TY  - CHAP
M1  - Book, Section
TI  - Genomic Stability and DNA Repair
A1  - Harding, Shane M.
A1  - Bristow, Robert G.
A1  - Harrington, Lea
A2  - Tannock, Ian F.
A2  - Hill, Richard P.
A2  - Bristow, Robert G.
A2  - Harrington, Lea
PY  - 2016
T2  - The Basic Science of Oncology, 5e
AB  - There  is  overwhelming  evidence  that  mutations  can  cause  cancer.  Major  evidence  for  the  genetic  origin  of  cancer  includes:  (a)  the  observation  of  Ames  (Ames  et  al,  1981)  that  many  carcinogens  are  also  mutagens,  and  (b),  the  finding  that  genetically  determined  traits  associated  with  a  deficiency  in  the  enzymes  necessary  to  repair  lesions  in  DNA  are  associated  with  an  increased  risk  of  cancer.  Mutations  may  occur  in  the  germline  of  an  individual  and  be  represented  in  every  cell  in  the  body,  or  they  may  occur  in  a  single  somatic  cell  and  be  identified  in  a  tumor  following  clonal  proliferation.  As  described  in  Chapter  6,  all  species  have  numerous  genes  called  cellular  oncogenes  (or  protooncogenes),  many  of  which  are  homologous  to  the  transforming  oncogenes  carried  by  specific  RNA  retroviruses.  Some  human  tumors  have  mutations  in  these  oncogenes  that  may  have  led  to  their  activation.  However,  there  is  no  evidence  for  germline  mutations  in  cellular  oncogenes,  perhaps  because  such  mutations  in  the  germline  are  lethal  even  in  the  heterozygous  state.  In  contrast,  there  is  good  evidence  for  germline  mutations  affecting  tumor-suppressor  genes,  which  can  lead  to  familial  clustering  of  cancer  or  transmission  of  predisposition  to  tumors.  In  such  cases,  the  loss-of-function  of  a  tumor-suppressor  gene  is  inherited  in  a  mendelian  manner.  
SN  - 
PB  - McGraw-Hill Education Medical
CY  - New York, NY
Y2  - 2024/04/16
UR  - accessbiomedicalscience.mhmedical.com/content.aspx?aid=1127471703
ER  -