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Article ; Online: Cancer: Context Is Key for E-cadherin in Invasion and Metastasis.

Fearon, Eric R

2019 Volume 29, Issue 21, Page(s) R1140–R1142

Abstract: A recent paper demonstrates how tissue context impacts the breast cancer cell phenotype. Loss of the E-cadherin tumor suppressor protein enhanced cell invasion, but inhibited multiple steps in metastatic spread due to the accumulation of reactive oxygen ... ...

Abstract	A recent paper demonstrates how tissue context impacts the breast cancer cell phenotype. Loss of the E-cadherin tumor suppressor protein enhanced cell invasion, but inhibited multiple steps in metastatic spread due to the accumulation of reactive oxygen species and induction of apoptosis.
MeSH term(s)	Apoptosis ; Breast Neoplasms ; Cadherins ; Humans ; Neoplasm Invasiveness ; Tumor Suppressor Proteins
Chemical Substances	Cadherins ; Tumor Suppressor Proteins
Language	English
Publishing date	2019-11-05
Publishing country	England
Document type	Journal Article ; Comment
ZDB-ID	1071731-6
ISSN	1879-0445 ; 0960-9822
ISSN (online)	1879-0445
ISSN	0960-9822
DOI	10.1016/j.cub.2019.09.054
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Zs.A 3208: Show issues

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Article: MOLECULAR FEATURES AND MOUSE MODELS OF COLORECTAL CANCER.

Fearon, Eric R

Transactions of the American Clinical and Climatological Association

2018 Volume 129, Page(s) 56–62

Abstract: Colorectal cancers (CRCs) harbor accumulated defects in key signaling pathways that regulate cell phenotypes, including proliferation, survival, metabolism, and differentiation. To study the functional contributions of the accumulated molecular defects ... ...

Abstract	Colorectal cancers (CRCs) harbor accumulated defects in key signaling pathways that regulate cell phenotypes, including proliferation, survival, metabolism, and differentiation. To study the functional contributions of the accumulated molecular defects in CRC, we have developed approaches to inactivate selected tumor suppressor and/or activate oncogenes in mouse colon epithelium. Conditional inactivation of the CDX2 tumor suppressor protein in conjunction with oncogenic activation of the BRAF protein promotes development of serrated glandular benign and malignant tumors in the mouse colon. The mouse tumors share significant morphological and molecular relationships with the 8% to 10% of human CRCs that manifest serrated morphology at diagnosis. The gene and protein expression patterns in the mouse tumors have informed understanding of the relationships between benign and malignant human serrated colon tumors. Our findings are consistent with prior work suggesting that perhaps upwards of one-third of human CRCs may arise from a precursor lesion with serrated morphology rather than a conventional adenoma.
MeSH term(s)	Animals ; Biomarkers, Tumor/genetics ; Biomarkers, Tumor/metabolism ; Cell Transformation, Neoplastic/genetics ; Cell Transformation, Neoplastic/metabolism ; Cell Transformation, Neoplastic/pathology ; Colorectal Neoplasms/genetics ; Colorectal Neoplasms/metabolism ; Colorectal Neoplasms/pathology ; Gene Expression Regulation, Neoplastic ; Genetic Predisposition to Disease ; Humans ; Mice ; Mutation ; Neoplasms, Experimental/genetics ; Neoplasms, Experimental/metabolism ; Neoplasms, Experimental/pathology ; Phenotype ; Prognosis ; Risk Factors ; Signal Transduction
Chemical Substances	Biomarkers, Tumor
Language	English
Publishing date	2018-08-30
Publishing country	United States
Document type	Journal Article
ZDB-ID	603823-2
ISSN	0065-7778
ISSN	0065-7778
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Article ; Online: Molecular genetics of colorectal cancer.

Fearon, Eric R

Annual review of pathology

2011 Volume 6, Page(s) 479–507

Abstract: Over the past three decades, molecular genetic studies have revealed some critical mutations underlying the pathogenesis of the sporadic and inherited forms of colorectal cancer (CRC). A relatively limited number of oncogenes and tumor-suppressor genes- ... ...

