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

Chen, Louise; Berenblum, I.

doi:10.1038/bjc.1968.69

Cited by 3 publications

(2 citation statements)

References 5 publications

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“…31,32) Strain difference in radiation effects on the thymus and bone marrow was investigated using susceptible B10 and resistant C3H or STS strains. 33) A study with radiation bone marrow chimeras revealed that the difference between B10 and C3H mice in lymphoma susceptibility was due to that of bone marrow-derived cells, and the resistance of STS, but not C3H, was ascribed to an intrinsic property of thymocytes.…”

Section: Discussionmentioning

confidence: 99%

The D4Mit12 locus on mouse chromosome 4 provides susceptibility to both γ‐ray‐induced and N‐methyl‐N‐nitrosourea‐induced thymic lymphomas

Sato¹,

Tamura²,

Ochiai³

et al. 2003

Cancer Science

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Low-penetrance genes control different susceptibilities to γ γ γ γ-rayinduced thymic lymphomas in mouse strains. Our previous genetic analyses with backcross mice between BALB/c and MSM strains and congenic lines localized one such gene near the D4Mit12 locus on chromosome 4. N-Methyl-N-nitrosourea (MNU) is a guanine base-alkylating agent and differs from γ γ γ γ-radiation in its mechanism of mutagenic action. Accordingly, in this study, we examined whether or not the locus also provides susceptibility to MNU-induced thymic lymphomas using 84 offsprings derived from congenic mice for D4Mit12. Association analysis provided a suggestive linkage at D4Mit12 (P = = = =0.0075) and the linkage was sustained by the peak of likelihood ratio statistical values being at the same position as that for the γ γ γ γ-ray-induced lymphomas. The results strongly suggest that the BALB/c allele near D4Mit12 is associated with susceptibility to lymphomas induced by two carcinogenic agents having different mechanisms of mutagenic action. (Cancer Sci 2003; 94: 668-671) enetic variation plays a key role in determining the range of individual susceptibility to cancers within human population, and there is increasing evidence that a high proportion of cancers arise in a susceptible subpopulation that carries lowpenetrance genes. [1][2][3][4][5] The importance of susceptibility genes has been underlined, because the identification of such genes has possible public health implications, and can be achieved using information from the human genome project. Mouse thymic lymphomas are one of the classical models of radiation-induced and chemical carcinogen-induced malignancies, [6][7][8] and the model involves low-penetrance susceptibility genes in mouse strains. For instance, BALB/c (C) is susceptible to the development of γ-ray-induced thymic lymphomas 9, 10) while MSM (M), an inbred strain derived from Japanese wild mice, Mus musculus molossinus, shows resistance. 11) Our previous analyses of backcross mice between sensitive and resistant strains and congenic lines localized one of the susceptibility genes near the D4Mit12 locus on chromosome 4. 12) Mice with the C/M genotype at D4Mit12 showed an incidence twice as high as that in mice with the M/M genotype. This indicated that the BALB/c allele near D4Mit12 provides susceptibility in a dominant manner, although the nature of the susceptibility locus is not clear.N-Methyl-N-nitrosourea (MNU) is an alkylating agent that can modify guanine bases in DNA and some of the modified guanines are changed to adenine after DNA replication. The mode of action differs from that of radiation; i.e., the major type of radiation-induced DNA change is large mutations, such as deletion and translocation.13) It is of interest, therefore, to know whether or not the BALB/c allele near the D4Mit12 locus provides susceptibility to MNU-induced thymic lymphomas as well. This may give a clue to the function of the susceptibility gene in lymphomagenesis. In this study we have investigated this issue using congenic mice ...

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Section: Discussionmentioning

confidence: 99%

The D4Mit12 locus on mouse chromosome 4 provides susceptibility to both γ‐ray‐induced and N‐methyl‐N‐nitrosourea‐induced thymic lymphomas

Sato¹,

Tamura²,

Ochiai³

et al. 2003

Cancer Science

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“…On the other hand, involvement of the thymus and bone marrow is not well studied in thymic lymphomas induced by chemical carcinogens despite similar serological properties of lymphoma cells as those induced by radiation (36). It is noteworthy that the development of DMBA-induced thymic lymphomas was not suppressed by bone marrow transplantation (37,38).…”

Section: Discussionmentioning

confidence: 99%

The D5Mit7 locus on mouse chromosome 5 provides resistance to -ray-induced but not N-methyl-N-nitrosourea-induced thymic lymphomas

Kodama

Yoshikai²,

Tamura³

et al. 2003

Carcinogenesis

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Susceptibility to gamma-ray induction of thymic lymphomas in mouse strains is controlled by low-penetrance genetic variant alleles. Our previous genome-wide scan of a mouse backcross between BALB/c and MSM strains suggested the existence of a BALB/c resistance locus near D5Mit5 on chromosome 5. To confirm this resistance, we produced congenic mice carrying a 28.4 cM region between D5Mit4 and D5Mit315 from the MSM parental strain on the BALB/c background. Lymphomas were induced in their progeny by gamma-ray irradiation or administration of N-methyl-N-nitrosourea (MNU), an alkylating agent. The incidence of radiogenic lymphomas was 87.5% in mice of the M/M genotype at D5Mit7, significantly higher than the 46% incidence in mice of the C/M genotype, indicating highly significant linkage between the locus and the resistance (P = 0.000054). In contrast, the frequencies of MNU-induced thymic lymphomas were similar between the two genotypes (P = 0.35 in chi2 test). These results confirm the presence of a resistance allele for gamma-ray induction of thymic lymphomas near the D5Mit7 locus and strongly suggest that this locus modifies carcinogenic risk from exposure to radiation but not to alkylating agents.

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Effects of Syngeneic Bone Marrow Cells on Mice Given a Leukemogenic Treatment with Urethan

Razon

1973

Tumori

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A leukemogenic treatment with urethan in infant (SWR x C57BL)F1 mice (1 mg/g body weight, 5 times, once every second day) induced a marked reduction of the thymus and spleen weight, of the number of RBC, WBC, and bone marrow cells, with an inverted lymphoid/myeloid cell ratio in the bone marrow. An analysis of the bone marrow population showed that the carcinogen acted selectively on the lymphoid cells and, to a lesser extent, on the erythroblastic ones, while the myeloid cells did not appear to be involved. The damage was still present 10 days after the end of treatment. A single intracardiac inoculum of 15–20 × 106 syngeneic normal bone marrow cells, 3 days after the last urethan injection, determined a recovery of the spleen weight and of the cell ratio in the bone marrow, whereas the thymus weight and the blood and bone marrow cell counts were uneffected. Moreover the bone marrow inoculum failed to inhibit the induction of thymic lymphosarcomas.

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

Cited by 3 publications

References 5 publications

The D4Mit12 locus on mouse chromosome 4 provides susceptibility to both γ‐ray‐induced and N‐methyl‐N‐nitrosourea‐induced thymic lymphomas

The D4Mit12 locus on mouse chromosome 4 provides susceptibility to both γ‐ray‐induced and N‐methyl‐N‐nitrosourea‐induced thymic lymphomas

The D5Mit7 locus on mouse chromosome 5 provides resistance to -ray-induced but not N-methyl-N-nitrosourea-induced thymic lymphomas

Effects of Syngeneic Bone Marrow Cells on Mice Given a Leukemogenic Treatment with Urethan

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