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Showing posts with label Cancer Index. Show all posts
Showing posts with label Cancer Index. Show all posts

Biological Explanation: How Abortion Causes Breast Cancer

ABORTION-BREAST CANCER SUMMARY

THE COALITION'S HISTORY

The coalition was organized in 1999 by a group which includes cancer survivors, women who’ve had abortions and others whose family members have had the disease. We came together because of our deep concern that women haven’t been informed about strong biological evidence and epidemiological research published since 1957 which provide overwhelming support for a cause and effect relationship between abortion and breast cancer. More than two dozen peer-reviewed studies conducted in different parts of the world report increased risk. Most of these studies were conducted by scientists describing themselves as abortion supporters.

Many physicians, however, are unaware of the research because they’ve not been educated by the “gatekeepers” in organized medicine. Other physicians may be aware of the research, but refuse to acknowledge the preponderance of the evidence because of personal ideology or their own involvement in performing or referring patients for abortions. Regardless of personally ideology, physicians who fail to inform their abortion-bound patients of the breast cancer risk, violate their legal duty to obtain informed consent and expose themselves to the risk of medical malpractice lawsuits.

Only a few decades ago, breast cancer was known to be a grandmother’s disease. Because of abortion, it has become a young woman’s disease, and breast cancer rates have skyrocketed over 40% since the surgical procedure was legalized in the U.S. in 1973.

Observing that breast cancer has emerged as a young woman’s illness only in recent decades, New Jersey breast cancer surgeon, Angela Lanfranchi, M.D., F.A.C.S., declared under oath in a California lawsuit that she has discussed the research with many physicians and encouraged them to get reproductive histories from their patients. Among the doctors who have obtained these histories, they’ve “found as I did that ... cases of breast cancer in young women are associated with an abortion history.” [[Agnes Bernardo, Pamela Colip, and Saundra Duffy-Hawkins v. Planned Parenthood Federation of America and Planned Parenthood of San Diego and Riverside Counties; Superior Court of the State of California, County of San Diego, August 15, 2001]

Our purpose is to educate women about abortion as a risk factor for breast cancer, help preserve their health and save lives. Women have the exclusive right to be decision makers where their own health care is concerned. This is why we’ve provided a comprehensive listing all of the research in order to give women the opportunity to review it and decide for themselves whether or not abortion causes breast cancer.

ABORTION -- A PREVENTABLE RISK FACTOR

It is not true that all women who have breast cancer have had abortions. It’s also untrue that all women who’ve had abortions will get breast cancer. Induced abortion is only one of the risk factors for the illness. However, it is the most preventable risk factor for breast cancer.

TWO WAYS THAT ABORTION RAISES BREAST CANCER RISK

There are two ways that abortion raises a woman’s risk for breast cancer. The first way is not debated. It’s called the "protective effect of childbearing," and scientists have acknowledged this effect for centuries. The second way is debated, and scientists have studied this effect - known as the "independent link" - since 1957. It has to do with this question: Does an abortion leave a woman with more cancer-vulnerable breast tissue than she had before she became pregnant?

First Way - Loss of the Protective Effect of Childbearing: Delayed First Term Pregnancy, Childlessness, Fewer Births, Decreased Breastfeeding

Scientists first observed in the 17th century that women’s reproductive histories impacted their risk for breast cancer when it was noticed that nuns were at high risk for the disease. Scientists surmised that childbearing provides women with increased protection.

Today’s medical experts agree that the best way women can reduce their lifetime risk for breast cancer is by: 1) Having an early first full term pregnancy (FFTP) starting before age 24; 2) Bearing more children; and 3) Breastfeeding for a longer lifetime duration. It’s undeniable that abortion causes women to change their childbearing patterns. It leads them to forego the protective effects of early FFTP, increased childbearing and breastfeeding. Consequently, scientists do not debate that it increases breast cancer risk in this first of two ways.

Despite these truths, there is not one cancer fundraising business that uses the phrase, "Abortion raises breast cancer risk." Not one of them has ever denounced Planned Parenthood for depriving women of the protective effect of childbearing or acknowledged that abortion contributes to the nation’s breast cancer rates at least in this way.

If childbearing reduces breast cancer risk, then choosing not to have that child means a greater breast cancer risk for the woman. Therefore, there is no debate among scientists that the woman who aborts has a greater breast cancer risk than does the woman who has a baby (assuming that her pregnancy lasts at least 32 weeks).

The Strongest Protective Factor

Medical experts have universally recognized since the publication of a landmark Harvard study in 1970 that the earlier a woman has her first full term pregnancy (FFTP), the lower her risk for breast cancer is. [MacMahon et al. (1970) Bulletin of the World Health Org 43:209-21]

Anti-cancer groups tell women that late FFTP (30 years of age or older) increases risk, but this is a half truth. A late FFTP is at age 24 or older. Each year that a woman delays her FFTP, her risk climbs markedly. A subsequent Harvard study reported that for each one year delay of a first full term pregnancy, risk is elevated 3.5%. [Trichopolous D, Hsieh Cc, MacMahon B, Lin T, et al. Age at Any Birth and Breast Cancer Risk. International J Cancer (1983) 31:701-704]

Nancy Krieger, PhD, wrote in 1989 that early FFTP had “emerged as the strongest protective factor” against the disease. [Breast Cancer Research and Treatment, 13:205-223]

Joel Brind, PhD, the lead author of the only comprehensive review and meta-analysis of the abortion-breast cancer research, stated in an affidavit in a California lawsuit that a single year’s delay of a FFTP impacts a woman’s risk of dying from breast cancer so greatly that it is about 10 times more than her risk of dying in childbirth. [Lawsuit referenced above]

For this reason, we encourage married women not to delay their FFTPs. We do, however, encourage abstinence before marriage.

Increased Childbearing and Breastfeeding

Scientists have long considered breastfeeding a likely protective factor, but this wasn’t confirmed until recently. In July 2002, a large meta-analysis of 47 epidemiological studies conducted in 30 countries and published in the British medical journal, Lancet, determined that women can reduce their relative risk of the disease by 4.3% for every 12 months of breastfeeding and 7.0% for each birth. It was concluded that skyrocketing breast cancer rates in the developed nations could be reduced by more than one-half if only women would bear more children and breastfeed for longer duration. [Beral, V (July 20, 2002) Lancet 360:187-95]

Second Way - The Independent Link: An Increase in Cancer-Vulnerable Breast Tissue

Abortion has been implicated with breast cancer in yet another way, however, and estrogen overexposure is the explanation for it. There is staggering evidence of an independent link between abortion and breast cancer. What this means is that a woman who has an abortion is left with more cancer-vulnerable cells than she had before she ever became pregnant. Biological evidence and more than two dozen studies worldwide support a cause and effect relationship. Fifteen studies were conducted on American women, and 13 of them reported risk elevations. Seven found a more than a twofold elevation in risk. Seventeen are statistically significant, 16 of which demonstrated a positive association. The term “statistical significance” means that scientists are at least 95% certain that their findings are not due to chance or error.

The evidence of a causal relationship between abortion and breast cancer isn’t only based on a statistical relationship either. Scientists also require biological evidence and a reasonable biological explanation before concluding that there’s a causal relationship. These requirements have been met.

Biological Evidence

Researchers were able to demonstrate that 77.7% of a group of rats given abortions could be caused to develop breast cancers with the carcinogen DMBA. On the other hand, 0% of the rats allowed to have a full term pregnancy, but not allowed to nurse their pups, developed tumors when exposed to DMBA. Among a group of 9 rats allowed to have a full term pregnancy and nurse their pups, only one developed a tumor. Among two groups of virgin rats, 66.7% and 71.4% developed tumors after being exposed to the carcinogen. Rats with abortion histories were at the greatest risk of all 5 groups. The experiment demonstrated that an induced abortion resulted in close to a 80% risk elevation among rats. [Russo J, Russo IH (1980) Am J Pathol 100:497-512]

ESTROGEN - THE “SMOKING GUN”

Most of the risk factors associated with breast cancer involve estrogen overexposure. Women who experience more menstrual cycles are exposed to higher levels of estradiol, a form of estrogen, over the course of their lifetimes. Women who reach puberty at an early age or menopause at a late age or who have fewer or no children, experience more menstrual cycles. Ergo, they are known have a higher risk of breast cancer. Women who have more children and who nurse them, on the other hand, experience fewer menstrual cycles and reduce their risk of breast cancer by doing so. Similarly, a low fat diet and avoidance of alcohol reduce a woman’s exposure to estrogen.

Estrogen is a secondary carcinogen. It promotes the growth of normal and abnormal tissue. In fact, estrogen replacement therapy, which is generally the same chemical form as the estrogen naturally produced by a woman’s ovaries, was included on our nation’s list of known carcinogens in 2001.

For an exhaustive explanation of estrogen’s role in the promotion of breast cancer, see the Web Site for the Breast Cancer Prevention Institute at and click on “The Estrogen Connection,” www.BCPInstitue.org.

