What questions you would like to ask the experts about gyn cancer?
Women with gynecologic cancers, and their families and friends, have many questions
-- questions that we do not always think to ask at the doctor's office. "Answers from
the Pros" is our attempt to get answers from professionals
who deal with gyn cancers on a daily basis.
Please keep in mind the following guideline as your read through the
Answers from the Pros: We cannot provide treatment recommendations, possible diagnosis
or prognosis information for specific situations or individuals. Our panel of
medical professionals answer questions of a general nature that
may have relevance to others. Thank you.
Who are "the Pros"?
Editor Judy Knapp, Ph.D., MSW, will choose questions for
our EyesOnThePrize.org Medical Advisory Panel (MAP), a cross section
of medical professionals, who care for women with gyn cancers and related issues:
Please note that 'the pros' cannot give personal replies or medical advice--you
should check with your regular health care provider for direction about your
case. Please read our disclaimer.
We encourage you to seek answers to your questions in our FAQ
and Resources sections. You may also join
our discussion list to ask your questions of other cancer survivors.
Of course, ask your doctor questions about your specific situation.
Lynch Syndrome is a genetic condition that predisposes to cancer. The other name for Lynch syndrome is hereditary nonpolyposis colorectal cancer syndrome (HNPCC). As indicated in the name, HNPCC is an inherited predisposition to colon cancer that is associated with few colon polyps. HNPCC also results in susceptibility to cancers of the uterus, ovary, stomach, small intestine, urinary tract and less commonly brain tumors. Individuals with HNPCC have increased risks to develop more than one type of cancer due to the underlying genetic susceptibility. Families with HNPCC commonly have a history of colon and uterine cancers in several generations. Often the cancers are diagnosed prior to age 50.
HNPCC is caused by inheriting a nonfunctioning gene. Mutations (genetic changes) in one of three genes, MLH1, MSH2 and MSH6, account for most cases of HNPCC, though other genes have been associated. Everyone, men and women alike, have two copies of each of these genes. One copy of each gene is inherited from our mother and the other from our father, which means that a nonworking copy of the gene can be passed from either parent. An individual with HNPCC has a 50/50 chance to pass the susceptibility each time they parent a child. Genes usually play a role in correcting errors in the genetic information (DNA); however if one of these genes does not work due to a mutation, it cannot do its job. In these cases, DNA mistakes accumulate, which affects other important genes and there is an increased risk for cancer to develop.
HNPCC accounts for only about 5% of all cases of colon and uterine cancer. This means that most of these cancers are not due to an inherited susceptibility. If there is sufficient concern about your personal or family history, testing may be offered that can evaluate the DNA code of the MLH1, MSH2 and MSH6 genes to identify a mutation. To find a cancer genetic counselor in your area go to www.nsgc.org and click on find a counselor. For more information about HNPCC go to www.genetichealth.com.
The timeline for initial evaluation and treatment of gynecologic cancers is highly variable, depending on circumstances. For example, a woman in pain or severely bleeding should be seen rapidly, have her diagnosis confirmed with appropriate tests and have therapy instituted immediately. Generally, this process should be accomplished within a few days to a week. On the other hand, patients whose diagnosis arises without symptoms, perhaps as a result of participation in a screening program, may expect to wait for a convenient time to be seen by a specialist. Sometimes this can take weeks to months.
Many people are surprised that there is a delay in the diagnosis of cancer, because they are under the impression that cancers are easy to spot. Of course, it is easy in hindsight to look at a problem from the past and attribute it to an undiagnosed cancer. Many of my patients ask me when their cancer began. This question is unanswerable. It goes without saying that if the cancer were found at the instant it began, every effort would be made to stop it from progressing. Early diagnosis does indeed increase the odds of successful outcome.
Some cancers progress slowly, some more quickly. Some patients have rapid institution of treatment after evaluation, and others have extreme and inexcusable delays. Many delays are unavoidable. Sometimes the delay is due to the cumbersome health care system. Sometimes patients may not be able to get appointments for doctor's visits or x-rays. Unfortunately, many women do not have resources such as time off from their jobs, health insurance, transportation or child care so that they can obtain healthcare in a timely manner.
Any plan for managing a known diagnosis of cancer should be discussed with the patient and her support person at length within a day and implemented within the next several days. Patients who may have anxiety due to inadequate understanding about the risks associated with their diagnosis should not be allowed to increase that anxiety during the period of emotional adjustment. Instead they need to be given accurate, complete information about the benefits of methodical and thorough assessment of disease coupled with expeditious treatment appropriate to the specific clinical situation.
