Abstract
Despite significant improvements in breast cancer treatment outcomes over the past 25 years, especially in a subset of hormone-dependent and HER2-expressing tumors, the disease remains the leading cause of death in women in the developed world. With the development of molecular biology and genetics, previously pathologically homogeneous nosological units disintegrate into subgroups of tumors, which differ not only in their characteristics, but especially in their biological behavior and response to treatment.
Gene expression profiling allowed the classification of breast cancer into four subgroups, the so-called "intrinsic subtypes" (luminal A, luminal B, HER2-enriched and "basal-like" and normal "breast-like"). Individual subgroups differ in incidence, survival, and response to treatment.
At the same time, they complement the information of classical clinical-pathological markers. With the development of genetic studies, the identification of other specific subtypes can be expected.
Recently, another subtype has been identified in mouse tumors and breast cancer cell lines, "Claudin-low", characterized as triple-negative invasive ductal carcinoma with a high frequency of metaplastic and medullary differentiation. This new subclassification, together with classical clinicopathological markers, should contribute to improving the success of treatment at a time of widespread development of new molecules of targeted therapy.
Approximately 75% of all breast tumors express hormone receptors, estrogenic or progesterone. Hormone therapy - whether using selective estrogen receptor modulators (tamoxifen) or aromatase inhibitors - is effective in about 2/3 of patients.
However, up to 1/3 of breast cancers are tumors primarily resistant to hormone therapy, and most patients who initially responded to hormone therapy become resistant to this therapy.