The predisposition to endometrial cancer may be influenced by genetic variants in genes such as PTEN, MLH1, and PMS2, which are important in DNA repair and the regulation of cell growth. Mutations in these genes can lead to uncontrolled cell growth in the endometrium, increasing the risk of cancer development.

The susceptibility to breast cancer may be associated with genetic factors such as variants in genes like CHEK2, ATM, and PALB2, which may play a role in increasing the risk, although each of these genes contributes to a lesser extent to the overall risk. In addition, acquired somatic alterations in genes involved in cell cycle regulation, DNA repair, and hormonal signaling may also contribute to the development of this type of cancer. These include mutations in genes such as PIK3CA, TP53, and HER2, which can occur during a person's life and are not inherited from parents.

The predisposition to ovarian cancer may be related to mutations in genes such as BRCA1, BRCA2, and TP53. These mutations can compromise genomic integrity and cell cycle regulation, facilitating the development of cancerous cells in the ovaries.

Pancreatic cancer may be associated with mutations in genes such as BRCA2, KRAS, CDKN2A, and TP53. KRAS is one of the most common mutations in pancreatic tumors, driving uncontrolled cell growth. BRCA2, in addition to its role in breast and prostate cancer, also contributes to the risk of pancreatic cancer by affecting DNA repair. Variations in these genes may predispose to early and aggressive disease development.

The predisposition to prostate cancer may be influenced by variants in genes such as BRCA1, BRCA2, HOXB13, and genes of the HLA system. BRCA2, in particular, is associated with a higher risk of developing aggressive forms of the disease. Additionally, variants in genes that regulate androgen signaling, such as the androgen receptor (AR), may influence the progression of prostate cancer.

The predisposition to thyroid cancer may be influenced by genetic variants in genes such as RET, BRAF, and PTEN. Mutations in RET and BRAF are particularly associated with different types of thyroid cancer, including medullary carcinoma and papillary carcinoma, respectively.

The predisposition to develop uterine leiomyomas may be associated with variants in genes such as MED12, HMGA2, and COL4A5/COL4A6. These genes are involved in the regulation of smooth muscle growth and the extracellular matrix, contributing to the development of these benign tumors of the uterus.