Biological Explanation for the Link

The explanation for the independent link makes good biological sense. It remains unrefuted and unchallenged by scientists because it is physiologically correct.

A never-pregnant woman has a network of primitive, immature and cancer-vulnerable breast cells which make up her milk glands. It is only in the third trimester of pregnancy - after 32 weeks gestation - that her cells start to mature and are fashioned into milk producing tissue whose cells are cancer resistant.

When a woman becomes pregnant, her breasts enlarge. This occurs because a hormone called estradiol, a type of estrogen, causes both the normal and pre-cancerous cells in the breast to multiply terrifically. This process is called “proliferation.” By 7 to 8 weeks gestation, the estradiol level has increased by 500% over what it was at the time of conception.

If the pregnancy is carried to term, a second process called “differentiation” takes place. Differentiation is the shaping of cells into milk producing tissue. It shuts off the cell multiplication process. This takes place at approximately 32 weeks gestation.

If the pregnancy is aborted, the woman is left with more undifferentiated -- and therefore cancer-vulnerable cells -- than she had before she was pregnant. On the other hand, a full term pregnancy leaves a woman with more milk producing differentiated cells, which means that she has fewer cancer-vulnerable cells in her breasts than she did before the pregnancy.

In contrast, research has shown that most miscarriages do not raise breast cancer risk. This is due to a lack of estrogen overexposure. Miscarriages are frequently precipitated by a decline in the production of progesterone which is needed to maintain a pregnancy. Estrogen is made from progesterone, so the levels of each hormone rise and fall together during pregnancy.

For a thorough biological explanation of the abortion-breast cancer link, see this second website for the Breast Cancer Prevention Institute, www.BCPInstitute.org and click on its online booklet, “Breast Cancer Risks and Prevention.”

EPIDEMIOLOGICAL RESEARCH

The first epidemiological study was reported in an English language journal in 1957. Researchers found a 160% elevation in risk among women who’d obtained abortions. [Segi M., et al. GANN (1957); 48 (Suppl): 1-63]

The first study to examine the abortion-breast cancer link among American women was published in 1981 and reported that abortion “appears to cause a substantial increase in risk of subsequent breast cancer.” A 140% risk elevation was reported. [Pike MC et al., British Journal of Cancer (1981;43:72-6]

Howe et al. 1989, the only statistically significant study conducted on American women in which medical records of abortion were used, not interviews after the fact, reported a 90% increased risk of breast cancer among women in New York who had chosen abortion. [Howe et al. (1989) Int J Epidemiol 18:300-4]

Our bar graphs reveal the relative risk found for each epidemiological study. These graphs were developed for our website by Chris Kahlenborn, M.D., author of the book, Breast Cancer, Its Link to Abortion and the Birth Control Pill.

World’s Only Comprehensive Review and Meta-Analysis

In 1996, Professor Joel Brind of Baruch College in New York and his colleagues at Pennsylvania State Medical College conducted a review and meta-analysis of the studies. A meta-analysis pools together the data from the studies in an area of medicine - in this case, the abortion-breast cancer research - and comes up with an overall risk for a particular risk factor. The Brind team, half of whom included abortion supporters, found an overall 30% elevated risk among women choosing abortion after first full term pregnancy (FFTP) and a 50% elevated risk among women choosing abortion before FFTP. [Brind, et al. Jrnl of Epidemiol Community Health (1996);50:481-96]

Number of Additional Breast Cancer Cases

The average American woman already has a high lifetime risk of breast cancer - 12.5%. One in 8 women can be expected to be diagnosed with the disease in her lifetime. If this already high lifetime risk is increased by even a small percentage - 30% - then many thousands more women will develop breast cancer who would not otherwise have developed it.

Using conservative figures, Dr. Brind has estimated that there are presently an additional 5,000 to 8,000 cases of breast cancer per year due to earlier abortions and that by the year 2020 there will be an additional 40,000 to 50,000 cases of breast cancer yearly.

Royal College of Obstetricians and Gynecologists

On March 13, 2000 the U.K.'s Royal College of Obstetricians and Gynecologists became the first medical organization to warn its abortion practitioners, saying that Dr. Brind's review was methodologically sound and that the abortion-breast cancer research "could not be disregarded." [“Evidence-based Guideline No. 7: The Care of Women Requesting Induced Abortion” (2000) RCOG Press, p. 29-30]

Later that summer after the London press learned of the RCOG’s warning, the BBC and The Guardian strenuously objected. Angry, post-abortive women, who hadn’t been informed of the breast cancer risk, called their doctors to learn what they could do to reduce their risks and otherwise protect their health. After being intimidated by members of the press who don't respect human life, the RCOG put its tail between its legs and dutifully withdrew the warning.

The incident reveals the cowardice of the RCOG’s leadership. It demonstrates what the medical group was willing to say when it thought it was politically safe to do so.

Today, the RCOG says that the relationship between abortion and breast cancer is "inconclusive." The group repeats the falsehood that the abortion-breast cancer studies which relied on interviews, not medical records, contain a bias called "report bias." This hypothetical problem proposes that studies, which use interviews, are inherently flawed because there is allegedly a difference in the reporting levels between healthy women and unhealthy women. In other words, healthy women lie or underreport their abortions, but unhealthy women don’t. However, a far more reasonable hypothesis is that women, who don’t want to report their abortions to researchers truthfully, would refuse to participate in these studies in the first place.

If the RCOG’s claim of report bias were true, then the findings of scientists who relied on interviews would be inaccurate and artificial. However, the RCOG provides no citations to support its claim because there are none. The RCOG expects women to accept its phantom theory as if it were a fact. Truth is, there are no scientists who presently claim to have found credible evidence of such a bias or difference in reporting levels.

The RCOG says it relies on the supposed findings of an abortionist, David Grimes, who is affiliated with the population control group, Family Health International. Despite the fact that Grimes clearly does not respect human life, the RCOG repeats his unsupported assertion that the studies which relied on medical records are superior to those relying on interviews.

Janet Daling et al. 1994

One especially disturbing study on women was done by Dr. Janet Daling and her colleagues at Seattle’s Fred Hutchinson Cancer Research Center in 1994. Dr. Daling, an abortion supporter, found that “among women who had been pregnant at least once, the risk of breast cancer in those who had experienced an induced abortion was 50% higher than among other women.”

Daling’s team found that teenagers under age 18 and women over 29 years of age who procure an abortion increase their breast cancer risk by more than 100%. Those with a family history of the disease increase their risk 80%. Daling’s most alarming finding was that teenagers with a family history of breast cancer who procure an abortion face a risk of breast cancer that is incalculably high. All 12 women in her study with this history were diagnosed with breast cancer by the age of 45. [Janet R. Daling et al., “Risk of Breast Cancer Among Young Women: Relationship to Induced Abortion,” 86 Journal of the National Cancer Institute; (1994);1584]

The 1997 and 1999 Melbye Studies

The abortion industry relies heavily upon Melbye et al. 1997, a study conducted on Danish women, to dispute the abortion-breast cancer link and dismiss more than two dozen studies finding risk elevations. However, even this study reported that “{w}ith each one-week increase in the gestational age of the fetus...there was a 3 percent increase in the risk of breast cancer.” The researchers, nevertheless, reported no overall positive association between abortion and breast cancer. [Melbye, et al. “Induced Abortion and the Risk of Breast Cancer,” New England Journal of Medicine (1997);336:81-5]

The Brind team argued in a letter to the New England Journal of Medicine that serious errors of misclassification and data adjustment in the Melbye study likely masked a significant risk increase. For instance, 60,000 women whose abortions were recorded in the Danish Life Statistics between 1940 and 1973 were counted by Melbye et al. as not having had abortions, although a number of them developed breast cancer. Additionally, Melbye and colleagues started recording breast cancer cases in 1968, but recorded abortions starting in 1973. It is clearly unscientific to start counting cases of a disease before the proposed cause of that disease. [Joel Brind & Vernon Chinchilli, Letter, ” Induced Abortion and the Risk of Breast Cancer,” 336 New England Journal of Medicine (1997) 1834-35]

In addition, Melbye and colleagues implicitly corrected these errors in a subsequent study in 1999. [Melbye M., Wohlfahrt J., Anderson A.M., Westergaard T., Andersen P.K., “Preterm Delivery and Risk of Breast Cancer,” British Journal of Cancer (1999);80:609-613]

In February of 2000, the New England Journal of Medicine, possibly the world’s most influential medical journal, admitted evidence of an abortion-breast cancer link in the text of an article written by researchers at the University of Pennsylvania School of Medicine, in spite of having published the much criticized Melbye study three years earlier. In reviewing risk factors for breast cancer the article stated, "Other risk factors have been less consistently associated with breast cancer (such as diet, use of oral contraceptives, lactation, and abortion)." [Armstrong K., et al., “Assessing the Risk of Breast Cancer,”NEJM (2000);342:564-71]

EXPERT TESTIMONY FROM THE CENTER FOR REPRODUCTIVE LAW AND POLICY

Center for Reproductive Law and Policy expert, Dr. Lynn Rosenberg, a Boston University Medical School epidemiologist, testified in the fall of 1999 in a Florida case on the abortion-breast cancer link. When asked by an attorney whether a pregnant 15 year old who aborts her pregnancy has a higher risk of breast cancer than one who carries her pregnancy to term, Dr. Rosenberg answered, “Probably, yes." [Dr. Joel Brind, “ABC in the Courts: Dramatic ABC Testimony in Florida’s Parental Notification Appeal,” Abortion-Breast Cancer Quarterly Update, (Fall, 1999) Vol. 2, No. 3, p. 1].

