Collateral lethality: a new therapeutic strategy in oncology

Muller, Florian L.; Aquilanti, Elisa A.; DePinho, Ronald A.

doi:10.1016/j.trecan.2015.10.002

Cited by 134Cancer-related Molecular PathwaysCancer Genomics and DiagnosticsChromatin Remodeling and Cancer

Collateral lethality: a new therapeutic strategy in oncology

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Muller, Florian L., Aquilanti, Elisa A., DePinho, Ronald A.·2015·Trends in Cancer

DOI 10.1016/j.trecan.2015.10.002PMC PMC4746004

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Abstract

Genomic deletion of tumor suppressor genes (TSG) is a rite of passage for virtually all human cancers. The synthetic lethal paradigm has provided a framework for the development of molecular targeted therapeutics that are functionally linked to the loss of specific TSG functions. In the course of genomic events that delete TSGs, a large number of genes with no apparent direct role in tumor promotion also sustain deletion as a result of chromosomal proximity to the target TSG. In this perspective, we review the novel concept of "collateral lethality", which has served to identify cancer-specific therapeutic vulnerabilities resulting from co-deletion of passenger genes neighboring TSG. The large number of collaterally deleted genes, playing diverse functions in cell homeostasis, offers a rich repertoire of pharmacologically targetable vulnerabilities presenting novel opportunities for the development of personalized anti-neoplastic therapies.

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Because cells often exhibit redundancy in essential pathways, passenger loss of metabolic genes can introduce a therapeutic opportunity termed collateral lethality.
“Because cells often exhibit redundancy in essential pathways, this phenomenon can introduce a therapeutic opportunity to target cancer cells that has been termed collateral lethality (Muller et al., 2015).”
From Targeting Metabolism for Cancer Therapy (2017) · cites this paper as Muller et al., 2015

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Targeting Metabolism for Cancer Therapy
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Targeting synthetic lethal paralogs in cancer
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Functional Genomics Reveals Synthetic Lethality between Phosphogluconate Dehydrogenase and Oxidative Phosphorylation
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Taking Aim at the Undruggable
Coleman, N., & Rodon, J. A. (2021) · American Society of Clinical Oncology Educational Book · doi:10.1200/edbk_325885 · Cited by 58 · see citing works
PTHrP Drives Pancreatic Cancer Growth and Metastasis and Reveals a New Therapeutic Vulnerability
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Integrative analysis of large-scale loss-of-function screens identifies robust cancer-associated genetic interactions
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Mutational inactivation of mTORC1 repressor gene DEPDC5 in human gastrointestinal stromal tumors
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Therapy-induced DNA methylation inactivates MCT1 and renders tumor cells vulnerable to MCT4 inhibition
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Targeting allosteric regulation of cancer metabolism
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Building a translational cancer dependency map for The Cancer Genome Atlas
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Prostate cancer research: The next generation; report from the 2019 Coffey‐Holden Prostate Cancer Academy Meeting
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Epigenetic based synthetic lethal strategies in human cancers
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FXR1 regulates transcription and is required for growth of human cancer cells with TP53/FXR2 homozygous deletion
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Lineage-specific silencing of PSAT1 induces serine auxotrophy and sensitivity to dietary serine starvation in luminal breast tumors
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Self-citation

Authors: Muller, F. L., Aquilanti, E. A., & DePinho, R. A.
Affiliations: Brigham and Women's Hospital (US)
The University of Texas MD Anderson Cancer Center (US)
Corresponding author: DePinho, Ronald A.
ORCID: Aquilanti, Elisa A.
DePinho, Ronald A.
Venue: Trends in Cancer
Publisher: Elsevier BV
Published: 2015-11
Volume: 1
Issue: 3
Pages: 161-173
ISSN: 2405-8025 (ISSN-L)
2405-8033
DOI: 10.1016/j.trecan.2015.10.002
PMC: PMC4746004
OpenAlex: W2179093278
Cited by: 132
References: 116
Citations by year: 2026: 10 · 2025: 12 · 2024: 10 · 2023: 9 · 2022: 18 · 2021: 14 · 2020: 17 · 2019: 15 · 2018: 11 · 2017: 10 · 2016: 6
FWCI: 0.97
Type: journal article
Language: en
Open access: green
www.ncbi.nlm.nih.gov
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations: Trends in cancer (publishedVersion)
PubMed (publishedVersion)
PubMed Central (acceptedVersion)
Funders: National Institutes of Health
National Cancer Institute (P01CA095616, P50CA127001)
Topics: Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer Genomics and Diagnostics
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Chromatin Remodeling and Cancer
Keywords: synthetic lethality, tumor suppressor, passenger genes, precision oncology, targeted cancer therapy

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Collateral lethality: a new therapeutic strategy in oncology

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