Detection of Proteins and their Therapeutic Effects in patients with Triple-Negative Breast Cancer

Abstract

Tumor-secreted substances such as cytokines, growth factors, proteases, inhibitors of proteases, membrane and extracellular vesicle proteins, peptide hormones, and metabolic proteins are all examples of extracellular matrix (ECM) proteins; these are actively included in cancer secretion. To prevent chemotherapy-dependent cytotoxicity, tumor-promoting factors known as TCS are released by cancer cells. Lung cancer is the most prevalent cause of cancer mortality, while breast cancer is the most common cancer among women. A novel way of classifying breast cancer emerged because of the development of gene expression profiling. Breast cancer has been classified into five categories using a DNA microarray molecular taxonomy: luminal types A and B, HER2/neu type, normal breast, and basal type (Figure 1) [1, 2]. Whereas basal-type breast cancers (BLBC) are triple-negative” breast cancers because they are negative for the three indicators estrogen receptor, progesterone receptor, and HER2/neu gene amplification. Luminal-type tumors are continuously estrogen receptor-positive and have a good prognosis (TNBCs). This feature has resulted in a widespread synonymy mistake where TNBCs and BLBCs are interchangeable. Much of the biological variation in human cells and malignancies is caused by variations in transcriptional processes. Each cell has signaling regulatory mechanisms that transmit information about the identity of the cell to the surrounding environment, which controls how much each gene in the genome is expressed. In the United States and around the world, breast cancer is the most common kind of cancer among women. Molecular subtypes of breast cancer can be distinguished based on differences in gene expression, prognosis, and available treatments. Because of its propensity to develop resistance to conventional chemotherapy after an initial positive response, triple-negative breast cancer (TNBC) poses a clinical challenge. This subtype of breast cancer lacks the expression of the estrogen receptor (ER), progesterone receptor (PR), and human epidermal growth factor receptor-2 (HER2), making it ineligible for ER and HER2 targeted therapy; instead, patients must rely on conventional chemotherapy [3, 4]. High test scores, a poor prognosis, and an early age are linked to BLBC. Such instances are frequently recognized clinically using the triple-negative phenotypic description (ER, PR, and HER-2, all negative). For typical pathology specimens, BLBC-positive markers that are easily accessible include EGFR and cytokeratin 5/6. Although patients initially react well to chemotherapy, resistance to chemotherapy drugs develops in 50% to 80% of TNBC patients, which is a substantial contributor to breast cancer mortality. Determining and characterizing additional molecular processes and downstream pathways significant for TNBC onset, chemotherapy resistance, and recurrence is thus an urgent unmet need. The interaction of released substances with the tumor cells or surrounding tumor microenvironment is one mechanism that may affect the emergence of chemoresistance in TNBC (TME). There are groups of co-expressed genes that have been found, and their mRNA level variation has been linked to physiological variational traits. Based on significant variations in their gene expression patterns, tumors can be divided into subtypes. For cancer patients, chemotherapy is a prominent kind of treatment. The tumor returns after chemotherapeutic treatment and does not respond to fresh chemotherapy treatments (chemoresistance). Chemotherapy exposure can also change the kinds and amounts of TCS constituents. Therapyinduced TCS is the name of this syndrome.