Evidence map›Paper›PMID 30898264›Full record

ReviewTrends in cancer2019

Polytherapy and Targeted Cancer Drug Resistance.

Nilanjana Chatterjee, Trever G Bivona

Abstract readReview
In one paragraph

Review in Trends in cancer, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 148 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
148citing papers in PubMed, 4 pooled it
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

148 citing papers in PubMed, 4 syntheses or guidelines pooled it.

  1. Pooled it
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  8. Rhein and its derivatives: potential anti-tumor drugs and corresponding targeted mechanism.Saudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society · 2026
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88 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors.

Nilanjana ChatterjeeDepartment of Medicine, University of California, San Francisco, 600 16(th) Street, Box 2140, Genentech Hall, San Francisco, CA 94158, USA; Department of Cellular and Molecular Pharmacology, University of California, San Francisco, 600 16(th) Street, Box 2140, Genentech Hall, San Francisco, CA 94158, USA; Helen Diller Family Comprehensive Cancer Center, University of California, San Francisco, 600 16(th) Street, Box 2140, Genentech Hall, San Francisco, CA 94158, USA.
Trever G BivonaDepartment of Medicine, University of California, San Francisco, 600 16(th) Street, Box 2140, Genentech Hall, San Francisco, CA 94158, USA; Department of Cellular and Molecular Pharmacology, University of California, San Francisco, 600 16(th) Street, Box 2140, Genentech Hall, San Francisco, CA 94158, USA; Helen Diller Family Comprehensive Cancer Center, University of California, San Francisco, 600 16(th) Street, Box 2140, Genentech Hall, San Francisco, CA 94158, USA. Electronic address: trever.bivona@ucsf.edu.

Funding

UCSF Project 1U54CA224081 · NCI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI CALVIN J KUO · 2017 to 2026
$12.9M
Molecular and Cellular Mechanisms in CancerT32CA108462 · NCI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI GOGA, ANDREI · 2004 to 2024
$10.4M
The Cancer Target Discovery and Development Network at UCSFU01CA217882 · NCI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI BANDYOPADHYAY, SOURAV, BIVONA, TREVER G · 2017 to 2021
$5.2M
Characterization of YAP as a rational companion target in lung cancerR01CA204302 · NCI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI Trever G Bivona · 2017 to 2026
$3.7M
Rational Combined Inhibition of NF-kB and EGFR to Optimize Lung Cancer TreatmentR01CA169338 · NCI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI BIVONA, TREVER G · 2013 to 2023
$3.4M
Optimizing biologically-based rational polytherapy in ALK+ lung cancerR01CA211052 · NCI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI BIVONA, TREVER G · 2017 to 2021
$1.8M
NCI NIH HHS R01 CA169338NCI NIH HHS R01 CA204302NCI NIH HHS R01 CA211052NCI NIH HHS T32 CA108462NCI NIH HHS U01 CA217882NCI NIH HHS U54 CA224081
6 · The paper itself

Abstract

A current challenge in cancer treatment is drug resistance. Even the most effective therapies often fail to produce a complete and durable tumor response and ultimately give rise to therapy resistance and tumor relapse. However, how resistance arises in cancer remains incompletely understood. While drug resistance in cancer is thought to be driven by irreversible genetic mutations, emerging evidence also implicates reversible proteomic and epigenetic mechanisms in the development of drug resistance. Tumor microenvironment-mediated mechanisms and tumor heterogeneity can significantly contribute to cancer treatment resistance. Here, we discuss the diverse and dynamic strategies that cancers use to evade drug response, the promise of upfront combination and intermittent therapies and therapy switching in forestalling resistance, and epigenetic reprogramming to combat resistance.

Indexed as

Biomarkers, TumorDrug Resistance, NeoplasmAntineoplastic AgentsAntineoplastic Combined Chemotherapy ProtocolsCellular ReprogrammingEpigenesis, GeneticHumansNeoplasmsAntineoplastic AgentsBiomarkers, Tumorcancer evolutiondrug resistanceepigeneticsgeneticsmolecular targetspolytherapytargeted therapy

Identifiers

PMID30898264
PMCPMC6446041

What Socratic holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.