Abstract	Over the past three decades, molecular genetic studies have revealed some critical mutations underlying the pathogenesis of the sporadic and inherited forms of colorectal cancer (CRC). A relatively limited number of oncogenes and tumor-suppressor genes-most prominently the APC, KRAS, and p53 genes-are mutated in a sizeable fraction of CRCs, and a larger collection of genes that are mutated in subsets of CRC have begun to be defined. Together with DNA-methylation and chromatin-structure changes, the mutations act to dysregulate conserved signaling networks that exert context-dependent effects on critical cell phenotypes, including the regulation of cellular metabolism, proliferation, differentiation, and survival. Much work remains to be done to fully understand the nature and significance of the individual and collective genetic and epigenetic defects in CRC. Some key concepts for the field have emerged, two of which are emphasized in this review. Specifically, the gene defects in CRC often target proteins and pathways that exert pleiotropic effects on the cancer cell phenotype, and particular genetic and epigenetic alterations are linked to biologically and clinically distinct subsets of CRC.
MeSH term(s)	Adenoma/genetics ; Adenoma/pathology ; Adenomatous Polyposis Coli/genetics ; Adenomatous Polyposis Coli/pathology ; Colorectal Neoplasms/genetics ; Colorectal Neoplasms/pathology ; Epigenesis, Genetic/physiology ; Genes, Tumor Suppressor/physiology ; Humans
Language	English
Publishing date	2011
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	2227429-7
ISSN	1553-4014 ; 1553-4006
ISSN (online)	1553-4014
ISSN	1553-4006
DOI	10.1146/annurev-pathol-011110-130235
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Article ; Online: Germline Sequence Variants and Ovarian Cancer: Known-Knowns and Known-Unknowns.

Stoffel, Elena M / Fearon, Eric R

JAMA oncology

2016 Volume 2, Issue 4, Page(s) 491–492

MeSH term(s)	Base Sequence ; Breast Neoplasms ; Female ; Genetic Predisposition to Disease ; Genetic Variation ; Germ Cells ; Germ-Line Mutation ; Humans ; Neoplasms ; Ovarian Neoplasms ; Risk Factors
Language	English
Publishing date	2016-04
Publishing country	United States
Document type	Comment ; Journal Article
ISSN	2374-2445
ISSN (online)	2374-2445
DOI	10.1001/jamaoncol.2015.5622
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Article ; Online: CDX2: Linking Cell and Patient Fates in Colon Cancer.

Fearon, Eric R / Huang, Emina H

Cell stem cell

2016 Volume 18, Issue 2, Page(s) 168–169

Abstract: Administering adjuvant chemotherapy to stage II colon cancer patients is controversial due to limited benefit observed for this subpopulation. Recently, Dalerba et al. (2016) identified a subgroup of stage II patients that might benefit from adjuvant ... ...

Abstract	Administering adjuvant chemotherapy to stage II colon cancer patients is controversial due to limited benefit observed for this subpopulation. Recently, Dalerba et al. (2016) identified a subgroup of stage II patients that might benefit from adjuvant chemotherapy based on lack of CDX2 expression in their cancer stem cells.
MeSH term(s)	CDX2 Transcription Factor ; Cell Lineage ; Chemotherapy, Adjuvant ; Colonic Neoplasms/drug therapy ; Colonic Neoplasms/pathology ; Homeodomain Proteins/metabolism ; Humans ; Neoplastic Stem Cells/pathology ; Trans-Activators/metabolism
Chemical Substances	CDX2 Transcription Factor ; Homeodomain Proteins ; Trans-Activators
Language	English
Publishing date	2016--04
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Comment
ZDB-ID	2375354-7
ISSN	1875-9777 ; 1934-5909
ISSN (online)	1875-9777
ISSN	1934-5909
DOI	10.1016/j.stem.2016.01.011
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Zs.A 6589: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular ab Jg. 2022: Lesesaal (EG)
Zs.MG 75: Show issues

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Article ; Online: Aging accelerates while multiparity delays tumorigenesis in mouse models of high-grade serous carcinoma.

Hou, Xiaoman / Zhai, Yali / Hu, Kevin / Liu, Chia-Jen / Udager, Aaron / Pearce, Celeste L / Fearon, Eric R / Cho, Kathleen R

Gynecologic oncology

2022 Volume 165, Issue 3, Page(s) 552–559

Abstract: Objectives: The "incessant ovulation" hypothesis links increased risk for tubo-ovarian high-grade serous carcinoma (HGSC) due to more ovulations and reduced risk conferred by pre-menopausal exposures like oral contraceptive use, multiparity, and ... ...

