Genetic aberration paves the way for new treatment of cancer disease
12-15 years of development and millions of dollars are typically the costs, when companies develop a new anti-cancer drug. Therefore all short cuts to a treatment are welcome…
12-15 years of development and millions of dollars are typically the costs, when companies develop a new anti-cancer drug. Therefore all short cuts to a treatment are welcome…
The study appears online in Nature Genetics. The discovery stems from a program at the U-M Comprehensive Cancer Center called Mi-ONCOSEQ in which patients with advanced cancer have their DNA and RNA sequenced to identify all types of genetic mutations that could play a role in the cancer. Researchers use the findings to help direct therapies they think will work best. But they also use the data to find new genetic links. …
The finding suggests that the fusion of NTRK1 to other genes fuels the growth of some lung adenocarcinomas (a form of non-small cell lung cancer), and that drugs that target NTRK1’s protein product could be effective in patients whose lung tumors harbor such fusions. "Treatment with targeted therapies is now superior to standard chemotherapy for many patients with lung cancers that harbor genetic changes including those with fusions involving the gene ALK," says Pasi A. Jänne, MD, PhD, of Dana-Farber, the senior co-author of the paper with Robert C. …
With the development of modern genomics sequencing tools, the discovery of additional genes implicated in breast cancer and the change in the legal status of genetic testing for BRCA1 and BRCA2, it is now possible to determine how often families in these circumstances actually do carry cancer-predisposing mutations in BRCA1, BRCA2, or another gene implicated in breast cancer, despite the results of their previous genetic tests. This was the challenge addressed by Mary-Claire King, Ph.D., American Cancer Society Professor of Medicine and Genome Sciences, and Tomas Walsh, Ph.D., Associate Research Professor of Medical Genetics, both at the University of Washington, Seattle. They conducted complete genomic sequencing of all genes implicated in breast cancer on DNA samples from breast cancer patients who had normal BRCA1 and BRCA2 commercial test results. …
In many cancers, a tumor suppressor protein called retinoblastoma is deactivated because of an increase in the activity of the proteins CDK 4 and 6. …
The findings were published in the journal Cancer Discovery and are currently available online. "We were able to demonstrate for the first time that different receptors within a single signaling pathway — in this case, the Wnt signaling pathway — can guide the phenotypic plasticity of tumor cells, and increased signaling of Wnt5A in particular can result in an increase in highly invasive tumor cells that are less sensitive to existing treatments for metastatic melanoma," said Ashani Weeraratna, Ph.D., assistant professor in the Tumor Microenvironment and Metastasis Program of Wistar’s NCI-designated Cancer Center, and senior corresponding author on the manuscript. …
The Lund University research team has looked at how cancer cells communicate with surrounding cells and how this encourages the development of malignant tumours. The idea is to try and inhibit tumours by disrupting this communication. The focus of their research is ‘exosomes’, small virus-like particles that serve as ‘transport packages’ for genetic material and proteins transmitted between cells. …
UCSF researcher Luika Timmerman, PhD, an investigator in the UCSF Helen Diller Family Comprehensive Cancer Center, found that many cell lines obtained from triple-negative breast cancer are especially dependent on cystine, one of the 20 amino acids that are the building blocks of proteins that all cells need. Timmerman used an FDA-approved drug to inhibit activity of a transporter protein that ferries cystine into triple-negative breast cancer cells, and found that it significantly inhibited their growth in culture and when the cancer cells were transplanted into mice…
"Doctors are looking for new ways to accurately predict prostate cancer patients’ prognoses, because the current methods that use disease stage, Gleason score, and PSA are not perfect," says Alan Meeker, Ph.D., assistant professor of pathology at The Johns Hopkins University School of Medicine and its Kimmel Cancer Center. "Telomere shortening is common in cancer, but the degree of shortening varies from one cancer cell to another within each patient, and this variability may give us a better idea of how prostate cancers behave." In the study, described in the October issue of Cancer Discovery, the scientists studied tissue samples from 596 men surgically treated for prostate cancer thought to be confined to the prostate and who were participants in a long-term follow-up study on men’s health. …
To investigate the function of LATs in prostate cancer, Qian Wang, Ph.D., of the Origins of Cancer Laboratory, Centenary Institute, Sydney, Australia, and colleagues studied LAT3 expression in tissue samples from prostate cancer patients, analyzed the function of LATs in cancer cells in vitro, used microarray data to determine which genes and pathways are associated with LAT function, and assessed the role of LAT1 and LAT3 in tumor formation, growth, and metastasis in mice. The researchers found that LAT3 was expressed at all stages of prostate cancer and that inhibition of LAT proteins inhibits nutrient signaling pathways and over 100 metastasis-related genes, including E2F transcription factors, resulting in cell cycle inhibition. In mice injected with prostate cancer cells, tumor formation, metastasis, and cell cycle progression were all inhibited when the LAT1 or LAT3 gene was knocked out. The authors conclude that "Targeting LAT transporters, thereby inhibiting leucine uptake, may offer a new therapeutic opportunity for metastatic CRPC, affecting tumor growth and metastasis through inhibition of M-phase cell cycle and mTORC1 signaling pathways." Wang et al…