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Recent News and Articles on the Keywords: cell death + new gene + new  Related to the article below (Last Update: 7/1/2008)

Cancer Cells Revert To Normal At Specific Signal Threshold ...
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AHN - Jun 25, 2008
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Source: Google News

A novel anti-apoptosis gene, survivin, expressed in cancer and lymphoma -
G Ambrosini, C Adida, DC Altieri? - Nature Medicine, 1997 - nature.com
... Inhibitors of programmed cell death (apoptosis) aberrantly prolonging cell viability
may ... the identification of several new apoptosis inhibitors ...

Bcl-2 initiates a new category of oncogenes: regulators of cell death -
SJ Korsmeyer - Blood, 1992 - bloodjournal.hematologylibrary.org
... PROVIDES THE BcI-2 GENE REGULATORS OF PROGRAMMED CELL DEATH: A NEW CATEGORY OF
ONCOGENES Malignancies usually possess aberrations in more than a single pathway ...

Control of programmed cell death in normal and leukemic cells: new implications for therapy. -
L Sachs, J Lotem - Blood, 1993 - ncbi.nlm.nih.gov
... death in normal and leukemic cells: new implications for ... Programmed cell death can
be induced in leukemic cells by ... or by the tumor-suppressor gene wild-type p53 ...

… -induced gene of the leucine zipper family protects T lymphocytes from TCR/CD3-activated cell death -
FD'Adamio, O Zollo, R Moraca, E Ayroldi, S … - Immunity, 1997 - actxdownload.immunity.com
... All rights reserved. Article. A New Dexamethasone-Induced Gene of the Leucine Zipper
Family Protects T Lymphocytes from TCR/CD3-Activated Cell Death. ...

… , a novel human apoptotic protein with homology to Caenorhabditis elegans cell death protein Ced-3 … -
T Fernandes-Alnemri, G Litwack, ES Alnemri - Journal of Biological Chemistry, 1994 - ASBMB
... The new gene encodes a 32-kDa putative cysteine protease (CPP32) with significant
homology to Caenorhabditis elegans cell death protein Ced- 3, mammalian ...

Programmed cell death in animal development -
MD Jacobson, M Weil, MC Raff? - Cell, 1997 - cell.com
... The strongest evidence that new gene transcription is involved in ... none of the normal
cell deaths occur ... genes activate the caspase-dependent death program in ...

[PDF] The Th1-Th2 hypothesis of HIV infection: new insights -
M Clerici, GM Shearer - Immunol Today, 1994 - aliveandwellsf.org
... new insights ... nmch quoted, viewpoint article, Mario Clerici and Gene Shearer examined ...
of activ, qon-induced, cytokine-nlodulated, progranmled cell death as a ...
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… deprived of trophic support in vitro require new gene expression to undergo programmed cell death. -
CE Milligan, RW Oppenheim, LM Schwartz - J Neurobiol, 1994 - ncbi.nlm.nih.gov
Motoneurons deprived of trophic support in vitro require new gene expression to
undergo programmed cell death. Milligan CE, Oppenheim RW, Schwartz LM. ...

Gene Expression Profile of Antithrombotic Protein C Defines New Mechanisms Modulating Inflammation … -
DE Joyce, L Gelbert, A Ciaccia, B DeHoff, BW … - Journal of Biological Chemistry, 2001 - ASBMB
... level and defines new relationships among hemostasis, inflammation, and cell
death/apoptosis. Moreover, our results demonstrate the value of gene profiling in ...

Tumor necrosis factor alpha-induced apoptosis in human neuronal cells: protection by the antioxidant … -
… , S Gummuluru, SM Fine, D New, LG Epstein, HE … - Molecular and Cellular Biology, 1995 - pubmedcentral.nih.gov
... University of Rochester Medical Center, New York 14642 ... Analysis of cell cycle-related
gene expression in ... induction of Cyclin D1 during programmed cell death. ...

Source: Google Scholar

Identification of new genes shows a complex path to cell death

UMass Medical School investigators define multi-step pathway that allows for cell survival and death

WORCESTER, Mass. — Can a tiny winged insect’s salivary glands really tell us about processes relevant to human disease" Yes, according to a new study by researchers at the University of Massachusetts Medical School (UMMS), who gained new insights into autophagy—a cellular degradation process associated with a form of programmed cell death—by studying the salivary gland cells of the fruit fly.

Since its initial discovery in the 1960s, programmed cell death has been a primary focus of studies for investigators across a wide array of scientific disciplines. An essential mechanism in development and homeostasis, programmed cell death allows for the clean intracellular destruction of unnecessary or damaged cells. While apoptosis is the most understood type of programmed cell death, recently scientists have begun to take a closer look at autophagy— a highly regulated, catabolic process that essentially allows a cell to eat itself. Paradoxically, autophagy is not only a major mechanism by which a starving cell reallocates nutrients to ensure survival, scientists are now demonstrating that autophagy also provides cells that cannot undergo apoptosis with an alternate form of self-destruction.

In “Growth arrest and autophagy are required for salivary gland cell degradation in Drosophila,” published in the December 14 issue of Cell, Eric Baehrecke, PhD, UMMS Associate Professor of Cancer Biology, and colleagues examined fly salivary glands, which contain all of the machinery required to dismantle and recycle their own cellular components and thus provide a genetic model system for elucidating the complex functions of autophagy. The paper describes the cellular components required for autophagic cell death and defines multiple pathways that cooperate in the clearance of cells during fly development. Further, their findings demonstrate a critical relationship between growth and this form of cell death.

“When cells keep growing, they don’t die well,” Dr. Baehrecke explained. “We show that an arrest of growth preceded the death of these cells. If we maintain growth by turning on certain genes, we can block the death of these cells, and this has potential clinical implications. Therapies directed at apoptotic mechanisms have resulted in limited success; we hope that further studies of autophagy could lead to new approaches to the treatment of human disease.”

“It’s becoming increasingly important to understand how the various cell death pathways connect and how they affect development, the stress response, and disease,” said Marion Zatz, PhD, who oversees cell death grants at the National Institute of General Medical Sciences, which funded the work. “While this research was done in fruit flies, findings made in model organisms are often the first step in understanding what goes on in humans. By shedding light on autophagic cell death, this work may help explain the pathway’s role in human diseases such as cancer, Alzheimer’s and Parkinson’s.”

“The role of autophagy during cell death remains controversial but is important to our understanding and treatment of many human disorders including cancer and neurodegeneration,” Baehrecke said. “It is important to understand the relationship between autophagy and cell death, as the association of autophagy with cell growth, nutrient utilization, survival and death indicates that this catabolic process is relevant to the treatment of many human disorders including cancer.”

###

About the University of Massachusetts Medical School

The University of Massachusetts Medical School, one of the fastest growing academic health centers in the country, has built a reputation as a world-class research institution, consistently producing noteworthy advances in clinical and basic research. The Medical School attracts more than $176 million in research funding annually, 80 percent of which comes from federal funding sources. The work of UMMS researcher Craig Mello, PhD, an investigator of the prestigious Howard Hughes Medical Institute (HHMI), and his colleague Andrew Fire, PhD, then of the Carnegie Institution of Washington, toward the discovery of RNA interference was awarded the 2006 Nobel Prize in Physiology or Medicine, hailed as the "Breakthrough of the Year" in 2002 by Science magazine and has spawned a new and promising field of research, the global impact of which may prove astounding. UMMS is the academic partner of UMass Memorial Health Care, the largest health care provider in Central Massachusetts. For more information, visit www.umassmed.edu.

 
 
 
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