THE NATIONAL CANCER INSTITUTE

In July 1998, Congressman Tom Coburn M.D., an obstetrician-gynecologist, questioned a representative from the National Cancer Institute (NCI), Dr. Edison Liu, during a Commerce Committee hearing on the State of Cancer Research. Congressman Coburn accused the NCI of misleading the public and "selectively releasing data" on the abortion-breast cancer link.

Dr. Brind accused the NCI of publishing an “outright lie” about the research on its website. Its website in 1999 said, “The scientific rationale for an association between abortion and breast cancer is based on limited experimental data in rats and is not consistent with human data.”

Commenting on this falsehood from the NCI, Dr. Brind said, “It is consistent with human data, and it is not just based upon limited data and rats. There is all the other biological evidence of what happens during pregnancy and what it is that makes breast cancer cells grow and what is the difference between a spontaneous and induced abortion. In other words, the whole biological story is consistent.” [Transcript of the talks by Professor Joel Brind and Professor Robert Burton at an Endeavour Forum Public Meeting on the 24th of August 1999, at Malvern, Vic. 3144, Australia]

After Congressmen Coburn and Dave Weldon, M.D. and other members of Congress called for hearings into the NCI’s scientific misconduct, the NCI revised its web site in 1999 and removed its falsehood. Nevertheless, its web page discussing the abortion-breast cancer link, as well as its web pages later published, remained conspicuous for what they still did not tell women (i.e., the number of studies - worldwide and American - reporting increased risk; the number of studies reporting a more than twofold risk elevation; the number of statistically significant studies and the biological evidence).

On June 7, 2002, twenty-eight members of Congress, including Congressmen Weldon and Coburn, sent a letter and petition with their own fact sheet to the Secretary of Health and Human Services, Tommy Thompson. They objected to the NCI’s reliance on Melbye et al. 1997, labeled it a “flawed study,” and called the NCI’s fact sheet “scientifically inaccurate and misleading to the public.” They pointed out that the NCI fact sheet erroneously stated, “The current body of scientific evidence suggests that women who have had either induced or spontaneous abortions have the same risk as other women for developing breast cancer.” Addressing this claim, the Congressmen asserted, “This glossing over of the weight of published scientific evidence does not provide the public with the information they deserve.”

The Congressmen asked Secretary Thompson to have the fact sheet “reevaluated for accuracy and bias.” Later that month, the NCI web page was taken down.

MEDICAL AUTHORITIES ACKNOWLEDGE LINK PRIVATELY, NOT PUBLICLY

There is good reason to believe that medical authorities at the highest levels of organized medicine are aware that abortion causes breast cancer, but they will not speak of it publicly because it is political dynamite. Angela Lanfranchi, M.D., declared under oath in the lawsuit, Bernardo et al. v. Planned Parenthood, et al., that “Over the past three or four years, I have spoken with many authorities and people in a position to be well-informed. Some have been straightforward and said that they know it is a risk factor but felt it was ‘too political’ to speak about.” [Lawsuit referenced above]

WOMEN’S RIGHT TO SUE

John Kindley, an attorney who authored an article for the Wisconsin Law Review in 1999, discussed the issues of informed consent and the abortion-breast cancer connection. Informed consent is a legal obligation requiring physicians to fully inform their patients of the risks associated with any surgical procedures recommended by them. Mr. Kindley argued that physicians who do not inform their patients of the breast cancer risk expose themselves to considerable legal liability and can be sued for medical malpractice. He represents a North Dakota woman in a false advertising suit against a clinic which was distributing a pamphlet denying the existence of studies reporting increased risk among women choosing abortion.

SIGNIFICANCE OF THE RISK

Mr. Kindley explains how the increased risk of breast cancer resulting from an induced abortion impacts a woman’s lifetime risk:

“The real significance of a relative risk increase depends upon the background risk which is increased. For example, although smoking increases the risk of lung cancer by a factor of 10.0, the background risk of lung cancer for nonsmokers is very low. By contrast, an average American woman’s lifetime risk of breast cancer is about twelve percent. A 1.3 relative risk increase from an induced abortion would therefore indicate about a four percent increase in absolute terms. Estimating a twenty-five percent mortality rate, this figure would suggest that about 1 out of 100 women who have had an induced abortion die from breast cancer attributable to the abortion.” www.johnkindley.com, “The Fit Between the Elements for an Informed Consent Cause of Action and the Scientific Evidence Linking Induced Abortion with Increased Breast Cancer Risk,” Wisconsin Law Review, (1999); Vol. 1998, No. 6; p. 1620]

A "HEALTH CARE TIME-BOMB"

Congressman Dave Weldon M.D. sent a “Dear Colleague” letter and a copy of Mr. Kindley’s law review article to all members of the U.S. House of Representatives on August 24, 1999. He discussed the duty of physicians to properly inform patients of the risks associated with surgical procedures.

Dr. Weldon called abortion a “significant health risk” and a “health care time-bomb” in his letter.

WORLD’S FIRST KNOWN ABORTION-BREAST CANCER SETTLEMENT

The world’s first known abortion-breast cancer settlement was reported in Australia in 2001. An Australian woman who’d obtained an abortion sued her physician for medical malpractice. She claimed he failed to inform her of the research linking abortion with breast cancer and the possibility of emotional damage which she might suffer as a result of her abortion. Although she hadn’t developed breast cancer, her attorney, Charles Francis, said she nevertheless received a significant sum. [Patrick Goodenough, “First Case Linking Abortion-Breast Cancer Settled,” Cybercast News Service, www.CNSNews.com, January 4, 2002]

A WOMAN'S RIGHT TO KNOW

Women have the right to know about the abortion-breast cancer research. In fact, we find it paternalistic that women have been prevented from making informed choices about this women’s health issue.

Public health authorities have been seriously remiss about educating women and their doctors about the weight of the research. These authorities include: the National Cancer Institute, research scientists and the nation’s anti-cancer organizations whose own web pages discussing the research, in some cases, cite irrelevant studies for which no abortion data were collected. Others contain much misinformation, omissions of most or all of the studies, half truths and even fabrications.

Because of induced abortion, anti-cancer organizations guarantee themselves an ever increasing pool of donors who’ve been unwittingly victimized by this cover up - breast cancer patients, survivors and their family members. Many of these donors have become activists who’ve lobbied Congress for billions of dollars of taxpayer money to support increasingly more research into the causes of breast cancer and methods of prevention. We’re not opposed to research, but any anti-cancer organization which fails to truthfully inform women about what scientists have known for five decades and taxpayers and donors have paid for has no right to continually return to the wells of public or private money.

We seek to reach women -- and those who love them -- with life-saving information, and our cause is extremely urgent. Will you help us to ensure that the public is finally told the truth about abortion? Please share this information with others and send us your donation now to help with our cause.

Donations can be mailed to the Coalition on Abortion/Breast Cancer, P.O. Box 152, Palos Heights, Illinois 60463. Our coalition is recognized by the IRS as a 501(c)3 organization.

Source

How Many Types of CANCER are there?

