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For Patient - Gynaecological Cancer |
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Cancer |
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CANCER : Gynaecological
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There are several different types of cancers that can start in a woman's reproductive system. These include:
- (Cancer of the neck of the womb)
- Uterine / Endometrial Cancer (Cancer of the body of the womb)
- Vulval Cancer (Cancer of the external genitals)
- Vaginal Cancer (Cancer of the birth canal)
The two common types of cancer among above are discussed below. |
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OVARIAN CANCER
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Ovarian cancer is a disease in which normal ovarian cells begin to grow in an uncontrolled, abnormal manner and produce tumors in one or both ovaries. Three basic types of ovarian tumors exist, designated by where they form in the ovary. They include:
- Epithelial tumors
About 85 percent to 90 percent of ovarian cancers develop in the epithelium - the thin layer of tissue that covers the ovaries. This form of ovarian cancer generally occurs in postmenopausal women.
- Germ cell tumors
These tumors occur in the egg-producing cells of the ovary and generally occur in younger women.
- Stromal tumors
These tumors develop in the estrogen- and progesterone-producing tissue that holds the ovary together.
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Risk factors |
Several factors may increase risk of ovarian cancer. Having one or more of these risk factors means a higher risk than that of the average woman for developing cancer. These risk factors include:
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| Inherited gene mutations |
The most significant risk factor for ovarian cancer is having an inherited mutation in one of two genes called breast cancer gene 1 (BRCA1) and breast cancer gene 2 (BRCA2). These genes were originally identified in families with multiple cases of breast cancer, but they're also responsible for about 5 percent to 10 percent of ovarian cancers. Another known genetic link involves an inherited syndrome called hereditary nonpolyposis colorectal cancer (HNPCC). Individuals in HNPCC families are at increased risk of cancers of the uterine lining (endometrium), colon, ovary, stomach and small intestine. However, risk of ovarian cancer associated with HNPCC is lower than is that of ovarian cancer associated with BRCA mutations.
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| Family history |
Sometimes, ovarian cancer occurs in more than one family member but isn't the result of any known inherited gene alteration. Having a family history of ovarian cancer increases the risk of the disease, but not to the same degree as does having an inherited genetic defect.
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| Age |
Ovarian cancer most often develops after menopause. Although most cases of ovarian cancer are diagnosed in postmenopausal women, the disease also occurs in premenopausal women.
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| Childbearing status |
Women who have had at least one pregnancy appear to have a lower risk of developing ovarian cancer. Similarly, the use of oral contraceptives appears to offer some protection against ovarian cancer.
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| Infertility |
Studies indicate that infertility increases the risk of ovarian cancer, even without use of fertility drugs. The risk appears to be highest for women with unexplained infertility and for women with infertility who never conceive. Research in this area is ongoing.
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| Ovarian cysts |
Cyst formation is a normal part of ovulation in premenopausal women. However, cysts that form after menopause have a greater chance of being cancerous. The likelihood of cancer increases with the size of the growth and with age.
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| Hormone replacement therapy (HRT) |
Findings about the possible link between postmenopausal use of the hormones estrogen and progestin and risk of ovarian cancer have been inconsistent. Some studies indicate a slightly increased risk of ovarian cancer in women taking estrogen after menopause, but other studies show no significant increase in risk. However, in a large study published in the Journal of the National Cancer Institute in October 2006, researchers report that women who haven't had a hysterectomy and who used menopausal hormone therapy for five or more years face a significantly increased risk of ovarian cancer.
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| Obesity in early adulthood |
Studies have suggested that women who are obese at age 18 are at increased risk of developing ovarian cancer before menopause. Obesity may also be linked to more aggressive ovarian cancers, which can result in a shorter time to disease relapse and a decrease in the overall survival rate. |
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Ovarian Cancer Staging (TNM System) |
| When ovarian cancer is suspected, patients usually undergo an exploratory laparotomy to determine the stage of the disease (i.e., how far it has spread). To stage the cancer, the physician reviews the histopathology report from the samples obtained during laparotomy, as well as results from needle biopsy, blood tests, imaging studies, or other tests. Staging provides an estimate of disease-free survival, overall survival, and the risk for recurrence or relapse. Staging also helps the physician to choose appropriate treatment. |
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Staging System |
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| Stage I: |
Ovarian cancer that is confined to one or both ovaries.
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| Stage II: |
Ovarian cancer that has spread to pelvic organs (e.g., uterus, fallopian tubes), but has not spread to abdominal organs.
