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Ionizing radiation, inflammation, and their interactions in colon carcinogenesis in Mlh1-deficient mice.

Morioka T, Miyoshi-Imamura T, Blyth BJ, Kaminishi M, Kokubo T, Nishimura M, Kito S, Tokairin Y, Tani S, Murakami-Murofushi K, Yoshimi N, Shimada Y, Kakinuma S - Cancer Sci. (2015)

Bottom Line: Mutations in the mutL homolog 1 (MLH1) gene, one of the DNA mismatch repair genes, are a main cause of hereditary colon cancer syndromes such as Lynch syndrome.Immunohistochemistry revealed that expression of both p53 and β-catenin and loss of p21 and adenomatosis polyposis coli proteins were observed at the later stages of carcinogenesis, suggesting a course of molecular pathogenesis distinct from typical sporadic or colitis-associated colon cancer in humans.In conclusion, radiation exposure could further increase the risk of colorectal carcinogenesis induced by inflammation under the conditions of Mlh1 deficiency.

View Article: PubMed Central - PubMed

Affiliation: Radiation Effect Accumulation and Prevention Project, Fukushima Project Headquarters, National Institute of Radiological Sciences, Chiba, Japan; Radiobiology for Children's Health Program, Research Center for Radiation Protection, National Institute of Radiological Sciences, Chiba, Japan.

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Macroscopic view of representative colon lesions from Mlh1−/− mice treated with X-ray irradiation and dextran sodium sulfate (DSS) alone or in combination. (a) X-rays (7 weeks) + DSS, female (arrow, single small protruded lesion). (b) X-rays (7 weeks) + DSS, male (arrow, single sessile polyp without hemorrhage). (c) DSS only, female (arrow, single large sessile polyp with hemorrhage). (d) X-rays (2 weeks) + DSS, male (arrow, single large sessile polyp with hemorrhage).
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fig02: Macroscopic view of representative colon lesions from Mlh1−/− mice treated with X-ray irradiation and dextran sodium sulfate (DSS) alone or in combination. (a) X-rays (7 weeks) + DSS, female (arrow, single small protruded lesion). (b) X-rays (7 weeks) + DSS, male (arrow, single sessile polyp without hemorrhage). (c) DSS only, female (arrow, single large sessile polyp with hemorrhage). (d) X-rays (2 weeks) + DSS, male (arrow, single large sessile polyp with hemorrhage).

Mentions: The typical gross appearance of colon lesions, which varied in size from 0.5 to 6 mm in diameter, is shown in Figure2. All lesions were sessile types and protruded into the lumen as a polyp (Fig.2b–d) or plaque (Fig.2a). The large lesions, but no small lesions, had hemorrhage on part of the upper surface (Fig.2c,d). No other tumors developed during the experimental period.


Ionizing radiation, inflammation, and their interactions in colon carcinogenesis in Mlh1-deficient mice.

Morioka T, Miyoshi-Imamura T, Blyth BJ, Kaminishi M, Kokubo T, Nishimura M, Kito S, Tokairin Y, Tani S, Murakami-Murofushi K, Yoshimi N, Shimada Y, Kakinuma S - Cancer Sci. (2015)

Macroscopic view of representative colon lesions from Mlh1−/− mice treated with X-ray irradiation and dextran sodium sulfate (DSS) alone or in combination. (a) X-rays (7 weeks) + DSS, female (arrow, single small protruded lesion). (b) X-rays (7 weeks) + DSS, male (arrow, single sessile polyp without hemorrhage). (c) DSS only, female (arrow, single large sessile polyp with hemorrhage). (d) X-rays (2 weeks) + DSS, male (arrow, single large sessile polyp with hemorrhage).
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4376429&req=5

fig02: Macroscopic view of representative colon lesions from Mlh1−/− mice treated with X-ray irradiation and dextran sodium sulfate (DSS) alone or in combination. (a) X-rays (7 weeks) + DSS, female (arrow, single small protruded lesion). (b) X-rays (7 weeks) + DSS, male (arrow, single sessile polyp without hemorrhage). (c) DSS only, female (arrow, single large sessile polyp with hemorrhage). (d) X-rays (2 weeks) + DSS, male (arrow, single large sessile polyp with hemorrhage).
Mentions: The typical gross appearance of colon lesions, which varied in size from 0.5 to 6 mm in diameter, is shown in Figure2. All lesions were sessile types and protruded into the lumen as a polyp (Fig.2b–d) or plaque (Fig.2a). The large lesions, but no small lesions, had hemorrhage on part of the upper surface (Fig.2c,d). No other tumors developed during the experimental period.

Bottom Line: Mutations in the mutL homolog 1 (MLH1) gene, one of the DNA mismatch repair genes, are a main cause of hereditary colon cancer syndromes such as Lynch syndrome.Immunohistochemistry revealed that expression of both p53 and β-catenin and loss of p21 and adenomatosis polyposis coli proteins were observed at the later stages of carcinogenesis, suggesting a course of molecular pathogenesis distinct from typical sporadic or colitis-associated colon cancer in humans.In conclusion, radiation exposure could further increase the risk of colorectal carcinogenesis induced by inflammation under the conditions of Mlh1 deficiency.

View Article: PubMed Central - PubMed

Affiliation: Radiation Effect Accumulation and Prevention Project, Fukushima Project Headquarters, National Institute of Radiological Sciences, Chiba, Japan; Radiobiology for Children's Health Program, Research Center for Radiation Protection, National Institute of Radiological Sciences, Chiba, Japan.

Show MeSH
Related in: MedlinePlus