Over the past decade, there have been significant advances in cancer treatment and research. A large part of this advancement is thanks to Targeted therapy’s success, otherwise known as precision medicine or personalized medicine that allows for individual cancer patients to receive treatment based on their own genetic information.
Because the target – (gene mutation or enzyme or receptor) may differ in each person even though the cancer may be the same type, target therapy is designed to reach the specific alteration or mutation on which tumors depend for their survival.
Target therapy aims to block the cancer cells’ signals/receptors, limiting the cancer cell’s life, destroying cancer cells without affecting healthy cells, and at the same time inducing less side effects.
Because Targeted therapies only work if the tumor has the right target. They can stop working if the target changes or if cancer finds a way around the treatment. In most cases, a patient’s tumor tissue must be tested to determine whether or not a target is present, with the understanding that not all types of cancers express the same targets.
For example, not every patient with breast cancer will have the mutated gene known as HER-2, the HER-2 protein may be a target in certain patients with breast cancer.
Also, in breast cancer and other hormonally promoted types of cancer such as ovaries and endometrial cancers, the presence of the estrogen receptor is a target for antiestrogen therapy with antihormonal such as Tamoxifen and aromatase inhibitors.
In patients with chronic myeloid leukemia – CML, the presence of an enzyme protein called BCR-ABL, which may have caused normal myeloid cells to start behaving like cancer cells, is the therapeutic target.
Other targeted therapies, called angiogenesis inhibitors, prevent blood supply formation causing the tumor to shrink. This is seen in some gastrointestinal and lung cancers.
The protein BRAF is present in its altered form BRAF V600E in many melanoma types. A drug that targets this mutant protein can be used to treat patients whose tumor contains this mutated BRAF protein. There are other cancers that might harbor this BRAF mutation such as colon cancer, lung cancer, etc.
PARP – poly-ADP ribose polymerase, a protein, and BRCA genes (BRCA1 and BRCA2) help repair DNA in cells. Gene mutations in the BRCA genes can cause damage to the PARP strands and block cell repair. PARP inhibitors are used to stop the PARP from repairing cancer cells. This targeted therapy may be offered to people with ovarian, fallopian tubes, peritoneal cancers, and metastatic HER2-negative breast cancer who have any of the BRCA gene mutations.
EGFR – epidermal growth factor receptor is a protein that helps cells grow and divide. Damage in a gene or mutation of the EGFR causes the EGFR to remain stuck, driving abnormal cell growth. Targeted therapy using drugs that block EGFR may be effective for people with non-small lung cancer with those EGFR mutations.
Although target therapy has become an essential part of cancer treatment, targeted therapy’s response depends widely on the cancer type and the corresponding molecular target. It remains a personalized approach for each individual with his/her own cancer-specific characteristics.
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