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Cellular origins of hematologic neoplasms

Article Abstract:

Blood cells arise from a small number of stem cells that continuously supply bone marrow with progenitor cells that are already committed to develop in specific ways. Once started down the road of development, progenitors can differentiate, or specialize, in many different ways, becoming erythrocytes (red blood cells), lymphocytes (a type of white blood cells), or members of other cell lineages. If a stem cell becomes cancerous, the possibility then exists for a tumor to be formed of mature cells that no longer divide but can still cause the tumor to grow, since it is constantly supplied with new members generated by the errant stem cell. Evidence of stem-cell defects in chronic myelogenous leukemia is discussed. It is not understood, however, why myeloid cells (one type of blood cell) or any single lineage, for that matter, predominate in the chronic phase of the disease, or why a blast crisis (tremendous multiplication of immature cells from all lineages) occurs. The existence of cells with markers (specific molecules) representative of more than one lineage on their surface could occur because cells can differentiate in the appropriate way up to some point beyond lineage commitment, regardless of genetic damage. This observation is consistent with the idea that the malignancy lies in an early progenitor cell. Researchers studying myeloma patients and reporting in the March 8, 1990 issue of The New England Journal of Medicine have found markers characteristic of the myeloid lineage on the patients' tumor cells. Myeloma cells have traditionally been thought to be plasma cells, from a different lineage. Although the authors of that report interpret their findings to support the existence of a transformation in an early stem cell that can give rise to many lineages (a multipotent stem cell), it is possible that they come about because laboratory conditions under which the myeloma cells were grown and studied induce the expression of normally quiescent (inactive) genes that regulate surface molecules characteristic of other lineages. This would implicate defective gene transcription, not a defective common precursor cell, as the agent in myeloma. If a genetic or chromosomal abnormality associated with multiple myeloma could be located, the point in blood cell development where the critical event takes place would be known. Such alterations have been documented for some types of lymphoma and leukemia. Insights about the cellular origins of cancer will come from collaboration among clinicians and cell and molecular biologists, since the techniques of all three are required to solve problems of the sort presented by myeloma. (Consumer Summary produced by Reliance Medical Information, Inc.)

Author: Schwartz, Robert S., Buchsbaum, Rachel J.
Publisher: Massachusetts Medical Society
Publication Name: The New England Journal of Medicine
Subject: Health
ISSN: 0028-4793
Year: 1990
Research, Multiple myeloma, editorial

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The case of the bare lymphocyte syndrome - tracking down faulty transcription factors

Article Abstract:

The bare lymphocyte syndrome is a good example of a disease caused by a mutation in the gene for a transcription factor. Transcription factors are proteins that turn on other genes. Patients with bare lymphocyte syndrome have a severe immunodeficiency that predisposes them to bacterial, viral and fungal infections. The immunodeficiency occurs because of a gene mutation that leads to a lack of major histocompatibility complex (MHC) class II molecules. These molecules are responsible for activating the immune system against foreign organisms. Without the molecules, the immune system is not activated.

Author: Schwartz, Robert S.
Publisher: Massachusetts Medical Society
Publication Name: The New England Journal of Medicine
Subject: Health
ISSN: 0028-4793
Year: 1997
Health aspects, Causes of, Physiological aspects, Gene mutations, Gene mutation, Genetic aspects, Immunological deficiency syndromes, Immunologic deficiency syndromes, Promoters (Genetics), Major histocompatibility complex

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Racial profiling in medical research

Article Abstract:

Doctors should stop focusing on racial differences and focus instead on the genetic factors that make some people more susceptible to disease than others. The Human Genome Project should facilitate this research, since race is often a social and cultural phenomenon rather than a biological one.

Author: Schwartz, Robert S.
Publisher: Massachusetts Medical Society
Publication Name: The New England Journal of Medicine
Subject: Health
ISSN: 0028-4793
Year: 2001
Analysis, Health, Health and race, Ethnic groups

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Subjects list: Editorial
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