Abstract	Objectives: The "incessant ovulation" hypothesis links increased risk for tubo-ovarian high-grade serous carcinoma (HGSC) due to more ovulations and reduced risk conferred by pre-menopausal exposures like oral contraceptive use, multiparity, and breastfeeding. However, most women diagnosed with HGSC are postmenopausal, implying age is a major risk factor for HGSC. Our mouse model for HGSC, based on tamoxifen (TAM)-induced somatic inactivation of the Brca1, Trp53, Rb1, and Nf1 (BPRN) tumor suppressor genes in oviductal epithelium, recapitulates key genetic, histopathologic, and biological features of human HGSCs. We aimed to credential the model for future efforts to define biological and risk modification factors in HGSC pathogenesis. Methods: BPRN mice were treated with TAM to induce tumors at defined ages and parity status. Results: BPRN mice aged 9-months prior to tumor induction had markedly shorter survival than 6-8 week old mice induced to form tumors (median 46.5 weeks versus 61.5 weeks, log-rank test P = 0.0006). No significant differences in cancer phenotypes were observed between multiparous versus nulliparous BPRN mice. However, using a modified tumor model with one wild-type Nf1 allele (BPRN Conclusions: Our findings show aging is associated with significantly shortened survival post tumor induction in the BRPN model and multiparity delays development and/or progression of HGSC in certain genetic contexts. The findings support relevance of our mouse model to gain mechanistic insights into how known factors exert their protective effects and to test novel approaches for HGSC prevention.
MeSH term(s)	Aging ; Animals ; Carcinoma ; Cell Transformation, Neoplastic/pathology ; Cystadenocarcinoma, Serous/pathology ; Disease Models, Animal ; Female ; Humans ; Mice ; Ovarian Neoplasms/pathology ; Parity ; Pregnancy
Language	English
Publishing date	2022-04-09
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	801461-9
ISSN	1095-6859 ; 0090-8258
ISSN (online)	1095-6859
ISSN	0090-8258
DOI	10.1016/j.ygyno.2022.03.030
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Zs.A 885: Show issues

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Article ; Online: PARsing the phrase "all in for Axin"- Wnt pathway targets in cancer.

Fearon, Eric R

Cancer cell

2009 Volume 16, Issue 5, Page(s) 366–368

Abstract: Genetic alternations resulting in constitutive stabilization of beta-catenin and altered transcription of beta-catenin/TCF-regulated genes are found in many cancers. A recent Nature paper offers insights into the role of tankyrase in regulating the Wnt/ ... ...

Abstract	Genetic alternations resulting in constitutive stabilization of beta-catenin and altered transcription of beta-catenin/TCF-regulated genes are found in many cancers. A recent Nature paper offers insights into the role of tankyrase in regulating the Wnt/beta-catenin pathway and suggests that compounds targeting tankyrase's poly-ADP-ribosylation (PARsylation) activity may hold promise for cancer therapy.
MeSH term(s)	Axin Protein ; Humans ; Neoplasms/genetics ; Neoplasms/metabolism ; Neoplasms/therapy ; Poly Adenosine Diphosphate Ribose/metabolism ; Repressor Proteins/genetics ; Repressor Proteins/metabolism ; Signal Transduction ; Tankyrases/genetics ; Tankyrases/metabolism ; Wnt Proteins/genetics ; Wnt Proteins/metabolism ; beta Catenin/genetics ; beta Catenin/metabolism
Chemical Substances	Axin Protein ; Repressor Proteins ; Wnt Proteins ; beta Catenin ; Poly Adenosine Diphosphate Ribose (26656-46-2) ; Tankyrases (EC 2.4.2.30)
Language	English
Publishing date	2009-11-06
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	2078448-X
ISSN	1878-3686 ; 1535-6108
ISSN (online)	1878-3686
ISSN	1535-6108
DOI	10.1016/j.ccr.2009.10.007
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Zs.A 5650: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
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Article ; Online: AXIN1 and AXIN2 variants in gastrointestinal cancers.

Mazzoni, Serina M / Fearon, Eric R

Cancer letters

2014 Volume 355, Issue 1, Page(s) 1–8

Abstract: Mutations in the APC (adenomatous polyposis coli) gene, which encodes a multi-functional protein with a well-defined role in the canonical Wnt pathway, underlie familial adenomatous polypsosis, a rare, inherited form of colorectal cancer (CRC) and ... ...

