Hereditary tendencies are an important factor in the development of a small proportion of epithelial ovarian cancers, so that people have already noticed the role of genetic factors in the etiology of ovarian tumors. It is estimated that about 10% to 15% of ovarian malignancies occur in the form of family clustering, of which only 5% are consistent with the dominant hereditary transmission pattern. The common types of hereditary ovarian malignancies are: concomitant with breast-ovarian cancer syndrome, hereditary non-polyposis colorectal cancer syndrome (I-ynch syndrome) type II, and hereditary ovarian cancer at specific sites. Ovarian cancer in the syndrome. The age of onset of ovarian cancer among these three types of ovarian cancer-prone family members was earlier than that of the general population. The average age at diagnosis was 49, 35, and 52 years respectively. The histological type of hereditary ovarian cancer was similar to that of ordinary ovarian cancer. The most common, moderately differentiated serous papillary cystadenoma. Less common are hereditary gastrointestinal polyposis with mucosal skin pigmentation (Peutz. Jeghers syndrome), ovarian granulosa-epitomal cell tumors, and ovarian fibroids in multiple sputum-like basal cell carcinoma syndromes. Cysts. Compared with ovarian epithelial tumors, hereditary ovarian germ cell tumors are rare, but the incidence of germ cell tumors in hereditary gonadal dysgenesis has been found to be relatively high. The high risk of ovarian cancer is determined based on pedigree analysis. In women of the first degree relatives, there are hereditary ovarian cancers or other related cancers (such as hereditary mammary gland cancer in the ovarian cancer syndrome). The risk of aberrant genotypes is 50%. It has been suggested that prophylactic oophorectomy is feasible for women with children and estimated hereditary ovarian cancer risk as high as 50%, but there is still the possibility of extraovarian serous papillary carcinoma arising from pelvic gastrointestinal epithelium.
First, the cytogenetics of tumors
The abnormality of chromosome number and structure of ovarian tumors has a reference value in the evaluation of prognosis. The survival rate of normal karyotype group is higher than that of abnormal karyotype group. The survival rate of complex abnormal karyotype group is obviously lower than that of normal karyotype group and simple abnormal karyotype. group.
(I) Abnormal chromosome number The chromosome changes in benign ovarian tumors are not significant, the most common being trisomy 12.
The number of chromosome changes in malignant ovarian tumors can be classified into two types, ie, near-diploid and high-heteroploid, with near-diploid tumors with better prognosis.
(II) Chromosome abnormalities The chromosome structure of malignant ovarian tumors is relatively complex, mainly concentrated on chromosomes 1, 2, 3, 6, 7, 9, 11, 14, and 17, with chromosomes 1, 3, and 6 abnormal. Very common, mainly missing and rearranged, with breakpoints at 1
P3-4, lp36, 3p14-21, 6q15-21. Other more common rearrangements occur at 7p,. 10q, llp,. 14q and 19q. The abnormalities of 2, 4 and 5 chromosomes are rare. Eo junctional cystadenocarcinoma chromosome 10 trisomy may be a specific early chromosome change.
(C) Marker chromosomes The study of tumor-specific marker chromosomes revealed that the breakpoints seen in chromosome rearrangements are highly consistent with the locations of rare and common fragile sites and are characterized by non-random chromosomal abnormalities. Many of the genes at these frequent breakpoints are cell oncogenes that play an important role in tumor formation. The more important marker chromosomes for ovarian malignancies are the ischemic chromosomes i(1q), i(4p), i(5p), i(6p) and i(12p).
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