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Open AccessJournal ArticleDOI

Cyclin D1 transgene impedes lymphocyte maturation and collaborates in lymphomagenesis with the myc gene.

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TLDR
Findings indicate that this G1 cyclin can modulate differentiation and collaborate with myc‐like genes in oncogenesis, as well as indicating that this cyclin D1 expression is lymphomagenic.
Abstract
Cyclin D1 is the regulatory subunit of certain protein kinases thought to advance the G1 phase of the cell cycle Deregulated cyclin D1 expression has been implicated in several human neoplasms, most consistently in centrocytic B lymphoma, where the cyclin D1 gene usually has been translocated to an immunoglobulin locus To determine directly whether constitutive cyclin D1 expression is lymphomagenic, transgenic mice were generated having the cyclin D1 gene linked to an immunoglobulin enhancer Despite abundant transgene expression, their lymphocytes were normal in cell cycle activity, size and mitogen responsiveness, but young transgenic animals contained fewer mature B- and T-cells Although spontaneous tumours were infrequent, lymphomagenesis was much more rapid in mice that co-expressed the cyclin D1 transgene and a myc transgene than in mice expressing either transgene alone Moreover, the spontaneous lymphomas of myc transgenic animals often ectopically expressed the endogenous cyclin D1 gene These findings indicate that this G1 cyclin can modulate differentiation and collaborate with myc-like genes in oncogenesis

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Cancer Cell Cycles

TL;DR: Genetic alterations affecting p16INK4a and cyclin D1, proteins that govern phosphorylation of the retinoblastoma protein and control exit from the G1 phase of the cell cycle, are so frequent in human cancers that inactivation of this pathway may well be necessary for tumor development.
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The oncogene and Polycomb-group gene bmi-1 regulates cell proliferation and senescence through the ink4a locus

TL;DR: This work shows that bmi-1-deficient primary mouse embryonic fibroblasts are impaired in progression into the S phase of the cell cycle and undergo premature senescence, and connects transcriptional repression by Polycomb-group proteins with cell-cycle control and senescences.
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Robustness in bacterial chemotaxis

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