TY - JOUR
T1 - Natural diversity facilitates the discovery of conserved chemotherapeutic response mechanisms
AU - Zdraljevic, Stefan
AU - Andersen, Erik C.
N1 - Funding Information:
The authors would like to thank members of the Andersen laboratory for critical reading of this manuscript. This work was supported by a National Institutes of Health R01 subcontract to E.C.A. (GM107227), the Chicago Biomedical Consortium with support from the Searle Funds at the Chicago Community Trust, a Sherman-Fairchild Cancer Innovation Award to E.C.A., and an American Cancer Society Research Scholar Grant to E.C.A. (127313-RSG-15-135-01-DD), along with support from the Cell and Molecular Basis of Disease training grant (T32GM008061) to S.Z.
Publisher Copyright:
© 2017 The Authors
PY - 2017/12
Y1 - 2017/12
N2 - Organismal fitness depends on adaptation to complex niches where chemical compounds and pathogens are omnipresent. These stresses can lead to the fixation of alleles in both xenobiotic responses and proliferative signaling pathways that promote survival in these niches. However, both xenobiotic responses and proliferative pathways vary within and among species. For example, genetic differences can accumulate within populations because xenobiotic exposures are not constant and selection is variable. Additionally, neutral genetic variation can accumulate in conserved proliferative pathway genes because these systems are robust to genetic perturbations given their essential roles in normal cell-fate specification. For these reasons, sensitizing mutations or chemical perturbations can disrupt pathways and reveal cryptic variation. With this fundamental view of how organisms respond to cytotoxic compounds and cryptic variation in conserved signaling pathways, it is not surprising that human patients have highly variable responses to chemotherapeutic compounds. These different responses result in the low FDA-approval rates for chemotherapeutics and underscore the need for new approaches to understand these diseases and therapeutic interventions. Model organisms, especially the classic invertebrate systems of Caenorhabditis elegans and Drosophila melanogaster, can be used to combine studies of natural variation across populations with responses to both xenobiotic compounds and chemotherapeutics targeted to conserved proliferative signaling pathways.
AB - Organismal fitness depends on adaptation to complex niches where chemical compounds and pathogens are omnipresent. These stresses can lead to the fixation of alleles in both xenobiotic responses and proliferative signaling pathways that promote survival in these niches. However, both xenobiotic responses and proliferative pathways vary within and among species. For example, genetic differences can accumulate within populations because xenobiotic exposures are not constant and selection is variable. Additionally, neutral genetic variation can accumulate in conserved proliferative pathway genes because these systems are robust to genetic perturbations given their essential roles in normal cell-fate specification. For these reasons, sensitizing mutations or chemical perturbations can disrupt pathways and reveal cryptic variation. With this fundamental view of how organisms respond to cytotoxic compounds and cryptic variation in conserved signaling pathways, it is not surprising that human patients have highly variable responses to chemotherapeutic compounds. These different responses result in the low FDA-approval rates for chemotherapeutics and underscore the need for new approaches to understand these diseases and therapeutic interventions. Model organisms, especially the classic invertebrate systems of Caenorhabditis elegans and Drosophila melanogaster, can be used to combine studies of natural variation across populations with responses to both xenobiotic compounds and chemotherapeutics targeted to conserved proliferative signaling pathways.
UR - http://www.scopus.com/inward/record.url?scp=85028944623&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=85028944623&partnerID=8YFLogxK
U2 - 10.1016/j.gde.2017.08.002
DO - 10.1016/j.gde.2017.08.002
M3 - Review article
C2 - 28892780
AN - SCOPUS:85028944623
SN - 0959-437X
VL - 47
SP - 41
EP - 47
JO - Current Opinion in Genetics and Development
JF - Current Opinion in Genetics and Development
ER -