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We are analyzing https://www.nature.com/articles/335440a0.

Title:
Bcl-2 gene promotes haemopoietic cell survival and cooperates with c-myc to immortalize pre-B cells | Nature
Description:
A common feature of follicular lymphoma, the most prevalent haematological malignancy in humans, is a chromosome translocation (t(14;18)) that has coupled the immunoglobulin heavy chain locus to a chromosome 18 gene denoted bcl-2 (refs 1–6). By analogy with the translocated c-myc oncogene in other B-lymphoid tumours (reviewed in ref. 7), bcl-2 is a candidate oncogene, but no biological effects of bcl-2 have yet been reported. To test whether bcl-2 influences the growth of haematopoietic cells, either alone or together with a deregulated c-myc gene, we have introduced a human bcl-2 complementary DNA (ref. 3) using a retroviral vector into bone marrow cells from either normal or Eµ-myc transgenic mice, in which B-lineage cells constitutively express the c-myc gene8–10. Bcl-2 cooperated with c-myc to promote proliferation of B-cell precursors, some of which became tumorigenic. To determine how bcl-2 expression impinges on growth factor requirements, the gene was introduced into a lymphoid and a myeloid cell line that require interleukin 3 (IL-3) (refs 11 and 12). In the absence of IL-3, bcl-2 promoted the survival of the infected cells but they persisted in a G0 state, rather than proliferating. These results argue that bcl-2 provided a distinct survival signal to the cell and may contribute to neoplasia by allowing a clone to persist until other oncogenes, such as c-myc, become activated.
Website Age:
30 years and 10 months (reg. 1994-08-11).

Matching Content Categories {📚}

  • Education
  • Telecommunications
  • Science

Content Management System {📝}

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Custom-built

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🌠 Phenomenal Traffic: 5M - 10M visitors per month


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$63,100 per month
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Keywords {🔍}

article, google, scholar, cas, nature, cell, bcl, access, cory, content, cmyc, cells, adams, pubmed, cookies, gene, oncogene, privacy, open, research, data, september, survival, ads, cancer, advertising, information, journal, subscribe, vaux, myeloid, institution, buy, death, croce, embo, schrader, molec, biol, dexter, metcalf, press, mulligan, permissions, essential, optional, media, personal, parties, policy,

Topics {✒️}

nature portfolio permissions reprints privacy policy cancer research vol medical research advertising subscribe nature social media nature 318 nature 303 nature 335 nature eµ-myc transgenic mice deregulated c-myc gene personal data springerlink instant access data protection permissions leukemia cancer cells anti-cancer effects myeloid cell line myeloid cell components translocated c-myc oncogene privacy distinct survival signal b-cell precursors b-cell malignancies bcl-2 expression impinges bcl-2 protein family explore content subscription content cell tissue kinet european economic area prevalent haematological malignancy institutional subscriptions read harcourt brace jovanovich eliza hall institute cellular mechanisms mediating dual–trigger release mesoporous silica nanospheres accepting optional cookies suzanne cory & jerry c-myc gene8–10 bone marrow cells journals search log b-lymphoid tumours issue learn savory essential oil manage preferences growth factor requirements

Schema {🗺️}

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         description:A common feature of follicular lymphoma, the most prevalent haematological malignancy in humans, is a chromosome translocation (t(14;18)) that has coupled the immunoglobulin heavy chain locus to a chromosome 18 gene denoted bcl-2 (refs 1–6). By analogy with the translocated c-myc oncogene in other B-lymphoid tumours (reviewed in ref. 7), bcl-2 is a candidate oncogene, but no biological effects of bcl-2 have yet been reported. To test whether bcl-2 influences the growth of haematopoietic cells, either alone or together with a deregulated c-myc gene, we have introduced a human bcl-2 complementary DNA (ref. 3) using a retroviral vector into bone marrow cells from either normal or Eµ-myc transgenic mice, in which B-lineage cells constitutively express the c-myc gene8–10. Bcl-2 cooperated with c-myc to promote proliferation of B-cell precursors, some of which became tumorigenic. To determine how bcl-2 expression impinges on growth factor requirements, the gene was introduced into a lymphoid and a myeloid cell line that require interleukin 3 (IL-3) (refs 11 and 12). In the absence of IL-3, bcl-2 promoted the survival of the infected cells but they persisted in a G0 state, rather than proliferating. These results argue that bcl-2 provided a distinct survival signal to the cell and may contribute to neoplasia by allowing a clone to persist until other oncogenes, such as c-myc, become activated.
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      headline:Bcl-2 gene promotes haemopoietic cell survival and cooperates with c-myc to immortalize pre-B cells
      description:A common feature of follicular lymphoma, the most prevalent haematological malignancy in humans, is a chromosome translocation (t(14;18)) that has coupled the immunoglobulin heavy chain locus to a chromosome 18 gene denoted bcl-2 (refs 1–6). By analogy with the translocated c-myc oncogene in other B-lymphoid tumours (reviewed in ref. 7), bcl-2 is a candidate oncogene, but no biological effects of bcl-2 have yet been reported. To test whether bcl-2 influences the growth of haematopoietic cells, either alone or together with a deregulated c-myc gene, we have introduced a human bcl-2 complementary DNA (ref. 3) using a retroviral vector into bone marrow cells from either normal or Eµ-myc transgenic mice, in which B-lineage cells constitutively express the c-myc gene8–10. Bcl-2 cooperated with c-myc to promote proliferation of B-cell precursors, some of which became tumorigenic. To determine how bcl-2 expression impinges on growth factor requirements, the gene was introduced into a lymphoid and a myeloid cell line that require interleukin 3 (IL-3) (refs 11 and 12). In the absence of IL-3, bcl-2 promoted the survival of the infected cells but they persisted in a G0 state, rather than proliferating. These results argue that bcl-2 provided a distinct survival signal to the cell and may contribute to neoplasia by allowing a clone to persist until other oncogenes, such as c-myc, become activated.
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External Links {🔗}(77)

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