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Rising expectations from new yeast study

Researchers at the University of Illinois Chicago have discovered a signaling mechanism in yeast cells that controls cell growth and differentiation, with potential implications for cancer treatment. The study found that pheromone triggers cells to stop dividing and orient their growth toward the source of pheromone.

SourceUniversity of Illinois Chicago·JournalScience·DateMay 23, 2002

Researchers solve killer protein's 'crime'

Researchers at Rockefeller University have discovered that the 'Reaper' protein triggers programmed cell death by instructing a fly cell's principal guard protein, DIAP1, to self-destruct. This finding may lead to novel strategies for targeting immortal cancer cells without harming healthy cells.

SourceRockefeller University·JournalNature Cell Biology·DateMay 20, 2002

How aging cells retire

Aging cells retire when their telomeres become too short to function, according to a new Rockefeller University study. The researchers found that protein TRF2 helps critically short telomeres function better, allowing old cells to live longer.

SourceRockefeller University·JournalScience·DateMar 28, 2002

New method for anticancer drug discovery developed

Researchers at the Fred Hutchinson Cancer Research Center have developed a new cell-based approach for anticancer drug discovery, which identified 39 new compounds selective for yeast cells with faulty DNA repair enzymes. This approach is adaptable to high-throughput screening methods and complements target-based screening, potentially...

SourceJournal of the National Cancer Institute·JournalJNCI Journal of the National Cancer Institute·DateJan 15, 2002

Arsenic and old telomeres

Telomeres, protective caps on chromosome ends, are shorter in people exposed to arsenic, increasing cancer risk. Long-term arsenic exposure has been associated with accelerated telomere shortening, a potential biomarker for arsenic poisoning.

SourceJCI Journals·JournalJournal of Clinical Investigation·DateNov 14, 2001

UIC researchers find "fountain of youth" gene

Scientists at UIC found that increasing FoxM1B gene expression restored liver cell growth rates and division activity in aged mice, potentially treating aging-related diseases such as cancer and Alzheimer's. This breakthrough could lead to new therapies for the elderly using gene therapy.

SourceUniversity of Illinois Chicago·JournalProceedings of the National Academy of Sciences·DateSep 24, 2001

Genomes on 'chips' boon to cancer research

Researchers used DNA-coated microchips to discover that flavopiridol works by broadly inhibiting messenger RNA molecules, which are responsible for carrying genetic information to cellular protein factories. This inhibition ultimately leads to a halt in the production of certain proteins, allowing normal cellular processes to continue.

SourceBMC (BioMed Central)·JournalGenome Biology·DateSep 13, 2001

NYU researchers have transformed a virus into a better cancer killer

Researchers have isolated a new version of a herpesvirus that kills cancer cells but spares normal tissue, dramatically reducing prostate cancer tumors in mice. The new virus contains an extra genetic mutation that enables more robust reproduction and prevents the cell from mounting a response to stop viral replication.

SourceNYU Langone Health / NYU Grossman School of Medicine·JournalProceedings of the National Academy of Sciences·DateJul 12, 2001

Cancer's penchant for developing drug resistance is a result of chromosome reassortment, UC Berkeley scientist proposes

A UC Berkeley scientist proposes that chromosome reassortment, rather than genetic mutations, is the cause of cancer's tendency to develop drug resistance. This theory suggests aneuploid cells, with abnormal numbers of chromosomes, are more prone to producing drug-resistant cancer cells.

SourceUniversity of California - Berkeley·JournalProceedings of the National Academy of Sciences·DateJan 28, 2001

Study reveals microscopic interaction of cancer cells and blood vessels in tumor formation

Researchers documented the earliest steps of tumor formation in mice and rats, showing that cancer cells can grow new blood vessels when just hundreds are present. The study suggests that angiogenesis inhibitors might be useful at the earliest stages of tumor development to prevent recurrence and spread.

SourceDuke University Medical Center·JournalJNCI Journal of the National Cancer Institute·DateJan 17, 2000

How A Common Protein Becomes A Cancer Killer

A new study by University of Wisconsin-Madison biochemist Ron Raines found that a ribonuclease A protein in humans has the same cancer-fighting potential as a frog-derived protein. The finding opens a door to creating a new class of natural drugs aimed at fighting cancer without side effects.

SourceUniversity of Wisconsin-Madison·JournalProceedings of the National Academy of Sciences·DateAug 31, 1998

Cancer Cells Self-Destruct When "Sweet Tooth" Is Thwarted

Researchers found cancer cells self-destruct when glucose is cut off, suggesting a potent new way to fight cancer with few side effects. The discovery was made using a compound that disrupts glycolysis, the process that produces energy from sugar, and could be used in combination with existing treatments.

SourceJohns Hopkins Medicine·JournalProceedings of the National Academy of Sciences·DateFeb 17, 1998

Green Tea Ingredient Can Kill Cancer Cells

Researchers at Case Western Reserve University have discovered that epigallocatechin-3-gallate, a green tea compound, can induce programmed cell death in cancer cells without harming healthy cells. This finding offers new hope for cancer prevention and treatment, and may lead to the development of purified polyphenolic derivatives.

SourceCase Western Reserve University·JournalJNCI Journal of the National Cancer Institute·DateDec 17, 1997

Pawpaw Shows Promise In Fighting Drug-Resistant Tumors

Researchers have discovered compounds in the bark of the pawpaw tree that show preliminary success in fighting some drug-resistant cancers. The compounds, called Annonaceous acetogenins, preferentially kill multidrug-resistant cells by inhibiting ATP production, pulling the plug on their energy source.

SourcePurdue University·JournalCancer Letters·DateSep 4, 1997