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|a Chen, Xiaowei
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|a Massachusetts Institute of Technology. Department of Biological Engineering
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|a Massachusetts Institute of Technology. Division of Comparative Medicine
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|a Koch Institute for Integrative Cancer Research at MIT
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|a Miller, Cassandra L.
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|a Muthupalani, Sureshkumar
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|a Shen, Zeli
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|a Drees, Frauke
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|a Ge, Zhongming
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|a Feng, Yan
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|a Gong, Guanyu
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|a Gertler, Frank
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|a Fox, James G
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|a Nagar, Karan K.
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|a Wang, Timothy C.
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|a Miller, Cassandra L.
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|a Muthupalani, Sureshkumar
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|a Shen, Zeli
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|a Drees, Frauke
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|a Ge, Zhongming
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|a Feng, Yan
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|a Gong, Guanyu
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|a Gertler, Frank
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|a Fox, James G
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|a Lamellipodin-Deficient Mice: A Model of Rectal Carcinoma
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|b Public Library of Science,
|c 2017-05-31T13:20:47Z.
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|z Get fulltext
|u http://hdl.handle.net/1721.1/109443
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|a During a survey of clinical rectal prolapse (RP) cases in the mouse population at MIT animal research facilities, a high incidence of RP in the lamellipodin knock-out strain, C57BL/6-Raph1[superscript tm1Fbg] (Lpd[superscript -/-]) was documented. Upon further investigation, the Lpd[superscript -/-] colony was found to be infected with multiple endemic enterohepatic Helicobacter species (EHS). Lpd[superscript -/-] mice, a transgenic mouse strain produced at MIT, have not previously shown a distinct immune phenotype and are not highly susceptible to other opportunistic infections. Predominantly male Lpd[superscript -/-] mice with RP exhibited lesions consistent with invasive rectal carcinoma concomitant to clinically evident RP. Multiple inflammatory cytokines, CD11b+Gr1+ myeloid-derived suppressor cell (MDSC) populations, and epithelial cells positive for a DNA damage biomarker, H2AX, were elevated in affected tissue, supporting their role in the neoplastic process. An evaluation of Lpd[superscript -/-] mice with RP compared to EHS-infected, but clinically normal (CN) Lpd[superscript -/-] animals indicated that all of these mice exhibit some degree of lower bowel inflammation; however, mice with prolapses had significantly higher degree of focal lesions at the colo-rectal junction. When Helicobacter spp. infections were eliminated in Lpd[superscript -/-] mice by embryo transfer rederivation, the disease phenotype was abrogated, implicating EHS as a contributing factor in the development of rectal carcinoma. Here we describe lesions in Lpd[superscript -/-] male mice consistent with a focal inflammation-induced neoplastic transformation and propose this strain as a mouse model of rectal carcinoma.
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|a United States. National Institutes of Health (T32-OD010978)
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|a United States. National Institutes of Health (R01-OD011141)
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|a United States. National Institutes of Health (P30-ES002109)
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|a Massachusetts Institute of Technology. Ludwig Center for Molecular Oncology (U54- CA114462)
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|a National Cancer Institute (U.S.) (P30-CA14051)
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|a en_US
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|a Article
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|t PLOS ONE
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