A

Acute Lymphoblastic Leukaemia, Adult
Acute Lymphoblastic Leukaemia, Childhood
Acute Myeloid Leukaemia, Adult
Acute Myeloid Leukaemia, Childhood
Adrenocortical Carcinoma
Adrenocortical Carcinoma, Childhood
AIDS-Related Lymphoma
Anal Cancer
Astrocytoma, Childhood Cerebellar
Astrocytoma, Childhood Cerebral

B

Basal Cell Carcinoma, see Skin Cancer (non-Melanoma)
Bile Duct Cancer, Extrahepatic
Bladder Cancer
Bladder Cancer, Childhood
Bone Cancer, Osteosarcoma/Malignant Fibrous Histiocytoma
BRCA 1 & BRCA 2 Gene Testing
Brain Stem Glioma, Childhood
Brain Tumour, Adult
Brain Tumours, Childhood
Brain Tumour, Brain Stem Glioma, Childhood
Brain Tumour, Cerebellar Astrocytoma, Childhood
Brain Tumour, Cerebral Astrocytoma/Malignant Glioma, Childhood
Brain Tumour, Ependymoma, Childhood
Brain Tumour, Medulloblastoma, Childhood
Brain Tumour, Supratentorial Primitive Neuroectodermal Tumours, Childhood
Brain Tumour, Visual Pathway and Hypothalamic Glioma, Childhood
Breast Cancer
Breast Cancer and Pregnancy
Breast Cancer, Childhood
Breast Cancer, Male
Bronchial Adenomas/Carcinoids, Childhood
Burkitt's Lymphoma

C

Carcinoid Tumour, Childhood
Carcinoid Tumour,Gastrointestinal
Carcinoma of Unknown Primary
Central Nervous System Lymphoma, Primary
Cerebellar Astrocytoma, Childhood
Cerebral Astrocytoma/Malignant Glioma, Childhood
Cervical Cancer
Chronic Lymphocytic Leukaemia
Chronic Myelogenous Leukaemia
Chronic Myeloproliferative Disorders
CNS Lymphoma, Primary
Colon Cancer
Colorectal Cancer, Childhood
Cutaneous T-Cell Lymphoma, see Mycosis Fungoides and Sézary Syndrome

E

Endometrial Cancer
Ependymoma, Childhood
Esophageal Cancer
Esophageal Cancer, Childhood
Ewing's Family of Tumours
Extracranial Germ Cell Tumour, Childhood
Extragonadal Germ Cell Tumour
Extrahepatic Bile Duct Cancer
Eye Cancer, Intraocular Melanoma
Eye Cancer, Retinoblastoma

G

Gallbladder Cancer
Gastric (Stomach) Cancer
Gastric (Stomach) Cancer, Childhood
Gastrointestinal Carcinoid Tumour
Gene Therapy for Cancer
Germ Cell Tumour, Extracranial, Childhood
Germ Cell Tumour, Extragonadal
Germ Cell Tumour, Ovarian
Gestational Trophoblastic Tumour
Glioma, Adult
Glioma, Childhood Brain Stem
Glioma, Childhood Cerebral Astrocytoma
Glioma, Childhood Visual Pathway and Hypothalamic

H

Hairy Cell Leukaemia
Hepatocellular (Liver) Cancer, Adult (Primary)
Hepatocellular (Liver) Cancer, Childhood (Primary)
Histiocytoma of Bone, Malignant Fibrous/Osteosarcoma
Hodgkin's Lymphoma, Adult
Hodgkin's Lymphoma, Childhood
Hodgkin's Lymphoma During Pregnancy
Hypopharyngeal Cancer
Hypothalamic and Visual Pathway Glioma, Childhood

I

Intraocular (Eye) Melanoma
Islet Cell Carcinoma (Endocrine Pancreas)

K

Kaposi's Sarcoma
Kidney (Renal Cell) Cancer
Kidney (Renal Pelvis and Ureter, Transitional Cell) Cancer
Kidney Tumours of Childhood, Wilms' Tumour and Other

L

Laryngeal Cancer
Laryngeal Cancer, Childhood
Leukaemia, Acute Lymphoblastic, Adult
Leukaemia, Acute Lymphoblastic, Childhood
Leukaemia, Acute Myeloid, Adult
Leukaemia, Acute Myeloid, Childhood
Leukaemia, Chronic Lymphocytic
Leukaemia, Chronic Myelogenous
Leukaemia, Hairy Cell
Lip and Oral Cavity Cancer
Liver Cancer, Adult (Primary)
Liver Cancer, Childhood (Primary)
Lung Cancer, Non-Small Cell
Lung Cancer, Small Cell
Lymphoma, AIDS-Related
Lymphoma, Burkitt's
Lymphoma, Cutaneous T-Cell, see Mycosis Fungoides and Sézary Syndrome
Lymphoma, Hodgkin's, Adult
Lymphoma, Hodgkin's, Childhood
Lymphoma, Hodgkin's During Pregnancy
Lymphoma, Non-Hodgkin's, Adult
Lymphoma, Non-Hodgkin's, Childhood
Lymphoma, Non-Hodgkin's During Pregnancy
Lymphoma, Primary Central Nervous System

M

Macroglobulinemia, Waldenström's
Malignant Fibrous Histiocytoma of Bone/Osteosarcoma
Medulloblastoma, Childhood
Melanoma
Melanoma, Intraocular (Eye)
Merkel Cell Carcinoma
Mesothelioma, Adult Malignant
Mesothelioma, Childhood
Metastatic Squamous Neck Cancer with Occult Primary
Multiple Endocrine Neoplasia Syndrome, Childhood
Multiple Myeloma/Plasma Cell Neoplasm
Mycosis Fungoides
Myelodysplastic Syndromes
Myelodysplastic/Myeloproliferative Diseases
Myelogenous Leukaemia, Chronic
Myeloid Leukaemia, Adult Acute
Myeloid Leukaemia, Childhood Acute
Myeloma, Multiple
Myeloproliferative Disorders, Chronic

N

Nasal Cavity and Paranasal Sinus Cancer
Nasopharyngeal Cancer
Nasopharyngeal Cancer, Childhood
Neuroblastoma
Neuroectodermal Tumours and Pineoblastoma, Childhood Supratentorial Primitive
Non-Hodgkin's Lymphoma, Adult
Non-Hodgkin's Lymphoma, Childhood
Non-Hodgkin's Lymphoma During Pregnancy
Non-Small Cell Lung Cancer

O

Ooesophageal Cancer
Ooesophageal Cancer, Childhood
Oral Cancer, Childhood
Oral Cavity Cancer, Lip and
Oropharyngeal Cancer
Osteosarcoma/Malignant Fibrous Histiocytoma of Bone
Ovarian Cancer, Childhood
Ovarian Epithelial Cancer
Ovarian Germ Cell Tumour
Ovarian Low Malignant Potential Tumour

P

Pancreatic Cancer
Pancreatic Cancer, Childhood
Pancreatic Cancer, Islet Cell
Paranasal Sinus and Nasal Cavity Cancer
Parathyroid Cancer
Penile Cancer
Phaeochromocytoma
Pineoblastoma and Supratentorial Primitive Neuroectodermal Tumours, Childhood
Pituitary Tumour
Plasma Cell Neoplasm/Multiple Myeloma
Pleuropulmonary Blastoma
Pregnancy and Breast Cancer
Pregnancy and Hodgkin's Lymphoma
Pregnancy and Non-Hodgkin's Lymphoma
Primary Central Nervous System Lymphoma
Primitive Neuroectodermal Tumours, Childhood Supratentorial and Pineoblastoma
Prostate Cancer

R

Rectal Cancer
Renal Cell (Kidney) Cancer
Renal Cell (Kidney) Cancer, Childhood
Renal Pelvis and Ureter, Transitional Cell Cancer
Retinoblastoma
Rhabdomyosarcoma, Childhood

S

Salivary Gland Cancer
Salivary Gland Cancer, Childhood
Sarcoma, Ewing's Family of Tumours
Sarcoma, Kaposi's
Sarcoma, Soft Tissue, Adult
Sarcoma, Soft Tissue, Childhood
Sarcoma, Uterine
Sezary Syndrome
Skin Cancer (non-Melanoma)
Skin Cancer, Childhood
Skin Cancer (Melanoma)
Skin Carcinoma, Merkel Cell
Small Cell Lung Cancer
Small Intestine Cancer
Soft Tissue Sarcoma, Adult
Soft Tissue Sarcoma, Childhood
Squamous Cell Carcinoma, see Skin Cancer (non-Melanoma)
Squamous Neck Cancer with Occult Primary, Metastatic
Stomach (Gastric) Cancer
Stomach (Gastric) Cancer, Childhood
Supratentorial Primitive Neuroectodermal Tumours, Childhood

T

T-Cell Lymphoma, Cutaneous, see Mycosis Fungoides and Sézary Syndrome
Testicular Cancer
Thymoma, Childhood
Thymoma and Thymic Carcinoma
Thyroid Cancer
Thyroid Cancer, Childhood
Transitional Cell Cancer of the Renal Pelvis and Ureter
Trophoblastic Tumour, Gestational

U

Unknown Primary Site, Carcinoma of, Adult
Unknown Primary Site, Cancer of, Childhood
Unusual Cancers of Childhood
Ureter and Renal Pelvis, Transitional Cell Cancer
Urethral Cancer
Uterine Cancer, Endometrial
Uterine Sarcoma

V

Vaginal Cancer
Visual Pathway and Hypothalamic Glioma, Childhood
Vulvar Cancer

W

Waldenström's Macroglobulinaemia
Wilms' Tumour

TESTICULAR CANCER

Testicular cancer is a disease in which malignant (cancer) cells form in the tissues of one or both testicles.

The testicles are 2 egg-shaped glands located inside the scrotum (a sac of loose skin that lies directly below the penis). The testicles are held within the scrotum by the spermatic cord, which also contains the vas deferens and vessels and nerves of the testicles.

The testicles are the male sex glands and produce testosterone and sperm. Germ cells within the testicles produce immature sperm that travel through a network of tubules (tiny tubes) and larger tubes into the epididymis (a long coiled tube next to the testicles) where the sperm mature and are stored.

