The variant, a difference in just one of the three billion “letters” in the human genome known as a single-nucleotide polymorphism (SNP), originates from indigenous Americans and confers significant protection from breast cancer, particularly the more aggressive estrogen receptor-negative forms of the disease, which generally have a worse prognosis. …
“According to research evidence, survival rates are considered equal,” explained dean Nancy Fahrenwald of the South Dakota State University College of Nursing. Working through the South Dakota Women’s Cancer Network, the South Dakota Comprehensive Cancer Control Program and seven cancer treatment centers in the state, Fahrenwald got responses from 1,093 breast cancer survivors who had been diagnosed in the last five years. To determine which of the nine independent variables tipped the scales toward mastectomy, she turned to associate professor Chris Saunders of the mathematics and statistics department. “The statistics were not meant to be innovative but to provide an answer that is robust and rigorous,” said Saunders, who used logistic regression to analyze the survey results…
The ARMC5 gene was discovered by independent workgroups studying benign tumors — so-called adrenal adenomas — in connection with Cushing’s syndrome. In this disease, the body produces too much of the hormone cortisol. Now, for the first time, a mutation of ARMC5 has been characterized as the cause behind the growth of meningeal tumors. …
At the heart of this pathway lies PPARγ (peroxisome proliferation-activated receptor gamma), a protein that regulates glucose and lipid metabolism in normal cells. Researchers demonstrated that by activating PPARγ with antidiabetic drugs in lung cancer cells, they could stop these tumor cells from dividing. “We found that activation of PPARγ causes a major metabolic change in cancer cells that impairs their ability to handle oxidative stress,” said Dr…
A new study by researchers at The Ohio State University Comprehensive Cancer Center — Arthur G. James Cancer Hospital and Richard J. Solove Research Institute (OSUCCC — James) shows that a molecule called nuclear factor kappa B (NF-kB) helps cancer cells by suppressing the immune system’s ability to detect and destroy them. …
CLIP2 serves as a radiation marker: After exposure to radiation from radioiodine, both the genetic activity and the protein expression are increased, as the scientists’ studies were able to substantiate. CLIP2 appears to be particularly significant in the development of tumours in the thyroid gland after radiation exposure…
In the quest to solve cancer’s mysteries, they come in handy when describing tongue-twisting processes and pathways that somehow allow tumors to form and thrive. …
The results reported in the journal of Clinical Cancer Research, a publication of the American Association of Cancer Research, indicate the KLK3 gene — a gene on chromosome 19 responsible for encoding the prostate-specific antigen (PSA) — is not only associated with prostate cancer aggression, but a single nucleotide polymorphism (SNP) on it is more apparent in cancer patients with GS7. Researchers have linked Gleason score, an important predictor of prostate cancer outcomes, to several clinical end points, including clinical stage, cancer aggression and survival. There has been much research associated with prostate cancer outcomes as well as GS7 prostate cancers, which is an intermediate grade of cancer accounting for 30 to 40 percent of all prostate cancers. “This is the first report that I am aware of that indicates a genetic variant can stratify GS7 prostate cancer patients,” said Jian Gu, Ph.D., associate professor at MD Anderson, and a key investigator on the study. …
In experiments in animals, researchers from the University of Michigan Medical School showed that adding rapamycin to an immunotherapy approach strengthened the immune response against brain tumor cells. What’s more, the drug also increased the immune system’s “memory” cells so that they could attack the tumor if it ever reared its head again…
Scientists at the University of Michigan and the U-M Health System recently discovered a protein mutation that causes the devastating disease dyskeratosis congenita, in which precious hematopoietic stem cells can’t regenerate and make new blood. People with DC age prematurely and are prone to cancer and bone marrow failure. But the study findings reach far beyond the roughly one in 1 million known DC patients, and could ultimately lead to developing new drugs that prevent cancer from spreading, said Jayakrishnan Nandakumar, assistant professor in the U-M Department of Molecular, Cellular, and Developmental Biology. …