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Volume 28 Issue 2, June 2001

Stained glass by Susan Bayer-Fishman.

Editorial

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News & Views

  • Somatic loss-of-heterozygosity can result in the complete loss of function of tumor suppressor genes in human cancer. Mitotic recombination between homologous chromosomes can cause loss of heterozygosity, leading to tumorigenesis. However, the molecular mechanisms triggering and controlling mitotic recombination are largely unknown. A new study shows that genetic divergence between homologous chromosomes suppresses mitotic recombination to a varying degree in different tissues of the mouse.

    • Harry Vrieling
    News & Views
  • Control of lifespan in Caenorhabditis elegans by the DAF-2 insulin-like signaling pathway requires daf-16, which encodes a member of the forkhead family of transcription factors. A new study provides evidence that DAF-2 negatively regulates DAF-16 activity by promoting its retention in the cytoplasm. But, constitutive targeting of DAF-16 to the nucleus is not sufficient to extend lifespan, revealing a new layer of complexity in the genetic control of aging in the nematode.

    • Pamela L Larsen
    News & Views
  • The mitochondrial genomes of tumor cells accumulate mutations during transformation. A new study raises questions regarding the way in which mutations accumulate and has implications for the potential role of mitochondrial function in tumor phenotype.

    • Leonard H Augenlicht
    • Barbara G Heerdt
    News & Views
  • Three years after MADH4 (also known as SMAD4) was identified as a gene critical to juvenile polyposis, BMPR1A, encoding a receptor in the same pathway, has been identified as another susceptibility gene. The TGFβ/BMP superfamily of molecules has not only been shown to be defective in neoplasia but also in the non-cancer developmental syndromes primary pulmonary hypertension and hereditary hemorrhagic telangiectasia.

    • Charis Eng
    News & Views
  • Selective death of motor neurons beginning in mid life is the hallmark of the most abundant motor-neuron disease of adults, amyotrophic lateral sclerosis (ALS). An unexpected insight into potential causes of the disorder is now provided by mice lacking the hypoxia response element of the promoter of the gene encoding the vascular endothelial cell growth factor (VEGF). This elicits age-dependent, selective degeneration of motor neurons, and indicates that a primary cause of ALS may be chronic deficits in VEGF-dependent vascular perfusion or a direct neurotrophic effect of VEGF on motor neurons.

    • JH Pate Skene
    • Don W Cleveland
    News & Views
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Book Review

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Progress

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Brief Communication

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Article

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Letter

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Correction

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