Almost all testicular cancers start in the germ cells. The two main types of testicular germ cell tumours are seminomas and nonseminomas. These 2 types grow and spread differently and are treated differently. Nonseminomas tend to grow and spread more quickly than seminomas. Seminomas are more sensitive to radiation. A testicular tumour that contains both seminoma and nonseminoma cells is treated as a nonseminoma.

Testicular cancer is the most common cancer in men 20 to 35 years old.

Health history can affect the risk of developing testicular cancer.

Anything that increases the chance of getting a disease is called a risk factor. Risk factors for testicular cancer include:

  • Having had an undescended testicle.
  • Having had abnormal development of the testicles.
  • Having a personal or family history of testicular cancer.
  • Having Klinefelter's syndrome.
  • Being white.

Possible signs of testicular cancer include swelling or discomfort in the scrotum.

These and other symptoms may be caused by testicular cancer. Other conditions may cause the same symptoms. A doctor should be consulted if any of the following problems occur:

  • A painless lump or swelling in either testicle.
  • A change in how the testicle feels.
  • A dull ache in the lower abdomen or the groin.
  • A sudden build-up of fluid in the scrotum.
  • Pain or discomfort in a testicle or in the scrotum.

Tests that examine the testicles and blood are used to detect (find) and diagnose testicular cancer.

The following tests and procedures may be used:

  • Physical exam and history: An exam of the body to check general signs of health, including checking for signs of disease, such as lumps or anything else that seems unusual. The testicles will be examined to check for lumps, swelling, or pain. A history of the patient's health habits and past illnesses and treatments will also be taken.
  • Ultrasound exam: A procedure in which high-energy sound waves (ultrasound) are bounced off internal tissues or organs and make echoes. The echoes form a picture of body tissues called a sonogram.
  • Serum tumour marker test: A procedure in which a sample of blood is examined to measure the amounts of certain substances released into the blood by organs, tissues, or tumour cells in the body. Certain substances are linked to specific types of cancer when found in increased levels in the blood. These are called tumour markers. The following 3 tumour markers are used to detect testicular cancer:
  • o Alpha-fetoprotein (AFP).
    o Beta-human chorionic gonadotropin (β-hCG).
    o Lactate dehydrogenase (LDH).
    Tumour marker levels are measured before radical inguinal orchiectomy and biopsy, to help diagnose testicular cancer.
    • Radical inguinal orchiectomy and biopsy: A procedure to remove the entire testicle through an incision in the groin. A tissue sample from the testicle is then viewed under a microscope to check for cancer cells. (The surgeon does not cut through the scrotum into the testicle to remove a sample of tissue for biopsy, because if cancer is present, this procedure could cause it to spread into the scrotum and lymph nodes.) If cancer is found, the cell type (seminoma or nonseminoma) is determined in order to help plan treatment.

    Certain factors affect prognosis (chance of recovery) and treatment options.

    The prognosis (chance of recovery) and treatment options depend on the following:

    • Stage of the cancer (whether it is in or near the testicle or has spread to other places in the body, and blood levels of AFP, β-hCG, and LDH).
    • Type of cancer.
    • Size of the tumour.
    • Number and size of retroperitoneal lymph nodes.

    Testicular cancer is often curable.

    Treatment for testicular cancer can cause infertility.

    Certain treatments for testicular cancer can cause infertility that may be permanent. Patients who may wish to have children should consider sperm banking before having treatment. Sperm banking is the process of freezing sperm and storing it for later use.

    Stages of Testicular Cancer

    Key Points for This Section

    • After testicular cancer has been diagnosed, tests are done to find out if cancer cells have spread within the testicles or to other parts of the body.
    • The following stages are used for testicular cancer:
    • o Stage 0
      o Stage I
      o Stage II
      o Stage III

      After testicular cancer has been diagnosed, tests are done to find out if cancer cells have spread within the testicles or to other parts of the body.

      The process used to find out if cancer has spread within the testicles or to other parts of the body is called staging. The information gathered from the staging process determines the stage of the disease. It is important to know the stage in order to plan treatment. The following tests and procedures may be used in the staging process:

      • Chest x-ray: An x-ray of the organs and bones inside the chest. An x-ray is a type of energy beam that can go through the body and onto film, making a picture of areas inside the body.
      • CT scan (CAT scan): A procedure that makes a series of detailed pictures of areas inside the body, taken from different angles. The pictures are made by a computer linked to an x-ray machine. A dye may be injected into a vein or swallowed to help the organs or tissues show up more clearly. This procedure is also called computed tomography, computerised tomography, or computerised axial tomography.
      • Lymphangiography: A procedure used to x-ray the lymph system. A dye is injected into the lymph vessels in the feet. The dye travels upward through the lymph nodes and lymph vessels, and x-rays are taken to see if there are any blockages. This test helps find out whether cancer has spread to the lymph nodes.
      • Abdominal lymph node dissection: A procedure to examine lymph nodes in the abdomen. Lymph nodes are removed and a pathologist checks them for cancer cells. For patients with nonseminoma, removing the lymph nodes may help stop the spread of disease. Cancer cells in the lymph nodes of seminoma patients can be treated with radiation therapy.
      • Radical inguinal orchiectomy and biopsy: A procedure to remove the entire testicle through an incision in the groin. A tissue sample from the testicle is then viewed under a microscope to check for cancer cells. (The surgeon does not cut through the scrotum into the testicle to remove a sample of tissue for biopsy, because if cancer is present, this procedure could cause it to spread into the scrotum and lymph nodes.)
      • Serum tumour marker test: A procedure in which a sample of blood is examined to measure the amounts of certain substances released into the blood by organs, tissues, or tumour cells in the body. Certain substances are linked to specific types or cancer when found in increased levels in the blood. These are called tumour markers. The following 3 tumour markers are used in staging testicular cancer:
      • o Alpha-fetoprotein (AFP)
        o Beta-human chorionic gonadotropin (β-hCG).
        o Lactate dehydrogenase (LDH).
        Tumour marker levels are measured again, after radical inguinal orchiectomy and biopsy, in order to determine the stage of the cancer. This helps to show if all of the cancer has been removed or if more treatment is needed. Tumour marker levels are also measured during follow-up as a way of checking if the cancer has come back.

        The following stages are used for testicular cancer:

        Stage 0

        In stage 0, abnormal cells are found only in the tiny tubules where the sperm cells begin to develop. The cells do not invade normal tissues. This is sometimes called a "precancerous condition." Stage 0 cancer is also called carcinoma in situ. All tumour marker levels are normal.

        Stage I

        Stage I is divided into stage IA, stage IB, and stage IS and is determined after a radical inguinal orchiectomy is done.

        • In stage IA, the cancer is in the testicle and epididymis and may have spread to the inner layer of the membrane surrounding the testicle. All tumour marker levels are normal.
        • In stage IB, the cancer:
        • o is in the testicle and the epididymis and has spread to the blood or lymph vessels in the testicle; or
          o has spread to the outer layer of the membrane surrounding the testicle; or
          o is in the spermatic cord or the scrotum and may be in the blood or lymph vessels of the testicle.
          All tumour marker levels are normal.
          • In stage IS, the cancer is found anywhere within the testicle, spermatic cord, or the scrotum and either:
          • o all tumour marker levels are slightly above normal; or
            o one or more tumour marker levels are moderately above normal or high.

            Stage II

            Stage II is divided into stage IIA, stage IIB, and stage IIC and is determined after a radical inguinal orchiectomy is done.

            • In stage IIA, the cancer:
            • o is anywhere within the testicle, spermatic cord, or scrotum; and
              o has spread to up to 5 lymph nodes in the abdomen, none larger than 2 centimeters.
              All tumour marker levels are normal or slightly above normal.
              • In stage IIB, the cancer is anywhere within the testicle, spermatic cord, or scrotum; and either:
              • o has spread to up to 5 lymph nodes in the abdomen; at least one of the lymph nodes is larger than 2 centimeters, but none are larger than 5 centimeters; or
                o has spread to more than 5 lymph nodes; the lymph nodes are not larger than 5 centimeters.
                All tumour markers levels are normal or slightly above normal.
                • In stage IIC, the cancer:
                • o is anywhere within the testicle, spermatic cord, or scrotum; and
                  o has spread to a lymph node in the abdomen that is larger than 5 centimeters.
                  All tumour marker levels are normal or slightly above normal.

                  Stage III

                  Stage III is divided into stage IIIA, stage IIIB, and stage IIIC and is determined after a radical inguinal orchiectomy is done.

