The retinoblastoma gene in myeloid leukaemias

Research output: Contribution to journalArticle

2 Citations (Scopus)

Abstract

The balance between self-renewal, differentiation and programmed cell death underlies normal haemopoiesis. Disruption of this balance results in leukaemogenesis which is believed to be a multi-step process, culminating in the clonal selection and expansion of an abnormal haemopoietic progenitor cell. The malignant cell clone is believed to have lost the capacity to control cell growth through a series of mutations resulting in the activation of oncogenes and/or inactivation of tumour suppressor genes. These genes are involved in signal transduction, cell proliferation, cell differentiation and cell death or apoptosis. One of the commonly mutated tumour suppressor genes is the retinoblastoma gene (RB1) which is responsible for the childhood tumour, retinoblastoma. Mutations in RB1 leading to inactivation of the retinoblastoma protein, pRB, have also been implicated in many different malignancies including breast cancer, lung cancer and leukaemias. The exact role for RB1 mutations in the pathogenesis of these malignancies remains unclear, however there is a strong body of evidence to indicate that inactivation of pRB is a frequent event in a subset of these tumours and has implications for tumour behaviour and disease outcome.

Original languageEnglish
Pages (from-to)43-51
Number of pages9
JournalHematology
Volume1
Issue number1
Publication statusPublished - 1996
Externally publishedYes

Fingerprint

Retinoblastoma Genes
Myeloid Leukemia
Neoplasms
Tumor Suppressor Genes
Mutation
Lung Neoplasms
Cell Death
Retinoblastoma Protein
Retinoblastoma
Oncogenes
Cell Differentiation
Signal Transduction
Leukemia
Stem Cells
Clone Cells
Cell Proliferation
Apoptosis
Breast Neoplasms
Growth
Genes

Keywords

  • Leukaemia
  • Myeloid
  • pRB
  • Retinoblastoma gene

ASJC Scopus subject areas

  • Hematology

Cite this

The retinoblastoma gene in myeloid leukaemias. / A. Jamal, A. Rahman.

In: Hematology, Vol. 1, No. 1, 1996, p. 43-51.

Research output: Contribution to journalArticle

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