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| Stage III: |
Ovarian cancer that has spread to abdominal organs (e.g., abdominal lymph nodes, liver, bowel).
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| Stage IV: |
Ovarian cancer that has spread outside to distant sites (e.g., lung, brain, lymph nodes in the neck).
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| Recurrent: |
Ovarian cancer that has recurred (come back) even though the patient has completed treatment. |
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Ovarian cancer staging usually is described in terms of the FIGO system (staging scheme developed by the International Federation of Gynecology and Obstetrics) and the TNM system (classification system developed by the American Joint Committee on Cancer [AJCC]). |
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According to the TNM system:
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T = Tumor Size N = Node Involvement M = Metastasis Status
Ovarian cancer treatment ultimately depends upon such staging. In general, the lower the stage, the more favorable is the prognosis. |
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Ovarian cancer treatment ultimately depends upon such staging. In general, the lower the stage, the more favorable is the prognosis.
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T Stage (Tumors)
The primary tumor (T) is classified according to the following categories:
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| T1: |
Tumor is limited to one or both ovaries.
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| T1a: |
Tumor is limited to one ovary. The capsule, or outer wall of the tumor, is intact, there is no tumor on the ovarian surface, and there are no cancer cells in ascites (abdominal fluid build-up) or peritoneal lavage ("washings" from the abdominal cavity).
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| T1b: |
Tumor is limited to both ovaries. The capsule is intact, there is no tumor on the ovarian surface, and there are no cancer cells in ascites or peritoneal lavage.
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| T1c: |
Tumor is limited to one or both ovaries with any of the following: ruptured capsule (burst outer wall of the tumor), tumor on ovarian surface, or cancer cells in the ascites or peritoneal lavage. |
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| T2: |
Tumor involves one or both ovaries with spread into the pelvis.
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| T2a: |
Tumor has spread and/or attaches to the uterus and/or fallopian tubes. There are no cancer cells in ascites or peritoneal lavage.
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| T2b: |
Tumor has spread to other pelvic tissues. There are no cancer cells in ascites or peritoneal lavage.
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| T2c: |
Tumor has spread to pelvic tissues, with cancer cells in ascites or peritoneal lavage. |

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| T3: |
Tumor involves one or both ovaries, with microscopically confirmed peritoneal metastasis outside the pelvis and/or metastasis to regional (nearby) lymph node(s).
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| T3a: |
Microscopic peritoneal metastasis beyond the pelvis.
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| T3b: |
Macroscopic (visible to the naked eye) peritoneal metastasis beyond the pelvis, 2 cm or less in greatest dimension.
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| T3c: |
Peritoneal metastasis beyond the pelvis, more than 2 cm in greatest dimension. |
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Nodal staging (N)
The regional lymph nodes (N) are clinically divided into the following categories:
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| N0: |
Regional lymph nodes contain no cancer cells.
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| N1: |
Evidence of lymph node metastasis. |
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Spread /Metastatic Staging (M):
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| M0: |
No distant metastases are found (this excludes peritoneal metastasis). |
| M1: |
Distant metastases are present. |
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Stage Grouping
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The TNM system places ovarian cancer growth at a particular stage. There are four basic stage groupings within the TNM system:
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| Stage Ia: |
T1a, N0, M0
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| Stage Ib: |
T1b, N0, M0
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| Stage Ic: |
T1c, N0, M0 |

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| Stage IIa: |
T2a, N0, M0
Stage IIb: T2b, N0, M0
Stage IIc: T2c, N0, M0
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| Stage IIIa: |
T3a, N0, M0
Stage IIIb: T3b, N0, M0
Stage IIIc: T3c, N0, M0, or T(any), N1, M0
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| Stage IV: |
T(any), N(any), M1 |
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Tumor Grade |
Tumor grade generally refers to the degree of differentiation - or maturity - of the cells that make up the tumor within the ovary. Yet, worldwide, there are many different systems for the grading of ovarian cancers, without a common standard. Most investigators use criteria such as the architectural "pattern" of the cells and their nuclear content (e.g., DNA "ploidy," or how many pairs of chromosomes are present), although additional factors may be considered, such as the tumor's margin, invasion of the blood vessels, and penetration of the ovarian capsule (surface).
Most epithelial cancers are categorized by three grades of cells:
- Grade 1 - the least malignant, with well-differentiated cells
- Grade 2 - intermediate, with moderately differentiated cells
- Grade 3 - the most malignant, with poorly differentiated cells
The low-grade (e.g., Grade 1) tumors grow more slowly and have a better prognosis than high-grade tumors.