The majority of ovarian cancer occurs for reasons that are not completely understood. About 10% of the time ovarian cancer is the result of an underlying hereditary (genetic) susceptibility. The susceptibility results from inheriting a nonfunctioning gene. Mutations (genetic changes) in either of two genes, BRCA1 and BRCA2, account for most of the genetic risk for ovarian cancer. Everyone, men and women alike, have two copies of each of the BRCA1 and BRCA2 genes. One copy of each is inherited from our mother and the other from our father, which means that a nonworking copy of the gene can be passed from either parent. These genes usually play a role in preventing tumors from forming; however if either of the genes does not work due to a mutation, it cannot do its job, and there is an increased risk for cancer to develop. Inheriting a nonfunctioning copy of one of these genes primarily increases the risk for ovarian and breast cancers, though the exact reasons for this are not yet known.
If a woman inherits one nonworking copy of either BRCA1 or BRCA2, her risk to develop ovarian cancer is increased and may be as high as 27-44% (general population less than 2%) in her lifetime and her risk to develop breast cancer may be as high as 50-87% (general population about 12%). Men who inherit a nonworking copy of the gene do have increased risks to develop breast and prostate cancers. However these risks are not as increased as those of the women who inherit the nonworking gene.
Most of the time, the family history provides clues to increase the suspicion for a hereditary susceptibility to cancer. Specifically, if there is a history of breast cancer before age 50 in one or more close relatives, if there is breast and ovarian cancer in the same bloodline, if there is a male with breast cancer and if there is a history of breast or ovarian cancer in several generations. In addition to family history, some ethnic groups such as the eastern European Jews (Ashkenazi) have a higher chance to carry a nonworking copy of the BRCA genes due to common ancestors. In some families, a hereditary susceptibility to ovarian cancer is due to mutations in other genes such as MLH1, MSH2, and MSH6 and known to cause a hereditary cancer syndrome called hereditary nonpolyposis colorectal cancer (HNPCC). In families with HNPCC, we can also commonly see a history of colon and uterine cancer, particularly at younger ages (before 50).
If you are concerned about your risk to have a hereditary susceptibility to cancer, there are genetics professionals with whom you can meet that can evaluate your risk to carry a nonworking copy of either BRCA1 or BRCA2. If there is sufficient concern about your personal or family history, a blood test may be offered that can evaluate the DNA code of the BRCA1 and BRCA2 genes to identify a mutation. To find a cancer genetic counselor in your area, go to www.nsgc.org and click on 'find a counselor'.
The recent news about the vaccine against cervical cancer is exciting. What is HPV (human papilloma virus) and how does it relate to cancer of the cervix? What does the vaccine do and who will benefit from it?
John Comerci, MD:
There are two main vaccine strategies historically speaking:
1. Live attenuated viruses are presented to the patient so he/she can make an immune response. Examples of these vaccines are smallpox, polio, measles, mumps, rubella, and chicken pox.
2. Proteins or killed viruses are presented to the patient to stimulate an immune response. Examples are pertussis, tetanus, influenza and hepatitis B.
The HPV vaccine falls into the second category. A virus like protein particle is generated via genetic recombination in yeast or bacterial cells. The virus like particle is the protein coat of the virus minus its genetic material so it is not considered live and therefore there is no risk of infection by the vaccine.
The vaccine is designed to stimulate the humoral immune system which means that specific antibodies are generated to prevent viral infection. The vaccine also stimulates immune cells (CD4 and CD8) to help prevent HPV infection.
There are two groups of HPV viruses; low risk and high risk subgroups. Low risk viruses (HPV 6 and 11) do not cause cervical cancer, but do cause gential warts. High risk HPV viruses (HPV 16 and 18) have been associated with precancerous lesions of the cervix and cervical cancer, and do not cause genitial warts.
The first HPV vaccine to show efficacy was a vaccine to HPV 16. The trial was published in the New England Journal of Medicine in 2002. It was a randomized double blinded study that had 2392 particiants. These participants received three consecutive doses of HPV 16 vaccine. The vaccine demonstrated 100 % efficacy in that there were no HPV infections detected in the vaccinated group of women nor were there any cases of cervical dysplasia. The most recent study published looked at a vaccine against both high risk and low risk HPV subtypes (6, 11, 16, 18). In this study, there was 100 % clinical efficacy in that there were no cases of genital warts or cervical dysplasia in the vaccinated group of women.
A cost estimate for the vaccine is $300. By vaccinating adolescent girls it is estimated that the vaccine would eliminate 224,255 cases of HPV, 112,710 cases of dysplasia, 33127 cases of cervical cancer, and 1340 deaths per year.
It is important to emphasize that the vaccine is not a treatment for women who already have cervical dysplasia or cancer. It would be administered as a preventive measure as most vaccines are in childhood or adolescence.
"Answers from the Pros" are given in general terms, and are not intended
to address individual medical needs. "Answers from the Pros" does not
give medical advice, but answers medical questions that always should
be verified with your doctor and care team. Do not rely solely on the
answers you receive from the "Answers from the Pros" section. Do not make any changes
in your treatment or medications, without consulting your doctor. If you
have an emergency, call 911 or your physician.