The DOI matches its Crossref record; 113 of the 116 references it cites were found in a registry or an index.
Collateral Lethality: A New Therapeutic Strategy in Oncology
Open accessAbstract
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, 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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Cerami, E., Gao, J., Dogrusoz, U., Gross, B. E., Sumer, S. O., Aksoy, B. A., Jacobsen, A., Byrne, C. J., Heuer, M. L., Larsson, E., et al. (2012) · Cancer Discovery · doi:10.1158/2159-8290.cd-12-0095 · Cited by 17,455
The Cancer Cell Line Encyclopedia enables predictive modelling of anticancer drug sensitivity
Barretina, J., Caponigro, G., Stransky, N., Venkatesan, K., Margolin, A. A., Kim, S., Wilson, C. J., Lehár, J., Kryukov, G. V., Sonkin, D., et al. (2012) · Nature · doi:10.1038/nature11003 · Cited by 7,950
A map of human genome variation from population-scale sequencing.
The 1000 Genomes Project Consortium (2010) · Nature · doi:10.1038/nature09534 · Cited by 7,877
Comprehensive genomic characterization defines human glioblastoma genes and core pathways
The Cancer Genome Atlas Research Network (2008) · Nature · doi:10.1038/nature07385 · Cited by 7,735
The genomic and transcriptomic architecture of 2,000 breast tumours reveals novel subgroups
METABRIC Group, Curtis, C., Shah, S. P., Chin, S.-F., Turashvili, G., Rueda, O. M., Dunning, M. J., Speed, D., Lynch, A. G., Samarajiwa, S., et al. (2012) · Nature · doi:10.1038/nature10983 · Cited by 6,097
Integrated genomic characterization of endometrial carcinoma
The Cancer Genome Atlas Research Network, & Levine, D. A. (2013) · Nature · doi:10.1038/nature12113 · Cited by 5,784
Genome-scale CRISPR-Cas9 knockout screening in human cells
Shalem, O., Sanjana, N. E., Hartenian, E., Shi, X., Scott, D. A., Mikkelsen, T. S., Heckl, D., Ebert, B. L., Root, D. E., Doench, J. G., et al. (2014) · Science · doi:10.1126/science.1247005 · Cited by 5,234
Trastuzumab after Adjuvant Chemotherapy in HER2-Positive Breast Cancer
Piccart-Gebhart, M. J., Procter, M., Leyland-Jones, B., Goldhirsch, A., Untch, M., Smith, I., Gianni, L., Baselga, J., Bell, R., Jackisch, C., et al. (2005) · New England Journal of Medicine · doi:10.1056/nejmoa052306 · Cited by 5,084
The Somatic Genomic Landscape of Glioblastoma
Brennan, C. W., Verhaak, R. G. W., McKenna, A., Campos, B., Noushmehr, H., Salama, S. R., Zheng, S., Chakravarty, D., Sanborn, J. Z., Berman, S. H., et al. (2013) · Cell · doi:10.1016/j.cell.2013.09.034 · Cited by 5,016
Trastuzumab-Induced Hepatotoxicity: A Case Report
Vucicevic, D., Carey, E. J., & Karlin, N. J. (2013) · Breast Care · doi:10.1159/000346844 · Cited by 4,432
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Targeting Metabolism for Cancer Therapy
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Metadata
- 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.
- Venue
- Trends in Cancer
- Publisher
- Elsevier BV
- Published
- 2015-11
- Volume
- 1
- Issue
- 3
- Pages
- 161-173
- ISSN
- 2405-8025 (ISSN-L)
- 2405-8033
- 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
- 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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