Can ovarian tumors be passed on to newborn babies?

Genetic predisposition is an important factor in the occurrence of a small number of epithelial ovarian cancers, and people have paid attention to the role of genetic factors in the etiology of ovarian tumors. It is estimated that about 10% to 15% of ovarian malignancies occur in familial clusters, of which only 5% conform to the dominant inheritance mode.

The high risk of ovarian cancer is determined based on pedigree analysis. If a woman's first-degree relatives have hereditary ovarian cancer or other related cancers (such as breast cancer in hereditary breast-ovarian cancer syndrome), the risk of their offspring having an abnormal genotype is 50%. Some people advocate that women with children whose estimated risk of hereditary ovarian cancer is as high as 50% can undergo preventive oophorectomy, but there is still a possibility of developing extraovarian serous papillary carcinoma originating from the pelvic intestinal epithelium after surgery.

Tumor cytogenetics

Abnormalities in chromosome number and structure in ovarian tumors have a reference value in assessing prognosis. The survival rate of the normal karyotype group is higher than that of the abnormal karyotype group, and the survival rate of the complex abnormal karyotype group is significantly lower than that of the normal karyotype group and the simple abnormal karyotype group.

1. Abnormal chromosome number: The chromosome changes in benign ovarian tumors are not significant, the most common being trisomy 12.

The changes in the number of chromosomes in malignant ovarian tumors can be divided into two categories, namely, near diploid and highly aneuploid, among which near diploid tumors have a better prognosis.

2. Chromosome structural abnormalities The changes in chromosome structure of malignant ovarian tumors are relatively complex, mainly concentrated on chromosomes 1, 2, 3, 6, 7, 9, 11, 14, and 17. Among them, the abnormalities of chromosomes 1, 3, and 6 are quite common, mainly deletions and rearrangements, and the breakpoints are located at 1p34, lp36, 3p14-21, and 6q15-21. Other common rearrangements occur in 7p, 10q, llp, 14q, and 19q. There are not many abnormalities in chromosomes 2, 4, and 5. Chromosome 10 trisomy in Eo borderline cystadenocarcinoma may be a specific change in the early stage of chromosomes.

3. Marker chromosomes Studies on tumor-specific marker chromosomes have found 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 cellular oncogenes that play an important role in tumor formation. The more important marker chromosomes for ovarian malignancies are isochromosomes i(1q), i(4p), i(5p), i(6p) and i(12p).