TY  - CHAP
M1  - Book, Section
TI  - Genomics and Cancer Biomarkers
A1  - Solomon, Benjamin D.
A1  - Vockley, Joseph G.
A1  - Niederhuber, John E.
A2  - Morita, Shane Y.
A2  - Balch, Charles M.
A2  - Klimberg, V. Suzanne
A2  - Pawlik, Timothy M.
A2  - Posner, Mitchell C.
A2  - Tanabe, Kenneth K.
PY  - 2018
T2  - Textbook of Complex General Surgical Oncology
AB  - Cancer  is  a  complex  disease  capable  of  manifesting  itself  as  many  different  disease  phenotypes  occurring  in  virtually  any  tissue  of  the  body.  This  complexity  can  be  the  result  of  inherited  single  gene  mutations  in  germline  DNA,  the  accumulation  of  acquired  genomic  alterations  over  time,  or  the  combination  of  both  germline  mutations  and  somatic  genomic  alterations.1  There  are  many  examples  of  inherited  or  de  novo  mutations  in  the  germline  contributing  to  cancer  susceptibility.  These  mutations  include  single  nucleotide  polymorphisms  (SNPs),  small  insertions  and  deletions  (InDels),  as  well  as  structural  variants  such  as  copy  number  variants,  translocations,  and  inversions.  In  addition,  somatic  genetic  and  epigenetic  changes  are  known  to  be  involved  in  the  earliest  steps  of  cancer  initiation  within  normal  cells  and  during  the  proliferation  of  these  transformed  cells  to  form  a  precursor  or  in  situ  cancer.2  As  transformed  cells  continue  to  grow,  they  undergo  further  genomic  alterations  taking  on  the  invasive,  immortal,  and  eventually  metastatic  properties  common  to  most  types  of  cancer.  Mutations  in  specific  and  well-characterized  genes,  occurring  during  these  earliest  steps  of  tumor  formation,  appear  to  cause  further  genetic  instability  within  the  tumor  cells  resulting  in  the  accumulation  of  even  more  deleterious  genomic  alterations,  sometimes  referred  to  as  acquiring  a  “mutator  phenotype.”3  The  summation  of  these  genetic,  epigenetic,  and  genomic  events  provides  the  tumor  cells  with  a  distinct  growth  advantage  characteristic  of  cancer  and  which  can  confer  resistance  to  therapy.  In  addition,  there  remains  an  open  question  about  the  potential  for  viral  genomes  to  interact  with  the  human  genome  throughout  life  to  initiate  the  molecular  changes  that  can  result  in  cancer.  
SN  - 
PB  - McGraw-Hill Education
CY  - New York, NY
Y2  - 2024/04/18
UR  - hemonc.mhmedical.com/content.aspx?aid=1145755509
ER  -