Breast cancer resistance to chemotherapy: When should we suspect it and how can we prevent it?

Abstract

Chemotherapy is an essential treatment for breast cancer, inducing cancer cell death. However, chemoresistance is a problem that limits the effectiveness of chemotherapy. Many factors influence chemoresistance, including drug inactivation, changes in drug targets, overexpression of ABC transporters, epithelial-to-mesenchymal transitions, apoptotic dysregulation, and cancer stem cells. The effectiveness of chemotherapy can be assessed clinically and pathologically. Clinical response evaluation is based on physical examination or imaging (mammography, ultrasonography, computed tomography scan, or magnetic resonance imaging) and includes tumor size changes after chemotherapy. Pathological response evaluation is a method based on tumor residues in histopathological preparations. We should be suspicious of chemoresistance if there are no significant changes clinically according to the Response Evaluation Criteria in Solid Tumors and World Health Organization criteria or pathological changes according to the Miller and Payne criteria, especially after 2–3 cycles of chemotherapy treatments. Chemoresistance is mostly detected after the administration of chemotherapy drugs. No reliable parameters or biomarkers can predict chemotherapy responses appropriately and effectively. Well-known parameters such as cancer type, grade, subtype, estrogen receptor, progesterone receptor, human epidermal growth factor receptor 2, Ki-67, and MDR-1/P-gP have been used for selecting chemotherapy regimens. Some new methods for predicting chemoresistance include chemosensitivity and chemoresistance assays, multigene expressions, and positron emission tomography assays. The latest approaches are based on evaluation of molecular processes and the metabolic activity of cancer cells. Some methods for preventing chemoresistance include using the right regimen, using some combination of chemotherapy methods, conducting adequate monitoring, and using drugs that could prevent the emergence of multidrug resistance.

Comparison of outcomes in patients with luminal type breast cancer treated with a gonadotropin-releasing hormone analog or bilateral salpingo-oophorectomy: A cohort retrospective study

“…Breast cancer is the leading cause cancer in women [ 13 ], with a 5-year overall survival rate of only 27% for individuals with metastatic breast cancer (MBC) [ 14 ]. A rapidly evolving understanding of cancer biology has led to the development of novel biomarkers and targeted therapy, even though significant improvement on the survival of patients with MBC remains elusive.…”

Synchronous breast cancer and non-Hodgkin lymphoma: A case report

“…3 ). After chemotherapy, the lump in the left breast had decreased to 0.5 cm in diameter based on ultrasonography (US) examination (i.e., partial clinical response according to RECIST criteria [1] , [5] ), whereas the lump in the neck had disappeared (i.e., complete clinical response according to RECIL criteria [6] ) ( Fig. 4 ).…”

“…Among women, breast cancer (BC) is the most prevalent type of cancer and the top cause of cancer deaths [1] . Following chemotherapy or radiotherapy, patients with BC are at greater risk of developing non-Hodgkin lymphoma (NHL), the most prevalent hematological cancer [2] .…”

Nanocarriers containing platinum compounds for combination chemotherapy

“…To evade apoptosis, platinum-resistant cancer cells often overexpress anti-apoptotic proteins (e.g., Bcl-2) ( Qin et al, 2018 ). It was also reported that pro-survival signal pathway (e.g., PI3K/AKT/mTOR pathway), epigenetic change, and tumor microenvironment also contributed to the development of drug resistance ( Hu et al, 2016 ; Prihantono and Faruk, 2021 ; Pomeroy et al, 2022 ). In addition, drug-induced autophagy increased in the platinum-resistant cells after treatment with platinum drugs, and the addition of autophagy inhibitors could effectively reduce drug resistance ( Lei et al, 2019 ).…”