                  • In stage IIIA, the cancer:
                  • o is anywhere within the testicle, spermatic cord, or scrotum; and
                    o may have spread to one or more lymph nodes in the abdomen; and
                    o has spread to distant lymph nodes or to the lungs.
                    The level of one or more tumour markers may range from normal to slightly above normal.
                    • In stage IIIB, the cancer:
                    • o is anywhere within the testicle, spermatic cord, or scrotum; and
                      o may have spread to one or more nearby or distant lymph nodes or to the lungs.
                      The level of one or more tumour markers may range from normal to high.
                      • In stage IIIC, the cancer:
                      • o is anywhere within the testicle, spermatic cord, or scrotum; and
                        o may have spread to one or more nearby or distant lymph nodes or to the lungs or anywhere else in the body.
                        The level of one or more tumour markers may range from normal to very high.

                        Recurrent Testicular Cancer

                        Recurrent testicular cancer is cancer that has recurred (come back) after it has been treated. The cancer may come back many years after the initial cancer, in the other testicle or in other parts of the body.

                        Treatment Option Overview

                        Key Points for This Section

                        • There are different types of treatment for patients with testicular cancer.
                        • Testicular tumours are divided into 3 groups, based on how well the tumours are expected to respond to treatment.
                        • o Good Prognosis
                          o Intermediate Prognosis
                          o Poor Prognosis
                        • Three types of standard treatment are used:
                        • o Surgery
                          o Radiation therapy
                          o Chemotherapy
                        • New types of treatment are being tested in clinical trials. These include the following:
                        • o High-dose chemotherapy with stem cell transplant
                        • Lifelong follow-up exams are very important for men who have had testicular cancer.

                        There are different types of treatment for patients with testicular cancer.

                        Different types of treatments are available for patients with testicular cancer. Some treatments are standard (the currently used treatment), and some are being tested in clinical trials. Before starting treatment, patients may want to think about taking part in a clinical trial. A treatment clinical trial is a research study meant to help improve current treatments or obtain information on new treatments for patients with cancer. When clinical trials show that a new treatment is better than the standard treatment, the new treatment may become the standard treatment.

                        Clinical trials are taking place in many parts of the country. Information about ongoing clinical trials is available from the NCI Web site. Choosing the most appropriate cancer treatment is a decision that ideally involves the patient, family, and health care team.

                        Testicular tumours are divided into 3 groups, based on how well the tumours are expected to respond to treatment.

                        Good Prognosis

                        For nonseminoma, all of the following must be true:

                        • The tumour is found only in the testicle or in the retroperitoneum (area outside or behind the abdominal wall); and
                        • The tumour has not spread to organs other than the lungs; and
                        • The levels of all the tumour markers are slightly above normal.

                        For seminoma, all of the following must be true:

                        • The tumour has not spread to organs other than the lungs; and
                        • The level of alpha-fetoprotein (AFP) is normal. Beta-human chorionic gonadotropin (β-hCG) and lactate dehydrogenase (LDH) may be at any level.

                        Intermediate Prognosis

                        For nonseminoma, all of the following must be true:

                        • The tumour is found in one testicle only or in the retroperitoneum (area outside or behind the abdominal wall); and
                        • The tumour has not spread to organs other than the lungs; and
                        • The level of any one of the tumour markers is more than slightly above normal.

                        For seminoma, all of the following must be true:

                        • The tumour has spread to organs other than the lungs; and
                        • The level of AFP is normal. β-hCG and LDH may be at any level.

                        Poor Prognosis

                        For nonseminoma, at least one of the following must be true:

                        • The tumour is in the center of the chest between the lungs; or
                        • The tumour has spread to organs other than the lungs; or
                        • The level of any one of the tumour markers is high.

                        There is no poor prognosis grouping for seminoma testicular tumours.

                        Three types of standard treatment are used:

                        Surgery

                        Surgery to remove the testicle (radical inguinal orchiectomy) and some of the lymph nodes may be done at diagnosis and staging. (Refer to the General Information and Stages sections of this summary.) Tumours that have spread to other places in the body may be partly or entirely removed by surgery.

                        Even if the doctor removes all the cancer that can be seen at the time of the surgery, some patients may be given chemotherapy or radiation therapy after surgery to kill any cancer cells that are left. Treatment given after the surgery, to increase the chances of a cure, is called adjuvant therapy.

                        Radiation therapy

                        Radiation therapy is a cancer treatment that uses high-energy x-rays or other types of radiation to kill cancer cells. There are two types of radiation therapy. External radiation therapy uses a machine outside the body to send radiation toward the cancer. Internal radiation therapy uses a radioactive substance sealed in needles, seeds, wires, or catheters that are placed directly into or near the cancer. The way the radiation therapy is given depends on the type and stage of the cancer being treated.

                        Chemotherapy

                        Chemotherapy is a cancer treatment that uses drugs to stop the growth of cancer cells, either by killing the cells or by stopping the cells from dividing. When chemotherapy is taken by mouth or injected into a vein or muscle, the drugs enter the bloodstream and can reach cancer cells throughout the body (systemic chemotherapy). When chemotherapy is placed directly into the spinal column, an organ, or a body cavity such as the abdomen, the drugs mainly affect cancer cells in those areas (regional chemotherapy). The way the chemotherapy is given depends on the type and stage of the cancer being treated.

                        New types of treatment are being tested in clinical trials. These include the following:

                        High-dose chemotherapy with stem cell transplant

                        High-dose chemotherapy with stem cell transplant is a method of giving high doses of chemotherapy and replacing blood-forming cells destroyed by the cancer treatment. Stem cells (immature blood cells) are removed from the blood or bone marrow of the patient or a donor and are frozen and stored. After the chemotherapy is completed, the stored stem cells are thawed and given back to the patient through an infusion. These reinfused stem cells grow into (and restore) the body’s blood cells.

                        Lifelong follow-up exams are very important for men who have had testicular cancer.

                        Men who have had testicular cancer have an increased risk of developing cancer in the other testicle. A patient is advised to regularly check the other testicle and report any unusual symptoms to a doctor right away.

                        Lifelong clinical exams are very important. The patient will probably have checkups once per month during the first year after surgery, every other month during the next year, and less often after that.

                        Treatment Options by Stage

                        Stage I Testicular Cancer

                        Treatment of stage I testicular cancer depends on whether the cancer is a seminoma or a nonseminoma.

                        Treatment of seminoma is usually surgery to remove the testicle, with or without radiation therapy to lymph nodes in the abdomen after the surgery, with lifelong follow-up.

                        Treatment of nonseminoma may include the following:

                        • Surgery to remove the testicle and lymph nodes in the abdomen, with lifelong follow-up.
                        • Surgery to remove the testicle, followed by chemotherapy and lifelong follow-up.
                        • Surgery to remove the testicle, with lifelong follow-up.

                        Stage II Testicular Cancer

                        Treatment of stage II testicular cancer depends on whether the cancer is a seminoma or a nonseminoma.

                        Treatment of seminoma may include the following:

                        • When the tumour is 5 centimeters or smaller, treatment is usually surgery to remove the testicle followed by radiation therapy to lymph nodes in the abdomen and pelvis, with lifelong follow-up.
                        • When the tumour is larger than 5 centimeters, treatment is usually surgery to remove the testicle followed by combination chemotherapy or radiation therapy to lymph nodes in the abdomen and pelvis, with lifelong follow-up.

                        Treatment of nonseminoma may include the following:

                        • Surgery to remove the testicle and lymph nodes, with lifelong follow-up.
                        • Surgery to remove the testicle and lymph nodes, followed by combination chemotherapy and lifelong follow-up.
                        • Surgery to remove the testicle followed by combination chemotherapy and a second surgery if cancer remains, with lifelong follow-up.
                        • Combination chemotherapy before surgery to remove the testicle, for cancer that has spread and is thought to be life-threatening.
                        • A clinical trial of combination chemotherapy instead of removing the lymph nodes.

                        Stage III Testicular Cancer

                        Treatment of stage III testicular cancer depends on whether the cancer is a seminoma or a nonseminoma.

                        Treatment of seminoma may include the following:

                        • Surgery to remove the testicle followed by combination chemotherapy. Any tumour remaining after treatment will need lifelong follow-up.
                        • A clinical trial of a new therapy.
                        • A clinical trial of high-dose chemotherapy with bone marrow transplant.

                        Treatment of nonseminoma may include the following:

                        • Surgery to remove the testicle, followed by combination chemotherapy.
                        • Combination chemotherapy followed by surgery to remove any remaining tumour. Additional chemotherapy may be given if the tumour tissue removed contains cancer cells that are growing.
                        • Combination chemotherapy combined with radiation therapy to the brain for cancer that has spread to the brain.
                        • Combination chemotherapy before surgery to remove the testicle, for cancer that has spread and is thought to be life-threatening.
                        • A clinical trial of a new therapy.
                        • A clinical trial of high-dose chemotherapy with bone marrow transplant.

