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Relevant bibliographies by topics / APCmin

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Journal articles

Academic literature on the topic 'APCmin'

Author: Grafiati

Published: 4 June 2021

Last updated: 1 February 2022

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Journal articles on the topic "APCmin"

1

Godavarthi, Jyotsna D., Shahrazad Polk, Lisa Nunez, Amruthesh Shivachar, Nancy L. Glenn Griesinger, and Angabin Matin. "Deficiency of Splicing Factor 1 (SF1) Reduces Intestinal Polyp Incidence in ApcMin/+ Mice." Biology 9, no. 11 (2020): 398. http://dx.doi.org/10.3390/biology9110398.

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Background: Splicing factor 1 (SF1) is a conserved alternative splicing factor expressed in many different mammalian cell types. The genetically modified Sf1+/− (or Sf1β-geo/+) mice express reduced levels of SF1 protein in mouse tissues, including in cells of the intestines. Mutational inactivation of human adenomatous polyposis coli (APC) gene deregulates the Wnt signaling pathway and is a frequent genetic event in colon cancers. Mice with a point mutation in the Apc gene (ApcMin/+) also develop numerous intestinal polyps at a young age. Our aim was to determine the effect of reduced SF1 leve

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2

Baltgalvis, Kristen A., Franklin G. Berger, Maria Marjorette O. Pena, J. Mark Davis, Stephanie J. Muga, and James A. Carson. "Interleukin-6 and cachexia inApcMin/+mice." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 294, no. 2 (2008): R393—R401. http://dx.doi.org/10.1152/ajpregu.00716.2007.

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The ApcMin/+mouse has a mutation in the Apc tumor suppressor gene and develops intestinal polyps, beginning at 4 wk of age. This mouse develops cachexia by 6 mo, characterized by significant loss of muscle and fat tissue. The purpose of the present study was to determine the role of circulating interleukin-6 (IL-6) and the polyp burden for the development of cachexia in ApcMin/+mice. At 26 wk of age, mice exhibiting severe cachectic symptoms had a 61% decrease in gastrocnemius muscle weight, complete loss of epididymal fat, a 10-fold increase in circulating IL-6 levels, and an 89% increase in

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3

Tanner, Scott M., Joseph G. Daft, Stephanie A. Hill, Colin A. Martin, and Robin G. Lorenz. "Altered T-Cell Balance in Lymphoid Organs of a Mouse Model of Colorectal Cancer." Journal of Histochemistry & Cytochemistry 64, no. 12 (2016): 753–67. http://dx.doi.org/10.1369/0022155416672418.

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The adenomatous polyposis coli ( APC) gene is a known tumor suppressor gene, and mice with mutations in Apc (ApcMin/+) spontaneously form multiple intestinal neoplasms. In this model of human colorectal cancer (CRC), it has been reported that CD4+ T-cell-derived interleukin 17 (IL-17) promotes intestinal tumor development, but it is not known if the Apc mutation actually directly alters T-cell function and subsequently tumor immunosurveillance. To investigate the ApcMin/+ mutation on T-cell function, flow cytometric, histochemical, and immunofluorescent studies on both wild-type (Apc+/+) and A

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4

Coletta, P. Louise, Albrecht M. Müller, Elena A. Jones, et al. "Lymphodepletion in the ApcMin/+ mouse model of intestinal tumorigenesis." Blood 103, no. 3 (2004): 1050–58. http://dx.doi.org/10.1182/blood-2003-03-0707.

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AbstractGerm line mutations in the Adenomatous polyposis coli tumor suppressor gene cause a hereditary form of intestinal tumorigenesis in both mice and man. Here we show that in ApcMin/+ mice, which carry a heterozygous germ line mutation at codon 850 of Apc, there is progressive loss of immature and mature thymocytes from approximately 80 days of age with complete regression of the thymus by 120 days. In addition, ApcMin/+ mice show parallel depletion of splenic natural killer (NK) cells, immature B cells, and B progenitor cells in bone marrow due to complete loss of interleukin 7 (IL-7)-dep

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5

De Santis, Stefania, Giulio Verna, Grazia Serino, et al. "Winnie-APCMin/+ Mice: A Spontaneous Model of Colitis-Associated Colorectal Cancer Combining Genetics and Inflammation." International Journal of Molecular Sciences 21, no. 8 (2020): 2972. http://dx.doi.org/10.3390/ijms21082972.

