Autophagy News and Research

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Autophagy is a normal process in which a cell destroys proteins and other substances in its cytoplasm (the fluid inside the cell membrane but outside the nucleus), which may lead to cell death. Autophagy may prevent normal cells from developing into cancer cells, but it may also protect cancer cells by destroying anticancer drugs or substances taken up by them.

Cancer cells 'addicted' to self-preservation process

A team of investigators at The Cancer Institute of New Jersey (CINJ); Rutgers, The State University of New Jersey; and Princeton University, have determined that cancer cells are "addicted" to a self-preservation process known as autophagy. They also showed that the inhibition of that process could prove to be a valuable treatment approach for aggressive cancers. CINJ is a Center of Excellence of UMDNJ-Robert Wood Johnson Medical School.

11 Feb 2011

CINJ clinical trial explores anti-malaria drug against melanoma

Building upon recent laboratory discoveries on resistance by cancer cells to therapies that attempt to starve cancer, scientists at The Cancer Institute of New Jersey (CINJ) are conducting a clinical trial that further explores how to prevent that action.

14 Jan 2011

Study highlights role of SIRT1 protein as tumor suppressor in prostate cancer

Researchers from the Kimmel Cancer Center at Jefferson and two other institutions have discovered new evidence that suggests the "longevity" protein SIRT1, known for its life-spanning effects in different species, can inhibit the development of a known precursor to prostate cancer, prostatic intraepithelial neoplasia.

14 Jan 2011

Study identifies over 30 breast cancer gene targets involved in drug resistance to chemotherapy

A new study conducted by Josh LaBaer's research team in the Biodesign Institute at Arizona State University has pinpointed more than 30 breast cancer gene targets ---including several novel genes---that are involved in drug resistance to a leading chemotherapy treatment.

11 Jan 2011

AMPK activates autophagy by activating ATG1 enzyme

Researchers at the Salk Institute for Biological Studies have discovered how AMPK, a metabolic master switch that springs into gear when cells run low on energy, revs up a cellular recycling program to free up essential molecular building blocks in times of need.

24 Dec 2010

Study broadens understanding of role of IDH1 and IDH2 mutations in AML

Agios Pharmaceuticals, the leading biopharmaceutical company focused on discovering and developing novel drugs in the rapidly emerging field of cancer metabolism, today announced the publication of a paper in Cancer Cell that illuminates the mechanism by which 2-hydroxyglutarate (2HG), and the mutations in the metabolic genes IDH1 and IDH2 that produce it, may be driving the growth of tumors in patients with acute myeloid leukemia (AML).

15 Dec 2010

New mechanism breaks drug resistance in ovarian cancer

Drug resistance is a major obstacle in curing ovarian cancer but new research from the Centenary Institute has discovered a treatment that kills ovarian cancer cells in a new way that can break the resistance mechanism.

16 Nov 2010

Agios receives two grants under QTDP program to develop novel cancer metabolism therapies

8 Nov 2010

Alpha-synuclein protein in Parkinson's disease inhibits autophagy: Research

A protein linked to Parkinson's disease may cause neurodegeneration by inhibiting autophagy-the process in which cells digest some of their contents-according to a study in the September 20 issue of the Journal of Cell Biology

21 Sep 2010

Research suggests blocking HMGB1 protein can benefit cancer patients

Like some people, cells eat when they are under pressure-but they consume parts of themselves. A multi-function protein helps control this form of cannibalism, according to a study in the September 6 issue of the Journal of Cell Biology.

7 Sep 2010

Berries help aging brain stay healthy

Scientists today reported the first evidence that eating blueberries, strawberries, and acai berries may help the aging brain stay healthy in a crucial but previously unrecognized way. Their study, presented at the 240th National Meeting of the American Chemical Society (ACS), concluded that berries, and possibly walnuts, activate the brain's natural "housekeeper" mechanism, which cleans up and recycles toxic proteins linked to age-related memory loss and other mental decline.

