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    Four oncology treatment advances to watch


    2. Immunotherapy: CAR-T cells

    CAR-T cell therapy genetically engineers the patient’s own T cells, a type of white blood cell known as a lymphocyte, to attack the cancer. They are then reinfused back into the patient.

    “This therapy will be life-saving in a small portion of children and young adults with acute lymphoblastic lymphoma and has encouraging results in patients with a recurrence of non-Hodgkin lymphoma. Additionally, early clinical trial data on chronic lymphocytic leukemia, lymphoma, and multiple myeloma suggests this technology might have broad applicability in the treatment of blood cancers,” Seiden says. “Along with immune-oncology drugs and other immune enhancing strategies, checkpoint inhibitors and CAR-T cells are rapidly bringing advances in immunology to patients with advanced cancers.”

    FDA’s approval of Kymriah marked the first time that the agency approved a gene therapy. The drug, a CAR-T cell therapy, is for treating certain pediatric and young adult patients with relapsed or refractory B-cell precursor acute lymphoblastic leukemia. “While $475,000 is the price of one treatment, it is anticipated to be a much less costly alternative compared to patients who require ongoing care measured in years,” DeRosa says.

    3. Precision oncology

    Dong Zhang, PhD, associate professor of biomedical sciences, New York Institute of Technology College of Osteopathic Medicine, Old Westbury, New York, sees precision oncology as the future of oncology treatment. Precision oncology means that before treating a cancer patient, the oncologist will first obtain a molecular profile of the patient’s tumor to see if a treatment strategy has been proven to be effective for that specific kind of tumor.

    The profiling can be based on gene transcription pattern, mutation pattern (BRCA1/2), overexpression of a known oncogene (e.g., HER2 in breast cancers, EGFR in lung cancers), or other biomolecular markers. A patient’s tumor profiling can be used for diagnosis, treatment, or both. For example, several molecularly targeted agents have been approved to treat some blood cancers, breast cancers, lung cancers, and skin cancers.

    A new family of precision oncology drugs, called PARP inhibitors, has been effective in killing cancer cells in patients with a certain genetic background. Two examples of PARP inhibitors include Lynparza (olaparib), which FDA approved for adult patients with recurrent epithelial ovarian, fallopian tube, or primary peritoneal cancer who had a complete or partial response to platinum-based chemotherapy, in August 2017. Earlier, FDA approved Rubraca (rucaparib) in 2016 for treating patients with a BRCA mutation associated advanced ovarian cancer who were treated with two or more chemotherapies. Previously in 2014, FDA approved olaparib capsules for treating patients with certain BRCA-mutated advanced ovarian cancer who were treated with three or more prior lines of chemotherapy.

    Zhang explains that women carrying BRCA1 or BRCA2 (BRCA1/2) mutations are often at a higher risk of developing breast and ovarian cancers. “Human beings have two copies of each gene, one copy from each parent. For women carrying BRCA1/2 mutations, they inherited one good copy and one bad copy of the BRCA1/2 gene from their parents,” he says. “During the development of breast or ovarian cancers, the good copy either mutates or becomes deleted in tumor cells. However, the non-tumor cells in those women still likely maintain the good copy.”

    Since both copies of the BRCA1/2 gene either mutate or become deleted in tumor cells, the DNA repair pathway is not functional in those tumor cells and is replaced by another type of DNA repair process that is heavily relied on by an enzyme called PARP. Further blocking of the PARP enzyme by PARP inhibitors (PARPi) will severely compromise the tumor cells’ ability to repair DNA and likely lead to death of those cells.

    The name of this cell death process is therefore called synthetic lethality or synthetic killing. “Since the non-tumor cells still have the good copy of BRCA1/2 genes, the DNA repair pathway is still functional. Therefore, PARPi will likely not harm the non-tumor cells that much,” Zhang explains. “Clinical trials of PARPi showed that PARPi is more effective in killing cancer cells that have lost both copies of BRCA1/2 while having less toxic effects to non-tumor cells, as reflected by fewer side effects. Therefore, this synthetic lethal family of drugs should have fewer side effects compared to conventional chemotherapy drugs.”

    Next: Advancement #4



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