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Diagnostic imaging Tests |
Ultrasound |
CT / MRI |
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Intravenous pyelogram (IVP) |
PET-CT Scan |
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Laboratory Tests |
In addition to imaging studies, other tests may be used to help verify a diagnosis of ovarian cancer. These include blood analyses for tumor markers, tests for genetic mutations, and the microscopic examination of ovarian cells.
CA125 is a blood protein known as a tumor marker. Research has shown that roughly 85% of women with clinically apparent ovarian cancer have increased levels of CA125. CA125 is not a fool proof test, as the protein also is increased during the first trimester of pregnancy, during menstruation, and in the presence of noncancerous illnesses (e.g., liver failure, pelvic inflammatory disease, endometriosis) and cancers of other sites (e.g., breast, lung, pancreas, colorectal). Some ovarian cancers may not have elevated CA125.
Women who are at high risk because of a positive family history of ovarian and/or breast cancer should be offered BRCA1 and BRCA2 mutation screening. |
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Treatment |
Treatment of ovarian cancer usually involves a combination of surgery and chemotherapy.
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| Surgery |
If you want to preserve the option to have children and if your tumor is discovered early, your surgeon may remove only the involved ovary and its fallopian tube. However, this situation is rare, and subsequent chemotherapy can cause infertility. The vast majority of women with ovarian cancer require a more extensive operation that includes removing both ovaries, fallopian tubes, and the uterus as well as nearby lymph nodes and a fold of fatty abdominal tissue known as the omentum, where ovarian cancer often spreads. Depending upon the stage and involvement by the tumour, surgeon may also remove part of your intestines.
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| Chemotherapy |
After surgery, treatment is carried out with chemotherapy. The initial regimen for ovarian cancer includes the combination of carboplatin (Paraplatin) and paclitaxel (Taxol) injected into the bloodstream (intravenous administration). Extensive clinical trials prove that this combination is the most effective, though studies continue to look for ways to improve on it. The carboplatin-paclitaxel combination reduces tumor volume in about 80 percent of women with newly diagnosed ovarian cancer. Studies have also shown that the combination results in longer survival, compared with that of previously used chemotherapy drugs and combinations.
A more intensive regimen has recently been shown to improve survival in women with advanced ovarian cancer by combining standard intravenous chemotherapy with chemotherapy injected directly into the abdominal cavity through a catheter placed at the time of the initial operation. This intra-abdominal infusion exposes hard-to-reach cancer cells to higher levels of chemotherapy than can be reached intravenously. This treatment typically involves six rounds of both intravenous and abdominal chemotherapy.
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| Radiation therapy is not commonly used in Ovarian cancer. |
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Other Therapies; |
Immunotherapy |
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Gene Therapy |
Gene therapy eventually may provide some control over cancer susceptibility and its treatment. Ovarian cancer, like all cancers, is believed to result from a build-up of genetic defects within the cells. Genetic engineers hope to correct such damage by transplanting copies of normal genes into cells with genetic defects. In addition, genetic manipulation may enable researchers to alter tumor cells so that they "commit suicide," are targeted by the immune system, or become more sensitive to chemotherapy. Investigators also have spent a lot of time trying to improve the resistance of bone marrow cells to chemotherapeutic agents, so that the doses of such drugs can be intensified. The practical applications of gene therapy are still being refined.
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Hormone Therapy
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There have been many reports of the potential benefits of hormone treatments in patients with ovarian cancer that does not respond to conventional therapy. For example, individuals with treatment-resistant (refractory) epithelial cancers have been treated with:
- progestins - crude forms of the female sex hormone progesterone
- oestrogens - for example, diethylstilbestrol (DES)
- combination estrogen/progestin therapy
- antiestrogens
- androgens - male sex hormones
- gonadotropin - releasing hormone (GnRH) - a hormone of the hypothalamus that stimulates the release of ovary-related hormones from the pituitary gland.
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Unfortunately, the responses to such therapies have been variable and not particularly effective in the management of this disease. Recent findings suggest that hormone replacement therapy (HRT) is not harmful to women who have been treated for epithelial ovarian cancer. But HRT therapy is controversial, since some physicians believe that the use of oestrogen might increase the likelihood of cancer recurrence, for example in women with well-differentiated endometrioid carcinomas that may be hormone-sensitive.
Your treating doctor will be the best person to discuss management plan with you.
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