Cellular Events in Radiation-induced Lymphomagenesis

Boniver, Jacques; Humblet, Chantal; Rongy, A. M.; Delvenne, Catherine; Delvenne, Philippe; Greimers, Roland; Thiry, Albert; Courtoy, R.; Defresne, Marie-Paule

doi:10.1080/09553009014550861

Cited by 10 publications

(3 citation statements)

References 19 publications

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“…Fractionated total body irradiation leads to thymocyte apoptosis and that in turn leads to differentiation arrest and population regeneration by the damaged but surviving thymocytes with tumorigenic potential [124,164,165,166]. Transplantation or intravenous infusion of unirradiated bone marrow into an irradiated host reduces lymphomagenesis possibly by restoring the thymic microenvironment and preventing clonal expansion of irradiated T-cell precursors.…”

Section: Resultsmentioning

confidence: 99%

Mouse Models for Efficacy Testing of Agents against Radiation Carcinogenesis — A Literature Review

Rivina

Schiestl

2012

IJERPH

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As the number of cancer survivors treated with radiation as a part of their therapy regimen is constantly increasing, so is concern about radiation-induced cancers. This increases the need for therapeutic and mitigating agents against secondary neoplasias. Development and efficacy testing of these agents requires not only extensive in vitro assessment, but also a set of reliable animal models of radiation-induced carcinogenesis. The laboratory mouse (Mus musculus) remains one of the best animal model systems for cancer research due to its molecular and physiological similarities to man, small size, ease of breeding in captivity and a fully sequenced genome. This work reviews relevant M. musculus inbred and F1 hybrid animal models and methodologies of induction of radiation-induced leukemia, thymic lymphoma, breast, and lung cancer in these models. Where available, the associated molecular pathologies are also included.

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Section: Resultsmentioning

confidence: 99%

Mouse Models for Efficacy Testing of Agents against Radiation Carcinogenesis — A Literature Review

Rivina

Schiestl

2012

IJERPH

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“…On chromosome 18 resides the Rbbp8 gene that encodes the CtIP protein, a suspected tumor suppressor. Boniver et al (1990aBoniver et al ( , 1990b, Hogarth, Edwards, et al (1982), Kaplan (1964), Kaplan, Brown, and Paull (1953), McMorrow, Newcomb, and Pellicer (1988), Mori and Takamori (1990), Okano et al (1999), Hilgers (1989, 1990), Payne and Dovat (2011), Saito et al (2001), Sasaki (1982), Shimada et al (2000), and Takabatake et al The fact that sporadic chromosome rearrangements bearing Rbbp8 gene have been reported in a variety of human neoplastic diseases including AML gives this gene more credibility (Darakhshan et al, 2006).…”

Section: Underlying Molecular Pathologies Of Ri Leukemiamentioning

confidence: 99%

“…Irradiation of these animals at 4-6 weeks of age for 4 weeks at 8-day intervals with 1.7 Gy/dose resulted in a 93% TL induction within 180-250 days. Thymic lymphoma with similar disease latency and penetrance can be induced in at least three other C57BL substrains: C57BL/6, C57BL/10, and C57BL/Ka (Boniver et al, 1990a(Boniver et al, ,1990bHumblet, Greimers, Boniver, & Defrense, 1997). Thymic lymphoma with similar disease latency and penetrance can be induced in at least three other C57BL substrains: C57BL/6, C57BL/10, and C57BL/Ka (Boniver et al, 1990a(Boniver et al, ,1990bHumblet, Greimers, Boniver, & Defrense, 1997).…”

Section: C57bl Modelmentioning

confidence: 99%

Mouse Models of Radiation-Induced Cancers

Rivina

Schiestl

2013

Advances in Genetics

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Radiation-induced (RI) secondary cancers were not a major clinical concern even as little as 15 years ago. However, advances in cancer diagnostics, therapy, and supportive care have saved numerous lives and many former cancer patients are now living for 5, 10, 20, and more years beyond their initial diagnosis. The majority of these patients have received radiotherapy as a part of their treatment regimen and are now beginning to develop secondary cancers arising from normal tissue exposure to damaging effects of ionizing radiation. Because historically patients rarely survived past the extended latency periods inherent to these RI cancers, very little effort was channeled towards the research leading to the development of therapeutic agents intended to prevent or ameliorate oncogenic effects of normal tissue exposure to radiation. The number of RI cancers is expected to increase very rapidly in the near future, but the field of cancer biology might not be prepared to address important issues related to this phenomena. One such issue is the ability to accurately differentiate between primary tumors and de novo arising secondary tumors in the same patient. Another issue is the lack of therapeutic agents intended to reduce such cancers in the future. To address these issues, large-scale epidemiological studies must be supplemented with appropriate animal modeling studies. This work reviews relevant mouse (Mus musculus) models of inbred and F1 animals and methodologies of induction of most relevant radiation-associated cancers: leukemia, lymphoma, and lung and breast cancers. Where available, underlying molecular pathologies are included.

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Flow-cytometric identification and follow-up of mice exposed to x-irradiation: Evaluation of a model system

Johannisson

Grawé

Nilsson

et al. 1995

Radiat Environ Biophys

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An experimental model system is presented that allows the identification and follow-up of mice exposed to ionizing radiation using flow-cytometric measurements of peripheral blood cells. In an experiment, properties of peripheral blood cells were analysed with flow cytometry for a rapid identification of individuals exposed to radiation. Individuals were then followed longitudinally in an attempt to identify those developing neoplasias. Male CBA mice, 25 days old, were subjected to fractionated x-irradiation (4 x 1.31 Gy) to induce haematopoietic malignancies. By repeated blood sampling followed by flow cytometry, frequencies of micronucleated erythrocytes and of proliferating nucleated cells were determined. Neoplasias were diagnosed by histopathology. Five days after the end of radiation exposure, increased frequencies of proliferating cells, polychromatic erythrocytes and micronucleated normochromatic erythrocytes clearly distinguished the exposed group from the control group. Increased cell proliferation in peripheral blood cells could be used to identify animals with manifest tumours, although these animals were at a late stage of tumour development. Animals with thymic lymphoma (not generalized) could not be identified with the flow-cytometric parameters used. We consider that this model system has a potential use when a small number of risk individuals need to be identified and monitored within a large population.

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Cellular Events in Radiation-induced Lymphomagenesis

Cited by 10 publications

References 19 publications

Mouse Models for Efficacy Testing of Agents against Radiation Carcinogenesis — A Literature Review

Mouse Models for Efficacy Testing of Agents against Radiation Carcinogenesis — A Literature Review

Mouse Models of Radiation-Induced Cancers

Flow-cytometric identification and follow-up of mice exposed to x-irradiation: Evaluation of a model system

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