Abstract	Mutations in the APC (adenomatous polyposis coli) gene, which encodes a multi-functional protein with a well-defined role in the canonical Wnt pathway, underlie familial adenomatous polypsosis, a rare, inherited form of colorectal cancer (CRC) and contribute to the majority of sporadic CRCs. However, not all sporadic and familial CRCs can be explained by mutations in APC or other genes with well-established roles in CRC. The AXIN1 and AXIN2 proteins function in the canonical Wnt pathway, and AXIN1/2 alterations have been proposed as key defects in some cancers. Here, we review AXIN1 and AXIN2 sequence alterations reported in gastrointestinal cancers, with the goal of vetting the evidence that some of the variants may have key functional roles in cancer development.
MeSH term(s)	Amino Acid Sequence ; Animals ; Axin Protein/genetics ; Axin Protein/metabolism ; Carcinoma, Hepatocellular/genetics ; Carcinoma, Hepatocellular/metabolism ; Carcinoma, Hepatocellular/pathology ; Gastrointestinal Neoplasms/genetics ; Gastrointestinal Neoplasms/metabolism ; Gastrointestinal Neoplasms/pathology ; Genetic Predisposition to Disease ; Hepatoblastoma/genetics ; Hepatoblastoma/metabolism ; Hepatoblastoma/pathology ; Humans ; Liver Neoplasms/genetics ; Liver Neoplasms/metabolism ; Liver Neoplasms/pathology ; Molecular Sequence Data ; Mutation ; Phenotype ; Risk Factors ; Wnt Signaling Pathway/genetics
Chemical Substances	AXIN1 protein, human ; AXIN2 protein, human ; Axin Protein
Language	English
Publishing date	2014-09-16
Publishing country	Ireland
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	195674-7
ISSN	1872-7980 ; 0304-3835
ISSN (online)	1872-7980
ISSN	0304-3835
DOI	10.1016/j.canlet.2014.09.018
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Article ; Online: KRAS and cancer stem cells in APC-mutant colorectal cancer.

Fearon, Eric R / Wicha, Max S

Journal of the National Cancer Institute

2014 Volume 106, Issue 2, Page(s) djt444

MeSH term(s)	Animals ; Cell Transformation, Neoplastic/metabolism ; Colorectal Neoplasms/metabolism ; Colorectal Neoplasms/pathology ; Female ; Humans ; Male ; Mutation ; Neoplastic Stem Cells/metabolism ; Proto-Oncogene Proteins/genetics ; Proto-Oncogene Proteins p21(ras) ; Wnt Proteins/metabolism ; beta Catenin/metabolism ; ras Proteins/genetics
Chemical Substances	CTNNB1 protein, human ; KRAS protein, human ; Proto-Oncogene Proteins ; Wnt Proteins ; beta Catenin ; Proto-Oncogene Proteins p21(ras) (EC 3.6.5.2) ; ras Proteins (EC 3.6.5.2)
Language	English
Publishing date	2014-02
Publishing country	United States
Document type	Editorial ; Comment
ZDB-ID	2992-0
ISSN	1460-2105 ; 0027-8874 ; 0198-0157
ISSN (online)	1460-2105
ISSN	0027-8874 ; 0198-0157
DOI	10.1093/jnci/djt444
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Article ; Online: Molecular subtyping of colorectal cancer: time to explore both intertumoral and intratumoral heterogeneity to evaluate patient outcome.

Fearon, Eric R / Carethers, John M

Gastroenterology

2014 Volume 148, Issue 1, Page(s) 10–13

MeSH term(s)	Adenocarcinoma/genetics ; Adenocarcinoma/pathology ; Biomarkers, Tumor/genetics ; Colonic Neoplasms/genetics ; Colonic Neoplasms/pathology ; Colorectal Neoplasms/genetics ; CpG Islands ; DNA Methylation ; DNA Mismatch Repair ; Female ; Humans ; Male ; Microsatellite Instability ; Mutation ; Proto-Oncogene Proteins/genetics ; Proto-Oncogene Proteins B-raf/genetics ; Proto-Oncogene Proteins p21(ras) ; ras Proteins/genetics
Chemical Substances	Biomarkers, Tumor ; KRAS protein, human ; Proto-Oncogene Proteins ; BRAF protein, human (EC 2.7.11.1) ; Proto-Oncogene Proteins B-raf (EC 2.7.11.1) ; Proto-Oncogene Proteins p21(ras) (EC 3.6.5.2) ; ras Proteins (EC 3.6.5.2)
Language	English
Publishing date	2014-11-22
Publishing country	United States
Document type	Editorial ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Comment
ZDB-ID	80112-4
ISSN	1528-0012 ; 0016-5085
ISSN (online)	1528-0012
ISSN	0016-5085
DOI	10.1053/j.gastro.2014.11.024
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Zs.MO 572: Show issues

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