Targeted cancer therapy is a newer treatment that may lessen traditional chemotherapy's adverse side effects. It works by recognizing specific mutations in cancer cells from patients. These mutations determine how well a specific medicine works against cancer. This means doctors can adapt their chemotherapy treatment to the exact malignancies causing issues.
Typically, 7% to 8% of cancer patients are suitable for targeted therapy because their cancer cells contain a specific mutation. Chronic myeloid leukemia (CML), characterized by the gene expression called BCR-ABL, is the first cancer type treated with this type of therapy. This medication has proven helpful in treating CML patients, and it is currently being utilized to treat other types of cancer.
Small compounds that penetrate the plasma membrane are used in targeted cancer therapy. They are directed at cancer cell surface receptors and intracellular signaling molecules. These chemicals can be taken orally and may be helpful in the treatment of cancer. These medications, however, must be closely managed. The success of targeted cancer therapy may differ from patient to patient, and many other factors must be considered, including the patient's ethnicity. The goal of targeted cancer therapy is to improve the quality of life for cancer patients.
Combination therapy with many medications can help to improve therapy efficacy by minimizing the need for each agent. Some combination medicines, however, may increase toxicity. Nevertheless, several combinations have been demonstrated to help shrink tumors and cancer stem cells. A combination of two medications, for example, can destroy cancer stem cells and heterogeneous cancer cells. Furthermore, combining a few anti-cancer medications can lower the likelihood of drug resistance while increasing the efficacy of the therapy.
Another primary type of targeted cancer therapy is medications targeting cancer proteins. For example, histone deacetylase (HDAC) inhibitors are increasingly being employed in clinical studies for a wide range of diseases. They cause apoptosis, reduce angiogenesis, and promote differentiation. For example, histone deacetylase inhibitors have been proven in studies to promote apoptosis in breast cancer and myeloma cells.
Primary care physicians are involved in a rising field of targeted cancer therapy. Understanding the side effects and drug interactions associated with these targeted cancer medicines is critical for cancer patients. For example, a patient with lung cancer may experience an unexpected side effect: new-onset acne. Erlotinib, an oral small molecule inhibitor, is another medication that may cause acne.
Targeting the heat-shock protein (HSP) receptor is another area of targeted cancer therapy. This molecule performs several tasks in the body, including playing a part in developing depression and violence. In addition, its ligand causes T-cell activation and programmed cell death. However, HSP expression is unusually high in malignancy. Furthermore, mutant versions of carcinogenic signaling proteins rely on HSP function.
Anti-angiogenic medicines are another successful technique for targeting cancer cells. They stop tumor cell growth by limiting them to oxygen and nutrients. This method is called metronomic chemotherapy, a new type of targeted cancer therapy. When combined with hypnotic therapies, these medicines can inhibit several pathways, reducing the likelihood of recurrence. However, it is vital to remember that numerous medicines are available to impede this process.
In addition to cancer cell targeting, nanoparticle-based drug delivery systems may aid in reversing tumor cell multidrug resistance. These nanoparticles can help patients endure higher dosages of chemotherapy by allowing medications to get through the body's immune system.
Another promising cancer therapeutic strategy inhibits the epidermal growth factor receptor (EGFR). By inhibiting EGFR with small-molecule tyrosine kinase inhibitors or antibodies targeting the receptor's extracellular domain, the ligand is prevented from binding to the receptor. The first anti-receptor medication targeting this pathway was produced for HER2 (HER2). Unfortunately, EGFR is overexpressed in a variety of malignancies. Furthermore, mutations that result in constitutive activation of the EGFR are linked to a variety of human malignancies.
Cancer stem cells are also vulnerable to epigenetic changes, which can be employed as therapeutic targets. For example, cancer stem cells harboring epigenetic modifier genes boosted proliferative activity in mice. However, the epigenome is highly malleable and reversible. HDACs and other epigenetic modifiers are common targets for cancer therapy. The dysregulation of these enzymes has been linked to the development of several forms of cancer.