Is ovarian tumor also a genetic disease?

Abnormalities in chromosome number and structure in ovarian tumors are of 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. So is ovarian tumor also a genetic disease?

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).

Malnutrition can reduce the number of ovulations. In fact, ovulation is an important carcinogenic factor. Periodic ovulation repeatedly causes damage and stimulation to the ovarian mesothelium, and also lacks a persistent physiological recovery period. This can explain why the ovarian mesothelium has a tendency to malignant transformation compared to the peritoneum. Ovulation also produces defects and unevenness on the ovarian surface, which easily forms ovarian mesothelial closed cysts, allowing carcinogenic factors to accumulate and stay there for a long time and attach to the mesothelium.