June 25, 2014
The National Cancer Institute awarded more than $2 million to a team at the Wilmot Cancer Institute to continue their study of a gene network that controls cancer progression, with a focus on pancreatic cancer.
The five-year grant will fund a series of new scientific experiments involving a gene known as Plac8. In earlier work, Wilmot investigators showed that by inactivating Plac8 they could stop or slow pancreatic tumor growth in mice and significantly extend survival – making Plac8 an attractive target for drug development.
Principle investigator Hartmut
HuckyLand, Ph.D., and co-investigator Aram Hezel, M.D., had been studying a wider system of genes and cellular events involved in cancer, when they discovered that Plac8 is a key driver in malignancies but is not essential to the function of normal tissue.
May 1, 2014
Cancer cells: blue is cell nucleus and yellow represents the garbage recycling process that occurs as cancer grows.
University of Rochester scientists have discovered a gene with a critical link to pancreatic cancer, and further investigation in mice shows that by blocking the gene’s most important function, researchers can slow the disease and extend survival.
Published online by Cell Reports, the finding offers a potential new route to intrude on a cancer that usually strikes quickly, has been stubbornly resistant to targeted therapies, and has a low survival rate. Most recent improvements in the treatment of pancreatic cancer, in fact, are the result of using different combinations of older chemotherapy drugs.
The research led by Hartmut
HuckyLand, Ph.D., and Aram F. Hezel, M.D., of UR Medicine's James P. Wilmot Cancer Center, identifies a new target in the process of garbage recycling that occurs within the cancer cell called autophagy, which is critical to pancreatic cancer progression and growth.
June 3, 2013
Researchers at the University of California, San Diego School of Medicine, with colleagues at the University of Rochester Medical Center, have identified a new mechanism that appears to suppress tumor growth, opening the possibility of developing a new class of anti-cancer drugs.
Writing in this week's online Early Edition of the Proceedings of the National Academy of Sciences, Willis X. Li, PhD, a professor in the Department of Medicine at UC San Diego, reports that a particular form of a signaling protein called STAT5A stabilizes the formation of heterochromatin (a form of chromosomal DNA), which in turn suppresses the ability of cancer cells to issue instructions to multiply and grow.
Co-authors are Xiaoyu Hu, Amy Tsurumi and Hartmut Land, Department of Biomedical Genetics, University of Rochester Medical Center; Pranabananda Dutta, Jinghong Li and Jingtong Wang, Department of Medicine, UCSD.
September 13, 2012
University of Rochester Medical Center scientists discovered new genetic evidence linking cholesterol and cancer, raising the possibility that cholesterol medications could be useful in the future for cancer prevention or to augment existing cancer treatment.
The data, published in the online journal Cell Reports, support several recent population-based studies that suggest individuals who take cholesterol-lowering drugs may have a reduced risk of cancer, and, conversely that individuals with the highest levels of cholesterol seem to have an elevated risk of cancer.
The cancer-cholesterol question has been debated since the early 20th century, and along with it doctors and scientists have observed various trends and associations. However, until now genetic evidence directly linking cholesterol and malignancy has been lacking, said senior author Hartmut (Hucky) Land, Ph.D., Robert and Dorothy Markin Professor and chair of the Department of Biomedical Genetics and Professor in the department of Biochemistry & Biophysics, and director of research and co-director of the James P. Wilmot Cancer Center at URMC.
May 28, 2008
A new approach to finding genes important in the onset of cancer is described in Nature. The findings could help to identify new targets for tumour therapy.
Several genes, or
oncogenes,cooperate with each other to transform normal cells into cancer cells. Hartmut Land and colleagues have now identified a list of other genes - termed
cooperation response genes(CRGs) - that are regulated downstream of these
oncogenes.By interfering with each CRG individually, the team were able to show that 14 out of 24 of them had a critical role in tumour formation. Restoring expression of these genes to the levels observed in normal cells prevented the formation of tumours. What's more, genetic perturbations of CRGs with relatively smaller effects when examined on their own show evidence of being essential when analysed in combination.
The findings represent an important step in the search for the chink in the armour in human cancer - the elusive gene that cancer cells simply cannot live without.
May 27, 2008
Pinpointing new targets for cancer treatments is as difficult as finding a needle in a haystack, yet a University of Rochester team has discovered an entire novel class of genes they believe will lead to a greater understanding of cancer cell function and the next generation of effective and less harmful therapies for patients.
February 20, 2007
University of Rochester scientists, while investigating the two most frequent types of mutations in cancer, discovered a possible new route to treatment that would take advantage of the mutations instead of trying to repair them. The research is reported online this week in the journal Nature Structural & Molecular Biology.
In experiments with rodent and human cells, co-authors Mingxuan Xia, Ph.D., and Hartmut Land, Ph.D., explored how the Rho family of proteins, which are involved in cell movement, and thus in the progression from benign to malignant cancer, are controlled by two well-known cancer genes, p53 and Ras. By closing in on this deadly collaboration, researchers showed for the first time why some molecules such as Rho are targeted by cancer genes - and how they might lead to a promising way to intervene against cancer.
We have very little understanding of how Ras and p53 or any other potent gene mutations cooperate to cause malignant tumors,said Land, who is professor and chair of the Department of Biomedical Genetics and scientific director of the James P. Wilmot Cancer Center at the University of Rochester.
But we have suspected for a long time that the way to develop rational searches for new drug targets is to first understand how these oncogenes cooperate. And in this study we've shown for the first time that this idea might work.
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