Lymphoma‐ and leukemia‐associated chromosomal translocations in healthy individuals
Abstract
Chromosomal translocations (CTs) are hallmark mutations of hematopoietic malignancy that result in the deregulated expression of oncogenes or the generation of novel fusion genes. The polymerase chain reaction (PCR) can be used to detect illegitimate recombinations of genomic DNA sequences as a more sensitive assay than cytogenetics for determining the presence of CTs. Both direct DNA-PCR and reverse transcriptase-PCR were used to examine healthy individuals for lymphoma- and leukemia-associated CTs. Two oncogene-activating CTs [t(14;18)(q32;q21) and t(8;14)(q24;q32)] and one fusion-gene CT [t(2;5)(p23;q35)] from lymphomas and five fusion-gene CTs from leukemia [t(9;22)(q34;q11), t(4;11)(q21;q23), t(15;17)(q22;q11), t(12;21)(p13;q22), t(8;21)(q22;q22)] were detected in such studies. The biological implication is that CTs associated with malignant tumors may also be found in cells that are not neoplastic. CTs are characteristic attributes of neoplastic clones but are by themselves insufficient to cause malignant transformation. A better understanding of the special biology of non-neoplastic CT-bearing cells will provide insight into their putative role as tumor precursors. Prospective epidemiological studies are needed to determine whether such cells in healthy individuals may, in some instances, become clonogenic founders of lymphoma or leukemia.
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MYC translocation and hyperexpression is a hallmark of endemic Burkitt lymphoma, but it in itself is not sufficient to induce lymphogenesis.
“Interestingly, while MYC translocation and hyperexpression is a hallmark of EBL, it in itself is not sufficient to induce lymphogenesis (143), which may at least in part explain why mutations in PLCγ2 are relevant to the disease initiation (142).”
From The role of PLCγ2 in immunological disorders, cancer, and neurodegeneration (2021) · cites this paper as [143]
Mutations in PLCγ2 are relevant to disease initiation in endemic Burkitt lymphoma.
“Interestingly, while MYC translocation and hyperexpression is a hallmark of EBL, it in itself is not sufficient to induce lymphogenesis (143), which may at least in part explain why mutations in PLCγ2 are relevant to the disease initiation (142).”
From The role of PLCγ2 in immunological disorders, cancer, and neurodegeneration (2021) · cites this paper as [143]
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References 125 · Cited by 149
- Authors
- Janz, S., Potter, M., & Rabkin, C. S.
- Affiliations
- National Institutes of Health (US)
- Corresponding author
- Janz, Siegfried
- Venue
- Genes, Chromosomes and Cancer
- Publisher
- Wiley
- Published
- 2003-01-23
- Volume
- 36
- Issue
- 3
- Pages
- 211-223
- ISSN
- 1045-2257 (ISSN-L)
- 1098-2264
- OpenAlex
- W2161229310
- Cited by
- 149
- References
- 125
- Citations by year
- 2025: 2 · 2023: 3 · 2022: 1 · 2021: 5 · 2020: 2 · 2019: 6 · 2018: 6 · 2017: 7 · 2016: 6 · 2015: 9 · 2014: 12 · 2013: 6 · 2012: 11
- FWCI
- 1.21
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Genes Chromosomes and Cancer (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genomic variations and chromosomal abnormalities
- Health Sciences › Medicine › Pathology and Forensic Medicine › Lymphoma Diagnosis and Treatment
- Health Sciences › Medicine › Public Health, Environmental and Occupational Health › Acute Lymphoblastic Leukemia research
- Keywords
- chromosomal translocation, lymphoma, leukemia, healthy individuals, 18)(q32, 14)(q24, 5)(p23, 22)(q34, 11)(q21, 17)(q22, 21)(p13, 21)(q22, fusion genes, oncogene activation, tumor precursors
- MeSH terms
- Animals, Disease Models, Animal, Humans, Leukemia, Lymphoma, Translocation, Genetic, Oncogene Proteins, Fusion
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