Cancer is the primary and one of the most prominent causes of the rising global mortality rate, accounting for nearly 10 million deaths annually. Specific methods have been devised to cure cancerous tumours. Effective therapeutic approaches must be developed, both at the cellular and genetic level. Immunotherapy offers promising results by providing sustained remission to patients with refractory malignancies. Genetically modified T‑lymphocytic cells have emerged as a novel therapeutic approach for the treatment of solid tumours, haematological malignancies, and relapsed/refractory B‑lymphocyte malignancies as a result of recent clinical trial findings; the treatment is referred to as chimeric antigen receptor T‑cell therapy (CAR T‑cell therapy). Leukapheresis is used to remove T‑lymphocytes from the leukocytes, and CARs are created through genetic engineering. Without the aid of a major histocompatibility complex, these genetically modified receptors lyse malignant tissues by interacting directly with the carcinogen. Additionally, the outcomes of preclinical and clinical studies reveal that CAR T‑cell therapy has proven to be a potential therapeutic contender against metastatic breast cancer (BCa), triple‑negative, and HER 2+ve BCa. Nevertheless, unique toxicities, including (cytokine release syndrome, on/off‑target tumour recognition, neurotoxicities, anaphylaxis, antigen escape in BCa, and the immunosuppressive tumour microenvironment in solid tumours, negatively impact the mechanism of action of these receptors. In this review, the potential of CAR T‑cell immunotherapy and its method of destroying tumour cells is explored using data from preclinical and clinical trials, as well as providing an update on the approaches used to reduce toxicities, which may improve or broaden the effectiveness of the therapies used in BCa.
Keywords: B‑lymphocyte non‑Hodgkin lymphoma; T‑cell receptors; US Food and Drug Administration; anaphylaxis; breast cancer; chimeric antigen receptor t‑cell therapy; clinical trial; cytokine release syndrome; neurotoxicity; relapsed/refractory B‑cell malignancies.