The Time Factor in Inhibition of Lymphoid-Tumor Development by Injection of Marrow Cell Suspensions into Irradiated C57BL Mice&lt;xref ref-type="fn" rid="fn1"&gt;2&lt;/xref&gt;&lt;xref ref-type="fn" rid="fn2"&gt;3&lt;/xref&gt;

The present experiments are an attempt to precise the type and localization of the cells involved in the protective effect of hemopoietic suspensions against the radiation-induced thymic lymphosarcoma (TLS) of C57BL/6 mice. Inocula containing variable numbers of BM or spleen CFUs from 60-day-old and 360-day-old donors were tested. According to their origin, the suspensions differed with respect to the CFU replication rate, the CFU ability to differentiate towards the T lineage and the content of the suspensions in thymic precursors. Two levels of inhibition were observed: BM suspensions from 60-day-old donors containing 1,500 CFUs had the best protective effect: 14.5% of TLS; 1,500 CFUs from 360-day-old donors were slightly but not significantly less efficient (28.5%). The second level of inhibition (36-46% of TLS) was obtained with all the following inocula: a) 1,200 and 300 spleen CFUs or 300 and 95 BM CFUs from 60-day-old donors, b) 1,500 spleen CFUs from aged donors. Seventy-six spleen CFUs from 60-day-old donors, 120 BM or 175 spleen CFUs from aged donors had no effect. These results suggest that in addition to the high replication rate of the BM CFUs as compared with spleen CFUs, cells endowed with an optimal protective effect are present in BM suspensions and are either absent or present in very small amount in spleen suspensions. These cells which induce an early repopulation of the thymus might correspond to thymic precursors.

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Protective effect of bone marrow and spleen suspensions on radiation-induced leukemogenesis in C57BL/6 mice

Legrand

Daculsi

Galiay

et al. 1984

Radiat Environ Biophys

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Failure of syngeneic bone marrow cells to protect against MC-induced lymphoma in dba/2 mice

Chen¹,

Berenblum²

1968

Br J Cancer

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Acute DNA damage activates the tumour suppressor p53 to promote radiation-induced lymphoma

et al. 2015

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Genotoxic cancer therapies, such as chemoradiation, cause hematologic toxicity primarily by activating the tumor suppressor p53. While inhibiting p53-mediated cell death during cancer therapy ameliorates hematologic toxicity, whether it also impacts carcinogenesis remains unclear. Here we utilize a mouse model of inducible p53 short hairpin RNA (shRNA) to show that temporarily blocking p53 during total-body irradiation (TBI) not only ameliorates acute toxicity, but also improves long-term survival by preventing lymphoma development. Using KrasLA1 mice, we show that TBI promotes the expansion of a rare population of thymocytes that express oncogenic KrasG12D. However, blocking p53 during TBI significantly suppresses the expansion of KrasG12D-expressing thymocytes. Mechanistically, bone marrow transplant experiments demonstrate that TBI activates p53 to decrease the ability of bone marrow cells to suppress lymphoma development through a non-cell-autonomous mechanism. Together, our results demonstrate that the p53 response to acute DNA damage promotes the development of radiation-induced lymphoma.

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The Time Factor in Inhibition of Lymphoid-Tumor Development by Injection of Marrow Cell Suspensions into Irradiated C57BL Mice<xref ref-type="fn" rid="fn1">2</xref><xref ref-type="fn" rid="fn2">3</xref>

Cited by 5 publications

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Protective effect of bone marrow and spleen suspensions on radiation-induced leukemogenesis in C57BL/6 mice

Protective effect of bone marrow and spleen suspensions on radiation-induced leukemogenesis in C57BL/6 mice

Failure of syngeneic bone marrow cells to protect against MC-induced lymphoma in dba/2 mice

Acute DNA damage activates the tumour suppressor p53 to promote radiation-induced lymphoma

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