TY  - CHAP
M1  - Book, Section
TI  - Stomach Cancer
A1  - Powell, Steven M.
A2  - Valle, David L.
A2  - Antonarakis, Stylianos
A2  - Ballabio, Andrea
A2  - Beaudet, Arthur L.
A2  - Mitchell, Grant A.
PY  - 2019
T2  - The Online Metabolic and Molecular Bases of Inherited Disease
AB  - Adenocarcinoma  comprises  the  vast  majority  of  malignant  tumors  arising  from  the  stomach.  Gastric  carcinoma  is  a  significant  worldwide  health  burden,  second  only  to  lung  tumors  as  a  leading  cause  of  cancer  deaths.  Significant  geographic  and  temporal  variances  are  observed  in  this  cancer's  incidence,  predominantly  of  the  intestinal  type.  Epidemiologic  studies  indicate  a  strong  environmental  component  in  the  acquisition  of  this  cancer.  Developing  countries  that  are  noted  to  have  a  high  prevalence  of  Helicobacter  pylori  infection  early  in  life  are  distinctly  prone  to  having  high  rates  of  gastric  adenocarcinomas.  Most  gastric  cancers  are  identified  in  advanced  stages  that  present  in  the  later  decades  of  adult  life,  commonly  resulting  in  a  lethal  outcome  shortly  thereafter.Gastric  cancers  exhibit  heterogeneity  in  clinical,  biologic,  and  genetic  aspects.  Multiple  pathologic  classifications  of  gastric  adenocarcinomas  exist,  including  those  with  morphologic  and  histologic  criteria.  The  TNM  staging  system  is  generally  used  as  the  basis  for  prognostication  in  this  cancer,  with  depth  of  infiltration  being  an  important  parameter.  Most  cases  of  stomach  cancer  are  sporadic  in  nature,  with  rare  reports  of  inherited  gastric  cancer  predisposition  traits  that  can  involve  germ-line  E-cadherin  alterations  or  in  conjunction  with  the  hereditary  nonpolyposis  colon  cancer  disease  entity.Cytogenetic  studies  have  been  unsuccessful  in  identifying  an  obvious  significant  chromosomal  aberration  in  gastric  cancers.  Loss  of  heterozygosity  studies  and  comparative  genomic  hybridization  analyses  have  identified  several  loci  with  significant  allelic  loss,  thus  indicating  the  possibility  of  harboring  a  tumor-suppressor  gene  important  in  gastric  tumorigenesis.  The  exact  target(s)  of  loss  or  gain  in  most  of  these  chromosomal  regions,  including  4q,  5q,  9p,  17p,  18q,  and  20q,  remains  to  be  clarified.  Additionally,  evidence  of  Epstein-Barr  virus  infection  can  be  found  in  a  minority  of  gastric  cancer  patients.Multiple  somatic  alterations  have  been  described  in  gastric  carcinomas  at  the  molecular  level.  The  significance  of  these  changes  in  gastric  tumorigenesis  remains  to  be  established  in  most  instances.  The  p53  gene  is  consistently  altered  in  a  majority  of  gastric  cancer  cases.  Microsatellite  instability  and  associated  alterations  of  the  transforming  growth  factor  βII  receptor,  IGFRII,  BAX,  E2F-4,  MSH3,  and  MSH6  genes  are  found  in  a  subset  of  gastric  carcinomas.  Cell  adhesion  abnormalities  such  as  E-cadherin  or  associated  molecule  alterations  may  play  an  important  role  in  diffuse-type  gastric  cancer  development.  A  detailed,  clear  working  model  of  gastric  tumorigenesis  has  yet  to  be  formulated.  Thus  improved  diagnostic,  prognostic,  therapeutic,  and  preventive  strategies  are  eagerly  awaited  for  gastric  carcinomas.  Critical  molecular  alterations  that  are  prevalent  in  these  cancers,  once  fully  characterized,  ultimately  may  provide  new  avenues  to  combat  this  lethal  disease.  
SN  - 
PB  - McGraw-Hill Education
CY  - New York, NY
Y2  - 2024/04/19
UR  - ommbid.mhmedical.com/content.aspx?aid=1181417465
ER  -