Medicines may one day target papillary thyroid cancer based on its genetic source
Given that thyroid cancer is a disease that originates in mutations of DNA, an Italian researcher recently reviewed the state of genomic medicine, a healthcare field that has the potential to treat malignancies based on their genetic origins.
Mario Vitale, an oncologist and endocrinologist at the University of Naples Federico II, published an editorial in the Journal of Clinical Endocrinology and Metabolism (JCEM) stating that medications targeting particular enzymes may be able to mitigate papillary thyroid cancer (PTC) growth in patients with mutations of the serine/threonine-protein kinase B-Raf (BRAF) gene.
This gene encodes information that regulates the creation of proto-oncogene c-Raf, an enzyme that plays a crucial role in the molecular chain of events controlling cell growth, division and death in many thyroid cancers.
Previous studies have linked dozens of mutations in the BRAF gene to common forms of cancer. A report appearing in a 2003 issue of the JCEM found that one specific mutation, known as V599E, was found in 49 out of 170 cases of PTC, making it a particularly vulnerable "hot spot" for cancer-causing genetic variation.
In the new report, Vitale stated that chemotherapies that inhibit specific molecular targets - like tyrosine kinase receptors, kinases or oncogenes - may be able to more effectively dampen the growth of PTC caused by changes to the BRAF sequence.
As an example, the researcher indicated that in laboratory rodent models, c-Raf inhibitors have been found to slow the growth of cancer cells carrying BRAF mutations.
Vitale also pointed to other cellular mechanisms that can be pharmacologically influenced in order to reduce tumor cell survival. He noted that for any PTC site to grow beyond a couple of millimeters in diameters, the tissue area must create new blood vessels to feed the tumor, a process known as neoangiogenesis.
The oncologist stated that medications like bevacizumab, which targets signaling proteins that stimulate vascular growth, have been shown to significantly limit the proliferation of PTC. Vitale concluded that genomic medication and targeted protein inhibition lies on the frontier of PTC treatment.
At least 70 percent of all diagnoses of thyroid cancer are PTC, according to the Columbia University Department of Surgery.
Mario Vitale, an oncologist and endocrinologist at the University of Naples Federico II, published an editorial in the Journal of Clinical Endocrinology and Metabolism (JCEM) stating that medications targeting particular enzymes may be able to mitigate papillary thyroid cancer (PTC) growth in patients with mutations of the serine/threonine-protein kinase B-Raf (BRAF) gene.
This gene encodes information that regulates the creation of proto-oncogene c-Raf, an enzyme that plays a crucial role in the molecular chain of events controlling cell growth, division and death in many thyroid cancers.
Previous studies have linked dozens of mutations in the BRAF gene to common forms of cancer. A report appearing in a 2003 issue of the JCEM found that one specific mutation, known as V599E, was found in 49 out of 170 cases of PTC, making it a particularly vulnerable "hot spot" for cancer-causing genetic variation.
In the new report, Vitale stated that chemotherapies that inhibit specific molecular targets - like tyrosine kinase receptors, kinases or oncogenes - may be able to more effectively dampen the growth of PTC caused by changes to the BRAF sequence.
As an example, the researcher indicated that in laboratory rodent models, c-Raf inhibitors have been found to slow the growth of cancer cells carrying BRAF mutations.
Vitale also pointed to other cellular mechanisms that can be pharmacologically influenced in order to reduce tumor cell survival. He noted that for any PTC site to grow beyond a couple of millimeters in diameters, the tissue area must create new blood vessels to feed the tumor, a process known as neoangiogenesis.
The oncologist stated that medications like bevacizumab, which targets signaling proteins that stimulate vascular growth, have been shown to significantly limit the proliferation of PTC. Vitale concluded that genomic medication and targeted protein inhibition lies on the frontier of PTC treatment.
At least 70 percent of all diagnoses of thyroid cancer are PTC, according to the Columbia University Department of Surgery.
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