## 2 Classification of Breast Cancer by Histological, Molecular, and Morphological Characteristics
### Molecular Classification of Breast Cancer  
The conventional classification of breast cancer divides the tumors into various categories with varying prognoses and behaviors using morphology [26]. It has limits despite offering high-quality data for a low cost; therefore, there has been a hope that the new molecular approaches may aid in the improvement of the classification algorithms. Although much has been learned in recent years, molecular taxonomy is still evolving and is likely to alter over the next few years. It remains to be seen whether molecular categorization is as helpful for specific subtypes of breast cancer as it has been for ductal carcinoma, which is not a distinct kind. With the possibility of stratifying this neoplasm into multiple entities that call for particular treatments and monitoring measures, as well as a better knowledge of the pathophysiological pattern and clinical prognosis, molecular subtyping altered the perspective on breast cancer. Breast cancer can be categorized into different molecular subtypes based on the status of the progesterone receptor (PR), estrogen receptor (ER), and HER2. These subtypes include HER2+ (ER-/PR-/HER2+) luminal B (ER+/PR+/HER2+), luminal type A (ER+/PR+/HER2-), and basal-like (ER-/PR-/HER2-) [27; 28].  
Luminal A, the most prevalent subtype of breast cancer, accounts for 60-70% of all cases and is characterized by positive statuses for estrogen and progesterone receptors but a negative HER2 status [29]. As a result, endocrine therapies are considered the primary treatment approach for luminal A breast cancer. For instance, by preventing the aromatization of androgens to estrogens, aromatase inhibitors prevent the synthesis of estrogen. On the other hand, selective estrogen receptor degraders (SERDs), such as elacetrant and fulvestrant, hinder the translocation of estrogen receptors to the nucleus and destroy them [30], while selective estrogen receptor modulators (SERMs), such as tamoxifen, prevent the binding of estrogen and estrogen receptors [30]. The prognosis of luminal A breast cancer is more varied than that of other breast cancer subtypes, and some patients with this subtype of breast cancer have intrinsic or acquired resistance to these endocrine therapies.  
About 20% to 30% of cases of invasive breast cancer are caused by the luminal B molecular subtype, with a lower expression of estrogen receptors (ERs) [31]. The more biologically and clinically diverse luminal B subtype necessitates a thorough characterization to determine the best course of treatment for every patient [32]. Patients with luminal B (HER2-negative) BC were specifically categorized for survival results and recurrence scores using progesterone receptor (PR) and proliferative regulator (Ki-67) experiments [33]. Triple-negative breast cancers (TNBCs) make up 15% to 20% of all breast cancer cases [34]. TNBC is more prevalent in premenopausal women under the age of 40 and is extremely aggressive, developing faster, having a higher risk of metastasizing, and having a worse clinical result than hormone receptor-positive and HER2-enriched breast tumors [35]. The age-related increases in cancer risk are as follows: 1.5% at age 40, 3% at age 50, and at least 4% at age 70 [36], which consist of ER, PR, and HER2 [37].