ArticleInternational journal of experimental pathology2006
Developmental abnormalities in multiple proliferative tissues of Apc(Min/+) mice.
Article in International journal of experimental pathology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
37 citing papers in PubMed, 48 citations in OpenAlex.
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- Cancer cachexia as a multiorgan failure: Reconstruction of the crime scene.Frontiers in cell and developmental biology · 2022Review
- Comparison of the fertility of tumor suppressor gene-deficient C57BL/6 mouse strains reveals stable reproductive aging and novel pleiotropic gene.Scientific reports · 2021Article
- MicroencapsulatedInternational journal of molecular sciences · 2021Article
- Analysis of mutations in tumor and normal adjacent tissue via fluorescence detection.Environmental and molecular mutagenesis · 2021Article
- HASPIN kinase inhibitor CHR-6494 suppresses intestinal polyp development, cachexia, and hypogonadism in Apcmin/+ mice.European journal of cancer prevention : the official journal of the European Cancer Prevention Organisation (ECP) · 2020Article
- Muscle metabolism and atrophy: let's talk about sex.Biology of sex differences · 2019Review
- Microtubule plus-end tracking Adenopolyposis Coli negatively regulates proplatelet formation.Scientific reports · 2018Article
- Generation of renewable mouse intestinal epithelial cell monolayers and organoids for functional analyses.BMC cell biology · 2018Article
- Mesenchymal MAPKAPK2/HSP27 drives intestinal carcinogenesis.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- Unique invariant natural killer T cells promote intestinal polyps by suppressing TH1 immunity and promoting regulatory T cells.Mucosal immunology · 2018Article
- Inhibition and deficiency of the immunoproteasome subunit LMP7 suppress the development and progression of colorectal carcinoma in mice.Oncotarget · 2017Article
- HuR Small-Molecule Inhibitor Elicits Differential Effects in Adenomatosis Polyposis and Colorectal Carcinogenesis.Cancer research · 2017Article
- Ovarian function's role during cancer cachexia progression in the female mouse.American journal of physiology. Endocrinology and metabolism · 2017Article
- Altered T-Cell Balance in Lymphoid Organs of a Mouse Model of Colorectal Cancer.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2016Article
- Increased variability in Apc(Min)/+ intestinal tissue can be measured with microultrasound.Scientific reports · 2016Article
Corrections and comments
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Authors and funding
14 authors at 3 institutions in 1 country.
Funding
Abstract
Germ-line mutation of the Apc gene has been linked to familial adenomatous polyposis (FAP) that predisposes to colon cancer. Apc(Min/+) mice, heterozygous for the Apc gene mutation, progressively develop small intestinal tumours in a manner that is analogous to that observed in the colon of patients with FAP (Su et al. 1992; Fodde et al. 1994; Moser et al. 1995). We have studied the effects of Apc gene mutation on murine intestinal and extra-intestinal, proliferatively active tissues. We have contrasted the histology to that of the age- and sex-matched wild-type C57BL/6 mice. Histological assessment of the normal appearing intestinal mucosa demonstrates minimal change in size of crypts. In contrast, villi are longer in the ileum of Apc(Min/+) mice relative to C57BL/6 mice at 12 and 15 weeks of age. Vigorous splenic haematopoiesis in Apc(Min/+) mice was seen at 12 and 15 weeks of age, as reflected by marked splenomegaly, increased splenic haematopoietic cells and megakaryocytes. Peripheral blood counts, however, did not differ between C57BL/6 and Apc(Min/+) mice at 15 weeks of age. Lymphoid depletion in Apc(Min/+) mice was characterized by diminished numbers of splenic lymphoid follicles and small intestinal Peyer's patches. The ovaries of 12- and 15-week-old Apc(Min/+) mice exhibited increased numbers of atretic follicles, and estrous cycling by serial vaginal smears showed tendency of elongation in the mutant mice during these age ranges. The testicles of 10-week-old Apc(Min/+) mice showed increased numbers of underdeveloped seminiferous tubules. Collectively, these data suggest that, in addition to its obvious effects upon intestinal adenoma formation, Apc gene mutation causes impairment of developmental and apparent differentiation blockade in proliferative tissues, including those of the haematopoietic system, lymphoid and reproductive tract.
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Registered trials
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