PubTransformer

A site to transform Pubmed publications into these bibliographic reference formats: ADS, BibTeX, EndNote, ISI used by the Web of Knowledge, RIS, MEDLINE, Microsoft's Word 2007 XML.

Multiple Roles of APC and its Therapeutic Implications in Colorectal Cancer.

Abstract Adenomatous polyposis coli (APC) is widely accepted as a tumor suppressor gene highly mutated in colorectal cancers (CRC). Mutation and inactivation of this gene is a key and early event almost uniquely observed in colorectal tumorigenesis. Alterations in the APC gene generate truncated gene products, leading to activation of the Wnt signaling pathway and deregulation of multiple other cellular processes. It has been a mystery why most patients with CRC retain a truncated APC protein, but accumulating evidence suggest that these C terminally truncated APC proteins may have gain of function properties beyond the well-established loss of tumor suppressive function. Here, we will review the evidence for both the loss of function and the gain of function of APC truncations and how together they contribute to CRC initiation and progression.
PMID
Related Publications

Expression and mutation pattern of β-catenin and adenomatous polyposis coli in colorectal cancer patients.

Ovarian steroid cell tumor with biallelic adenomatous polyposis coli inactivation in a patient with familial adenomatous polyposis.

Role of oncogenic K-Ras in cancer stem cell activation by aberrant Wnt/β-catenin signaling.

APC loss-induced intestinal tumorigenesis in Drosophila: Roles of Ras in Wnt signaling activation and tumor progression.

The 'just-right' signaling model: APC somatic mutations are selected based on a specific level of activation of the beta-catenin signaling cascade.

Authors

Mayor MeshTerms

Mutation

Keywords
Journal Title journal of the national cancer institute
Publication Year Start




PMID- 28423402
OWN - NLM
STAT- MEDLINE
DA  - 20170419
DCOM- 20170501
LR  - 20170501
IS  - 1460-2105 (Electronic)
IS  - 0027-8874 (Linking)
VI  - 109
IP  - 8
DP  - 2017 Aug 01
TI  - Multiple Roles of APC and its Therapeutic Implications in Colorectal Cancer.
LID - 10.1093/jnci/djw332 [doi]
AB  - Adenomatous polyposis coli (APC) is widely accepted as a tumor suppressor gene
      highly mutated in colorectal cancers (CRC). Mutation and inactivation of this
      gene is a key and early event almost uniquely observed in colorectal
      tumorigenesis. Alterations in the APC gene generate truncated gene products,
      leading to activation of the Wnt signaling pathway and deregulation of multiple
      other cellular processes. It has been a mystery why most patients with CRC retain
      a truncated APC protein, but accumulating evidence suggest that these C
      terminally truncated APC proteins may have gain of function properties beyond the
      well-established loss of tumor suppressive function. Here, we will review the
      evidence for both the loss of function and the gain of function of APC
      truncations and how together they contribute to CRC initiation and progression.
CI  - (c) The Author 2017. Published by Oxford University Press. All rights reserved.
      For Permissions, please e-mail: [email protected]
FAU - Zhang, Lu
AU  - Zhang L
AD  - Affiliations of authors: Department of Cell Biology, University of Texas
      Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, TX 75390, USA.
FAU - Shay, Jerry W
AU  - Shay JW
AD  - Affiliations of authors: Department of Cell Biology, University of Texas
      Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, TX 75390, USA.
LA  - eng
PT  - Journal Article
PT  - Review
PL  - United States
TA  - J Natl Cancer Inst
JT  - Journal of the National Cancer Institute
JID - 7503089
RN  - 0 (APC protein, human)
RN  - 0 (Adenomatous Polyposis Coli Protein)
RN  - 0 (Tumor Suppressor Proteins)
RN  - 0 (beta Catenin)
SB  - IM
MH  - Adenomatous Polyposis Coli Protein/*genetics
MH  - Cell Transformation, Neoplastic/*genetics
MH  - Colorectal Neoplasms/*genetics
MH  - Genetic Predisposition to Disease/*genetics
MH  - Humans
MH  - Models, Genetic
MH  - *Mutation
MH  - Tumor Suppressor Proteins/genetics
MH  - Wnt Signaling Pathway/genetics
MH  - beta Catenin/genetics
EDAT- 2017/04/20 06:00
MHDA- 2017/05/02 06:00
CRDT- 2017/04/20 06:00
PHST- 2016/09/21 [received]
PHST- 2016/12/21 [accepted]
AID - 3113843 [pii]
AID - 10.1093/jnci/djw332 [doi]
PST - ppublish
SO  - J Natl Cancer Inst. 2017 Aug 1;109(8). doi: 10.1093/jnci/djw332.

<?xml version="1.0" encoding="UTF-8"?>
<b:Sources SelectedStyle="" xmlns:b="http://schemas.openxmlformats.org/officeDocument/2006/bibliography"  xmlns="http://schemas.openxmlformats.org/officeDocument/2006/bibliography" >
</b:Sources>