24 Aug 2010

New study reveals potential role of TGF-β1 in kidney disease

Fibrosis in the kidney is one of the key causes of progressive renal failure. High levels of the inflammatory molecule TGF-β1 in the kidney tubules due to tissue damage can cause fibrosis as well as nephron degeneration, resulting in loss of kidney function. To clarify the mechanisms regulating TGF-β1-mediated renal fibrosis, Koesters et al expressed high levels of TGF-β1 in renal tubules of mice. Nephron degeneration in this system was mediated by decomposition of the tubular cells. These data suggest that TGF-β1 may play a novel role in cell death of renal cells, thus contributing to renal fibrosis.

28 Jul 2010

Calcium transfer impacts fuel mechanism for normal cell metabolism

University of Pennsylvania School of Medicine researchers have described a previously unknown biological mechanism in cells that prevents them from cannibalizing themselves for fuel. The mechanism involves the fuel used by cells under normal conditions and relies on an ongoing transfer of calcium between two cell components via an ion channel. Without this transfer, cells start consuming themselves as a way of to get enough energy.

28 Jul 2010

Enzyme mTOR regulates autophagy: Study

Cells that consume parts of themselves can stop this process autonomously as well. This was discovered by NWO researcher Judith Klumperman's group, in collaboration with colleagues from the National Institute of Health in Washington. The self-cannibalism is part of the normal digestive process of the cell, but also a survival mechanism in times of famine. This is what makes it difficult for doctors to 'starve out' cancer cells, for instance. The research results were published on 6 June in Nature.

15 Jul 2010

Anti-seizure drug can be used to treat AT deficiency: Pitt researchers

The liver scarring of α1-antitrypsin deficiency, the most common genetic cause for which children undergo liver transplantation, might be reversed or prevented with a medication that has long been used to treat seizures, according to findings from Children's Hospital of Pittsburgh of UPMC and the University of Pittsburgh School of Medicine that will published in Science and are available online today through the Science Express website.

4 Jun 2010

Cancer Institute of New Jersey investigators target autophagy

In an effort to improve current anticancer treatments, investigators at The Cancer Institute of New Jersey (CINJ) have been targeting a process known as autophagy, in which cancer cells eat themselves as a measure of self preservation under chemotherapy and radiation stress, thus prolonging tumor cell survival and inducing resistance to therapy.

21 May 2010

Roche's xCELLigence System helps study cell viability, cell death while testing cytotoxic compounds

Monitoring of cell viability and toxicity are critical to many areas of biological and biomedical research. This is true for understanding the molecular and biochemical pathways regulating cell viability, for developing therapeutic agents which modulate cell viability and for identifying potential cytotoxic side effects of potential therapeutic agents.

3 May 2010

CINJ trial targets new combination therapy for advanced solid tumors

Building off recent laboratory discoveries relating to how cancer cells become resistant to therapies that attempt to starve cancer, scientists at The Cancer Institute of New Jersey (CINJ) are now applying that knowledge to a process in which cancer cells eat themselves to downsize and resist therapy. The ultimate goal of this effort is to improve upon current anticancer treatments.

29 Apr 2010

The EMBO Meeting 2010: Over 120 researchers to present

More than 120 leading researchers from across the molecular life sciences will speak at The EMBO Meeting 2010 - the second annual life sciences conference to be organized by the European Molecular Biology Organization (EMBO) and held in Barcelona from 4 - 7 September 2010.

13 Apr 2010

Accumulation of mutated protein may explain damaging cellular behavior in Huntington's disease

In a step towards a possible treatment for Huntington's disease, scientists at Albert Einstein College of Medicine of Yeshiva University have shown for the first time that the accumulation of a mutated protein may explain damaging cellular behavior in Huntington's disease. Their research is described in the April 11 online edition of Nature Neuroscience.

12 Apr 2010