Monday, August 31, 2009
MONDAY, Aug. 31 (HealthCare tips), Scientists have isolated a group of hereditary mutations involved in the growth of melanoma, the deadliest form of skin cancer. Their work may lead to therapy with existing drugs that aim the same mutations.
Led by Yardena Samuels of the National Human Genome Research Institute, the research team from the U.S. National Institutes of Health (NIH) sequenced the protein tyrosine kinase (PTK) gene family in tumor and blood example from people with metastatic melanoma. Their study is published in the September issue of the journal Nature Genetics.
"We have found what appears to be an Achilles' heel of a sizable share of melanomas," Samuels, an examiner in the cancer genetics branch of the institute's Division of Intramural Research, said in a NIH news release.
The PTK family includes many genes that, when mutated, promote many types of cancer, including brain, gastric and lung malignancies, according to background information provided in the news release. In the new NIH study, one PTK gene that appeared mainly suspicious was the ERBB4 gene. Scientists found ERBB4 changes in 19 percent of patients' tumors, making it the most frequently mutated PTK gene in melanoma. Additional lab studies found that melanoma cells with the ERBB4 imperfection were dependent on the mutant gene for their growth.
The researchers also found that two extra PTK genes , FLT1 and PTK2B , were mutated in about 10 percent of the tumor samples.
The discoveries could open up new avenues for therapies. For example, the researchers exposed that melanoma cells grew much more slowly when exposed to lapatinib (Tykerb), a chemotherapy drug that inhibits ERBB4. Lapatinib is already in use by some breast cancer patients. The NIH team is preparing a clinical trial using lapatinib in patients with metastatic melanoma harboring ERBB4 mutations.
"Though additional work is needed to gain a more complete understanding of these genetic mutations and their roles in cancer biology, our findings open the door to pursuing specific therapy that may prove useful for the treatment of melanoma with ERBB4 mutations," Samuels stated.
Led by Yardena Samuels of the National Human Genome Research Institute, the research team from the U.S. National Institutes of Health (NIH) sequenced the protein tyrosine kinase (PTK) gene family in tumor and blood example from people with metastatic melanoma. Their study is published in the September issue of the journal Nature Genetics.
"We have found what appears to be an Achilles' heel of a sizable share of melanomas," Samuels, an examiner in the cancer genetics branch of the institute's Division of Intramural Research, said in a NIH news release.
The PTK family includes many genes that, when mutated, promote many types of cancer, including brain, gastric and lung malignancies, according to background information provided in the news release. In the new NIH study, one PTK gene that appeared mainly suspicious was the ERBB4 gene. Scientists found ERBB4 changes in 19 percent of patients' tumors, making it the most frequently mutated PTK gene in melanoma. Additional lab studies found that melanoma cells with the ERBB4 imperfection were dependent on the mutant gene for their growth.
The researchers also found that two extra PTK genes , FLT1 and PTK2B , were mutated in about 10 percent of the tumor samples.
The discoveries could open up new avenues for therapies. For example, the researchers exposed that melanoma cells grew much more slowly when exposed to lapatinib (Tykerb), a chemotherapy drug that inhibits ERBB4. Lapatinib is already in use by some breast cancer patients. The NIH team is preparing a clinical trial using lapatinib in patients with metastatic melanoma harboring ERBB4 mutations.
"Though additional work is needed to gain a more complete understanding of these genetic mutations and their roles in cancer biology, our findings open the door to pursuing specific therapy that may prove useful for the treatment of melanoma with ERBB4 mutations," Samuels stated.
Labels: Skin cancer