                        Treatment Options for Recurrent Testicular Cancer

                        Treatment of recurrent testicular cancer may include the following:

                        • Combination chemotherapy.
                        • High-dose chemotherapy with bone marrow transplant.
                        • Surgery to remove cancer that has either:
                        • o come back more than 2 years after complete remission; or
                          o come back in only one place and does not respond to chemotherapy.
                        • A clinical trial of a new therapy

Tamoxifen

Tamoxifen is an oral selective oestrogen receptor modulator which is used in breast cancer treatment, and is currently the world's largest selling breast cancer treatment. It is used for the treatment of early and advanced breast cancer in pre- and post-menopausal women. It is also approved by the Food and Drug Administration (FDA) for the reduction of the incidence of breast cancer in women at high risk of developing the disease. It has been further approved for the reduction of contralateral (in the opposite breast) breast cancer.

Tamoxifen competes with oestrogen in the body for oestrogen receptors in breast tissue so that transcription of oestrogen-responsive genes is inhibited.

Tamoxifen was invented by ICI Pharmaceuticals (now AstraZeneca) and is sold under the brand names Nolvadex, Istubal, and Valodex. It is also available as a generic drug in a number of countries. In the United States and other countries, Tamoxifen was almost always referred to by its generic name even before its patents expired.

A rare condition occasionally treated with tamoxifen is retroperitoneal fibrosis.

Tamoxifen is sometimes used to treat gynaecomastia in men. Tamoxifen is also used by bodybuilders in a steroid cycle to try and prevent or reduce drug-induced gynaecomastia caused by steroids that are used in the same cycle.

Tamoxifen is also used to treat infertility in women with anovulatory disorders. A dose of 10-40 mg per day is administered in days 3-7 of a woman's cycle.

On April 17, 2006, it was announced that raloxifene is equally effective in reducing the incidence of breast cancer, but caused fewer side effects.

Side effects

Tamoxifen is a selective oestrogen receptor modulator. Even though it is an antagonist in breast tissue it acts as partial agonist on the endometrium. Therefore endometrial changes, including cancer, are among tamoxifen's side effects. For some women, tamoxifen can cause a rapid increase in triglyceride concentration in the blood.

4-hydroxytamoxifen
4-hydroxytamoxifen is a form of the drug tamoxifen that is made by the body after taking tamoxifen. It can also be made in the laboratory, and may help decrease breast density. A topical form of 4-hydroxytamoxifen is being studied in breast cancer screening.

Pharmacogenetics

Patients with variant forms of the gene CYP2D6 (also called simply 2D6) may not receive full benefit from tamoxifen. On Oct 18, 2006 the Subcommittee for Clinical Pharmacology recommended relabeling tamoxifen to include information about this gene in the package insert.

Source: wikipedia GFDL

PROSTATE SPECIFIC ANTIGEN (PSA) SCREENING

Prostate-specific antigen (PSA) test is a test that measures the level of PSA in the blood. PSA is used to screen for prostate cancer.

PSA is a substance made by the prostate that may be found in an increased amount in the blood of men who have prostate cancer.

PSA levels may also be high in men who have an infection or inflammation of the prostate or BPH (an enlarged, but noncancerous, prostate).

PROSTATE CANCER

Prostate cancer is a disease in which malignant (cancer) cells form in the tissues of the prostate.

The prostate is a gland in the male reproductive system located just below the bladder (the organ that collects and empties urine) and in front of the rectum (the lower part of the intestine). It is about the size of a walnut and surrounds part of the urethra (the tube that empties urine from the bladder). The prostate gland produces fluid that makes up part of the semen.

Prostate cancer is found mainly in older men. As men age, the prostate may get bigger and block the urethra or bladder. This may cause difficulty in urination or can interfere with sexual function. The condition is called benign prostatic hyperplasia (BPH), and although it is not cancer, surgery may be needed to correct it. The symptoms of benign prostatic hyperplasia or of other problems in the prostate may be similar to symptoms of prostate cancer.

Possible signs of prostate cancer include a weak flow of urine or frequent urination.

These and other symptoms may be caused by prostate cancer. Other conditions may cause the same symptoms. A doctor should be consulted if any of the following problems occur:

  • Weak or interrupted flow of urine.
  • Frequent urination (especially at night).
  • Trouble urinating.
  • Pain or burning during urination.
  • Blood in the urine or semen.
  • A pain in the back, hips, or pelvis that doesn't go away.
  • Painful ejaculation.

Tests that examine the prostate and blood are used to detect (find) and diagnose prostate cancer.

The following tests and procedures may be used:

  • Digital rectal exam (DRE): An exam of the rectum. The doctor or nurse inserts a lubricated, gloved finger into the rectum and feels the prostate through the rectal wall for lumps or abnormal areas.
  • Prostate-specific antigen (PSA) test: A test that measures the level of PSA in the blood. PSA is a substance made by the prostate that may be found in an increased amount in the blood of men who have prostate cancer. PSA levels may also be high in men who have an infection or inflammation of the prostate or BPH (an enlarged, but noncancerous, prostate).
  • Transrectal ultrasound: A procedure in which a probe that is about the size of a finger is inserted into the rectum to check the prostate. The probe is used to bounce high-energy sound waves (ultrasound) off internal tissues or organs and make echoes. The echoes form a picture of body tissues called a sonogram. Transrectal ultrasound may be used during a biopsy procedure.
  • Biopsy: The removal of cells or tissues so they can be viewed under a microscope by a pathologist. The pathologist will examine the biopsy sample to check for cancer cells and determine the Gleason score. The Gleason score ranges from 2-10 and describes how likely it is that a tumour will spread. The lower the number, the less likely the tumour is to spread. There are 2 types of biopsy procedures used to diagnose prostate cancer:
  • o Transrectal biopsy: The removal of tissue from the prostate by inserting a thin needle through the rectum and into the prostate. This procedure is usually done using transrectal ultrasound to help guide the needle. A pathologist views the tissue under a microscope to look for cancer cells.
    o Transperineal biopsy: The removal of tissue from the prostate by inserting a thin needle through the skin between the scrotum and rectum and into the prostate. A pathologist views the tissue under a microscope to look for cancer cells.

    Certain factors affect prognosis (chance of recovery) and treatment options.

    The prognosis (chance of recovery) and treatment options depend on the following:

    • The stage of the cancer (whether it affects part of the prostate, involves the whole prostate, or has spread to other places in the body).
    • The patient's age and health.
    • Whether the cancer has just been diagnosed or has recurred (come back).

    Prognosis also depends on the Gleason score and the level of PSA.

    Stages of Prostate Cancer

    Key Points for This Section

    • After prostate cancer has been diagnosed, tests are done to find out if cancer cells have spread within the prostate or to other parts of the body.
    • The following stages are used for prostate cancer:
    • o Stage I
      o Stage II
      o Stage III
      o Stage IV

      After prostate cancer has been diagnosed, tests are done to find out if cancer cells have spread within the prostate or to other parts of the body.

      The process used to find out if cancer has spread within the prostate or to other parts of the body is called staging. The information gathered from the staging process determines the stage of the disease. It is important to know the stage in order to plan treatment. The following tests and procedures may be used in the staging process:

      • Radionuclide bone scan: A procedure to check if there are rapidly dividing cells, such as cancer cells, in the bone. A very small amount of radioactive material is injected into a vein and travels through the bloodstream. The radioactive material collects in the bones and is detected by a scanner.
      • MRI (magnetic resonance imaging): A procedure that uses a magnet, radio waves, and a computer to make a series of detailed pictures of areas inside the body. This procedure is also called nuclear magnetic resonance imaging (NMRI).
      • Pelvic lymphadenectomy: A surgical procedure to remove the lymph nodes in the pelvis. A pathologist views the tissue under a microscope to look for cancer cells.
      • CT scan (CAT scan): A procedure that makes a series of detailed pictures of areas inside the body, taken from different angles. The pictures are made by a computer linked to an x-ray machine. A dye may be injected into a vein or swallowed to help the organs or tissues show up more clearly. This procedure is also called computed tomography, computerised tomography, or computerised axial tomography.
      • Seminal vesicle biopsy: The removal of fluid from the seminal vesicles (glands that produce semen) using a needle. A pathologist views the fluid under a microscope to look for cancer cells.

      The stage of the cancer is based on the results of the staging and diagnostic tests, including the original tumour biopsy. The biopsy is used to determine the Gleason score. The Gleason score ranges from 2-10 and describes how different the cancer cells look from normal cells and how likely it is that the tumour will spread. The lower the number, the less likely the tumour is to spread.

      The following stages are used for prostate cancer:

      Stage I

      In stage I, cancer is found in the prostate only. It cannot be felt during a digital rectal exam and is not visible by imaging. It is usually found accidentally during surgery for other reasons, such as benign prostatic hyperplasia. The Gleason score is low. Stage I prostate cancer may also be called stage A1 prostate cancer.

      Stage II

      In stage II, cancer is more advanced than in stage I, but has not spread outside the prostate. The Gleason score can range from 2-10. Stage II prostate cancer may also be called stage A2, stage B1, or stage B2 prostate cancer.

      Stage III

      In stage III, cancer has spread beyond the outer layer of the prostate to nearby tissues. Cancer may be found in the seminal vesicles. The Gleason score can range from 2-10. Stage III prostate cancer may also be called stage C prostate cancer.

