A Convergence-Based Framework for Cancer Drug Resistance

Konieczkowski, David J.; Johannessen, Cory M.; Garraway, Levi A.

doi:10.1016/j.ccell.2018.03.025

Cited by 258Drug Transport and Resistance MechanismsCancer Cells and MetastasisCancer Immunotherapy and Biomarkers

A Convergence-Based Framework for Cancer Drug Resistance

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Konieczkowski, David J., Johannessen, Cory M., Garraway, Levi A.·2018·Cancer Cell

DOI 10.1016/j.ccell.2018.03.025PMC PMC5957297

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Abstract

Despite advances in cancer biology and therapeutics, drug resistance remains problematic. Resistance is often multifactorial, heterogeneous, and prone to undersampling. Nonetheless, many individual mechanisms of targeted therapy resistance may coalesce into a smaller number of convergences, including pathway reactivation (downstream re-engagement of original effectors), pathway bypass (recruitment of a parallel pathway converging on the same downstream output), and pathway indifference (development of a cellular state independent of the initial therapeutic target). Similar convergences may also underpin immunotherapy resistance. Such parsimonious, convergence-based frameworks may help explain resistance across tumor types and therapeutic categories and may also suggest strategies to overcome it.

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The modest benefits of KRASG12C inhibitors are attributable at least in part to resistance that almost invariably develops with single-agent therapy.
“The modest benefits are attributable, at least in part, to resistance that almost invariably develops with single-agent therapy90–92.”
From The current state of the art and future trends in RAS-targeted cancer therapies (2022) · cites this paper as [91]
G12C-Is will have limited impact as single agents due to drug resistance.
“These results suggest that, like other targeted therapies (Ahronian and Corcoran, 2017; Konieczkowski et al., 2018; Ryan and Corcoran, 2018), G12C-Is will have limited impact as single agents due to drug resistance.”
From SHP2 inhibition diminishes KRASG12C cycling and promotes tumor microenvironment remodeling (2021) · cites this paper as Konieczkowski et al., 2018

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Authors: Konieczkowski, D. J., Johannessen, C. M., & Garraway, L. A.
Affiliations: Harvard University (US)
Broad Institute (US)
Eli Lilly (United States) (US)
Corresponding author: Konieczkowski, David J.
ORCID: Konieczkowski, David J.
Johannessen, Cory M.
Garraway, Levi A.
Venue: Cancer Cell
Publisher: Elsevier BV
Published: 2018-05
Volume: 33
Issue: 5
Pages: 801-815
ISSN: 1535-6108 (ISSN-L)
DOI: 10.1016/j.ccell.2018.03.025
PMC: PMC5957297
OpenAlex: W2802173235
Cited by: 258
References: 185
Citations by year: 2026: 21 · 2025: 21 · 2024: 29 · 2023: 36 · 2022: 38 · 2021: 39 · 2020: 42 · 2019: 25 · 2018: 7
FWCI: 2.95
Type: journal article
Language: en
Open access: bronze
doi.org
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
www.elsevier.com/legal/tdmrep-license (tdm)
www.elsevier.com/open-access/userlicense/1.0/ (vor, 378 d)
Locations: Cancer Cell (publishedVersion)
PubMed (publishedVersion)
Europe PMC (PubMed Central) (acceptedVersion)
PubMed Central (acceptedVersion)
Funders: National Cancer Institute (R01CA219943, U54CA224068)
Topics: Health Sciences › Medicine › Oncology › Drug Transport and Resistance Mechanisms
Health Sciences › Medicine › Oncology › Cancer Cells and Metastasis
Health Sciences › Medicine › Oncology › Cancer Immunotherapy and Biomarkers
Keywords: chemoresistance, targeted therapy resistance, immunotherapy resistance, resistance mechanisms
MeSH terms: Humans, Immunotherapy, Neoplasms, Biomarkers, Tumor, Drug Resistance, Neoplasm, Precision Medicine, Molecular Targeted Therapy

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