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(1) Background: Colorectal cancer (CRC) is among the best examples of the relationship between inflammation and increased cancer risk. (2) Methods: To examine the effects of spontaneous low-grade chronic inflammation on the pathogenesis of CRC, we developed a new murine model of colitis-associated cancer (CAC) by crossing Mucin 2 mutated mice (Winnie) with ApcMin/+ mice. (3) Results: The resulting Winnie-ApcMin/+ model combines an inflammatory background with a genetic predisposition to small intestinal polyposis. Winnie-ApcMin/+ mice show an early occurrence of inflammatory signs and dysplast

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6

De Santis, Stefania, Marina Liso, Mirco Vacca, et al. "Dysbiosis Triggers ACF Development in Genetically Predisposed Subjects." Cancers 13, no. 2 (2021): 283. http://dx.doi.org/10.3390/cancers13020283.

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Background: Colorectal cancer (CRC) is the third most common cancer worldwide, characterized by a multifactorial etiology including genetics, lifestyle, and environmental factors including microbiota composition. To address the role of microbial modulation in CRC, we used our recently established mouse model (the Winnie-APCMin/+) combining inflammation and genetics. Methods: Gut microbiota profiling was performed on 8-week-old Winnie-APCMin/+ mice and their littermates by 16S rDNA gene amplicon sequencing. Moreover, to study the impact of dysbiosis induced by the mother’s genetics in ACF devel

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7

Lee, Yunna, Elise L. Ma, Marisa Patel, et al. "Corticotropin-Releasing Hormone Receptor Alters the Tumor Development and Growth in Apcmin/+ Mice and in a Chemically-Induced Model of Colon Cancer." International Journal of Molecular Sciences 22, no. 3 (2021): 1043. http://dx.doi.org/10.3390/ijms22031043.

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The neuroendocrine circuit of the corticotropin-releasing hormone (CRH) family peptides, via their cognate receptors CRHR1 and CRHR2, copes with psychological stress. However, peripheral effects of the CRH system in colon cancer remains elusive. Thus, we investigate the role of CRHR1 and CRHR2 in colon cancer. Human colon cancer biopsies were used to measure the mRNA levels of the CRH family by quantitative real-time PCR. Two animal models of colon cancer were used: Apcmin/+ mice and azoxymethane (AOM)/dextran sulfate sodium (DSS)-treated mice. The mRNA levels of CRHR2 and UCN III are reduced

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8

Zasadil, Lauren M., Eric M. C. Britigan, Sean D. Ryan, et al. "High rates of chromosome missegregation suppress tumor progression but do not inhibit tumor initiation." Molecular Biology of the Cell 27, no. 13 (2016): 1981–89. http://dx.doi.org/10.1091/mbc.e15-10-0747.

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Aneuploidy, an abnormal chromosome number that deviates from a multiple of the haploid, has been recognized as a common feature of cancers for >100 yr. Previously, we showed that the rate of chromosome missegregation/chromosomal instability (CIN) determines the effect of aneuploidy on tumors; whereas low rates of CIN are weakly tumor promoting, higher rates of CIN cause cell death and tumor suppression. However, whether high CIN inhibits tumor initiation or suppresses the growth and progression of already initiated tumors remained unclear. We tested this using the ApcMin/+ mouse intestinal

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9

Hetzler, Kimbell L., Justin P. Hardee, Holly A. LaVoie, E. Angela Murphy, and James A. Carson. "Ovarian function’s role during cancer cachexia progression in the female mouse." American Journal of Physiology-Endocrinology and Metabolism 312, no. 5 (2017): E447—E459. http://dx.doi.org/10.1152/ajpendo.00294.2016.

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Cachexia is a debilitating condition that occurs with chronic disease, including cancer; our research has shown that some regulation of cancer cachexia progression is affected by sex differences. The ApcMin/+ mouse is genetically predisposed to develop intestinal tumors; IL-6 signaling and hypogonadism are associated with cachexia severity in the male. This relationship in the female warrants further investigation, as we have shown that the ability of IL-6 to induce cachexia differs between the sexes. Since ovarian reproductive function relies on a complex system of endocrine signaling to affe

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10

Joyce, D. E., G. Mulji, L. S. Gutierrez, and F. J. Castellino. "Evaluation of the thrombospondin-1 analogue ABT-510 in the APCMin/+ mouse intestinal adenoma model." Journal of Clinical Oncology 24, no. 18_suppl (2006): 13545. http://dx.doi.org/10.1200/jco.2006.24.18_suppl.13545.

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13545 Background: The extracellular matrix protein Thrombospondin-1 (TSP-1) affects the angiogenic balance in cancer to suppress tumor growth. Exogenous TSP-1 or the peptide derivative ABT-510 (Abbott, Chicago, IL) can reverse this angiogenic switch from adenoma to carcinoma. We evaluated treatment effects of ABT-510 in the APCMin/+ mouse spontaneous intestinal adenoma model. This study determined reduction in intestinal adenoma number after ABT-510 or the combined treatment of ABT-510/bevacizumab (Genentech) compared to no treatment in APCMin/+. Proliferation, vascularity, and dysplasia were

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