      Stage IV

      In stage IV, cancer has metastasized (spread) to lymph nodes near or far from the prostate or to other parts of the body, such as the bladder, rectum, bones, liver, or lungs. Metastatic prostate cancer often spreads to the bones. The Gleason score can range from 2-10. Stage IV prostate cancer may also be called stage D1 or stage D2 prostate cancer.

      Recurrent Prostate Cancer

      Recurrent prostate cancer is cancer that has recurred (come back) after it has been treated. The cancer may come back in the prostate or in other parts of the body.

      Treatment Option Overview

      Key Points for This Section

      • There are different types of treatment for patients with prostate cancer.
      • Four types of standard treatment are used:
      • o Watchful waiting
        o Surgery
        o Radiation therapy
        o Hormone therapy
      • New types of treatment are being tested in clinical trials. These include the following:
      • o Cryosurgery
        o Chemotherapy
        o Biologic therapy
        o High-intensity focused ultrasound

        There are different types of treatment for patients with prostate cancer.

        Different types of treatment are available for patients with prostate cancer. Some treatments are standard (the currently used treatment), and some are being tested in clinical trials. Before starting treatment, patients may want to think about taking part in a clinical trial. A treatment clinical trial is a research study meant to help improve current treatments or obtain information on new treatments for patients with cancer. When clinical trials show that a new treatment is better than the standard treatment, the new treatment may become the standard treatment.

        Clinical trials are taking place in many parts of the country. Information about ongoing clinical trials is available from the NCI Web site. Choosing the most appropriate cancer treatment is a decision that ideally involves the patient, family, and health care team.

        Four types of standard treatment are used:

        Watchful waiting

        Watchful waiting is closely monitoring a patient's condition without giving any treatment until symptoms appear or change. This is usually used in older men with other medical problems and early-stage disease.

        Surgery

        Patients in good health are usually offered surgery as treatment for prostate cancer. The following types of surgery are used:

        • Pelvic lymphadenectomy: A surgical procedure to remove the lymph nodes in the pelvis. A pathologist views the tissue under a microscope to look for cancer cells. If the lymph nodes contain cancer, the doctor will not remove the prostate and may recommend other treatment.
        • Radical prostatectomy: A surgical procedure to remove the prostate, surrounding tissue, and seminal vesicles. There are 2 types of radical prostatectomy:
        • o Retropubic prostatectomy: A surgical procedure to remove the prostate through an incision (cut) in the abdominal wall. Removal of nearby lymph nodes may be done at the same time.
          o Perineal prostatectomy: A surgical procedure to remove the prostate through an incision (cut) made in the perineum (area between the scrotum and anus). Nearby lymph nodes may also be removed through a separate incision in the abdomen.
        • Transurethral resection of the prostate (TURP): A surgical procedure to remove tissue from the prostate using a resectoscope (a thin, lighted tube with a cutting tool) inserted through the urethra. This procedure is sometimes done to relieve symptoms caused by a tumour before other cancer treatment is given. Transurethral resection of the prostate may also be done in men who cannot have a radical prostatectomy because of age or illness.

        Impotence and leakage of urine from the bladder or stool from the rectum may occur in men treated with surgery. In some cases, doctors can use a technique known as nerve-sparing surgery. This type of surgery may save the nerves that control erection. However, men with large tumours or tumours that are very close to the nerves may not be able to have this surgery.

        Radiation therapy

        Radiation therapy is a cancer treatment that uses high-energy x-rays or other types of radiation to kill cancer cells. There are two types of radiation therapy. External radiation therapy uses a machine outside the body to send radiation toward the cancer. Internal radiation therapy uses a radioactive substance sealed in needles, seeds, wires, or catheters that are placed directly into or near the cancer. The way the radiation therapy is given depends on the type and stage of the cancer being treated.

        Impotence and urinary problems may occur in men treated with radiation therapy.

        Hormone therapy

        Hormone therapy is a cancer treatment that removes hormones or blocks their action and stops cancer cells from growing. Hormones are substances produced by glands in the body and circulated in the bloodstream. Some hormones can cause certain cancers to grow. If tests show that the cancer cells have places where hormones can attach (receptors), drugs, surgery, or radiation therapy are used to reduce the production of hormones or block them from working.

        Hormone therapy used in the treatment of prostate cancer may include the following:

        • Luteinizing hormone-releasing hormone agonists can prevent the testicles from producing testosterone. Examples are leuprolide, goserelin, and buserelin.
        • Antiandrogens can block the action of androgens (hormones that promote male sex characteristics). Two examples are flutamide and bicalutamide.
        • Drugs that can prevent the adrenal glands from making androgens include ketoconazole and aminoglutethimide.
        • Orchiectomy is a surgical procedure to remove one or both testicles, the main source of male hormones, to decrease hormone production.
        • Oestrogens (hormones that promote female sex characteristics) can prevent the testicles from producing testosterone. However, oestrogens are seldom used today in the treatment of prostate cancer because of the risk of serious side effects.

        Hot flashes, impaired sexual function, loss of desire for sex, and weakened bones may occur in men treated with hormone therapy.

        New types of treatment are being tested in clinical trials. These include the following:

        Cryosurgery

        Cryosurgery is a treatment that uses an instrument to freeze and destroy prostate cancer cells. This type of treatment is also called cryotherapy.

        Chemotherapy

        Chemotherapy is a cancer treatment that uses drugs to stop the growth of cancer cells, either by killing the cells or by stopping the cells from dividing. When chemotherapy is taken by mouth or injected into a vein or muscle, the drugs enter the bloodstream and can reach cancer cells throughout the body (systemic chemotherapy). When chemotherapy is placed directly into the spinal column, an organ, or a body cavity such as the abdomen, the drugs mainly affect cancer cells in those areas (regional chemotherapy). The way the chemotherapy is given depends on the type and stage of the cancer being treated.

        Biologic therapy

        Biologic therapy is a treatment that uses the patient's immune system to fight cancer. Substances made by the body or made in a laboratory are used to boost, direct, or restore the body's natural defenses against cancer. This type of cancer treatment is also called biotherapy or immunotherapy.

        High-intensity focused ultrasound

        High-intensity focused ultrasound is a treatment that uses ultrasound (high-energy sound waves) to destroy cancer cells. To treat prostate cancer, an endorectal probe is used to make the sound waves.

        Treatment Options by Stage

        Stage I Prostate Cancer

        Treatment of stage I prostate cancer may include the following:

        • Watchful waiting.
        • Radical prostatectomy, usually with pelvic lymphadenectomy, with or without radiation therapy after surgery. It may be possible to remove the prostate without damaging nerves that are necessary for an erection.
        • External-beam radiation therapy.
        • Implant radiation therapy.
        • A clinical trial of high-intensity focused ultrasound.
        • A clinical trial of radiation therapy.
        • A clinical trial evaluating new treatment options.

        Stage II Prostate Cancer

        Treatment of stage II prostate cancer may include the following:

        • Radical prostatectomy, usually with pelvic lymphadenectomy, with or without radiation therapy after surgery. It may be possible to remove the prostate without damaging nerves that are necessary for an erection.
        • Watchful waiting.
        • External-beam radiation therapy.
        • Implant radiation therapy.
        • A clinical trial of radiation therapy with or without hormone therapy.
        • A clinical trial of ultrasound-guided cryosurgery.
        • A clinical trial of hormone therapy followed by radical prostatectomy.
        • A clinical trial evaluating new treatment options.

        Stage III Prostate Cancer

        Treatment of stage III prostate cancer may include the following:

        • External-beam radiation therapy with or without hormone therapy.
        • Hormone therapy.
        • Radical prostatectomy, usually with pelvic lymphadenectomy, with or without radiation therapy after surgery.
        • Watchful waiting.
        • Radiation therapy, hormone therapy, or transurethral resection of the prostate as palliative therapy to relieve symptoms caused by the cancer.
        • A clinical trial of radiation therapy.
        • A clinical trial of ultrasound-guided cryosurgery.
        • A clinical trial evaluating new treatment options.

        Stage IV Prostate Cancer

        Treatment of stage IV prostate cancer may include the following:

        • Hormone therapy.
        • External-beam radiation therapy with or without hormone therapy.
        • Radiation therapy or transurethral resection of the prostate as palliative therapy to relieve symptoms caused by the cancer.
        • Watchful waiting.
        • A clinical trial of radical prostatectomy with orchiectomy.

        Treatment Options for Recurrent Prostate Cancer

        Treatment of recurrent prostate cancer may include the following:

        • Radiation therapy.
        • Prostatectomy for patients initially treated with radiation therapy.
        • Hormone therapy.
        • Pain medication, external radiation therapy, internal radiation therapy with radioisotopes such as strontium-89, or other treatments as palliative therapy to lessen bone pain.
        • A clinical trial of ultrasound-guided cryosurgery.
        • A clinical trial of chemotherapy or biological therapy.
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