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Figure 1. Breast cancer. Schematic classification of breast cancer subtypes with relative prognosis and therapy. HER2: human epidermal
growth factor receptor 2

HR+ tumors can be treated with tamoxifen, letrozole, anastrozole, or exemestane, while HER2+ tumors
can be treated with monoclonal antibodies such as trastuzumab or pertuzumab, or with the tyrosine
[17]
kinase inhibitor lapatinib. The triple negative subtype is the most aggressive among breast cancers ,
[18]
with the highest risk of relapse within 5 years . Other genes frequently mutated that have a pivotal role
in development and progression of breast cancer are BRCA1/2 and TP53 tumor suppressor genes [17,19,20] .
The clinical outcome depends on the tumor stage at diagnosis, the presence of mutations in specific genes
(e.g., BRCA1/2, TP53, PTEN) and the specific subtype, which affects the hormone-, chemo-, or molecular
therapy response [Figure 1] [17,21] .

Ovarian cancer
Ovarian cancer is the fourth cancer, in terms of incidence, and the fourth cancer for mortality, among
[16]
female malignancies .
The asymptomatic growth of ovarian cancer leads to a late stage diagnosis when it has already invaded the
[22]
peritoneum and metastasized to distant organs .

Ovarian cancers are classified as epithelial ovarian cancer (EOC), accounting for up to 90% of the total,
and non-epithelial ovarian cancers, which arise from stromal and germ cells . Histologically, EOCs are
[23]
classified into five different subtypes: high-grade serous (HGS, accounting for 70% of the total ovarian
cancers), low-grade serous (LGS, about 5%), endometrioid (about 10%), clear cell (about 10%), and
[24]
mucinous (about 3%) [Figure 2] . In addition, some ovarian cancers present a non-specific histological
pattern.

All these histological types, except HGS, derive from precursor lesions and grow in a stepwise manner; they
are indolent and show a stable genome characterized by point mutations or amplifications and deletions in
oncogenes and tumor suppressors. Serous and mucinous tumors are characterized by mutated oncogenes,
such as BRAF and KRAS, whereas endometroid tumors carry PTEN mutations. Particularly, HGS ovarian
cancer presents TP53 mutations in 95% of patients and germline mutations in BRCA genes in 65-85% of
cases; this histological subtype is characterized by rapid growth and high aggressiveness [23,25] . Based on