Evidence map›Paper›PMID 28431544›Full record

ReviewGenome medicine2017

Strategies for monitoring and combating resistance to combination kinase inhibitors for cancer therapy.

Leanne G Ahronian, Ryan B Corcoran

Abstract readReview
In one paragraph

Review in Genome medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
–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

28 citing papers in PubMed.

  1. Review
  2. Review
  3. Dammarolic acid improves tyrosine kinase inhibitor activity in lung cancer cells.Naunyn-Schmiedeberg's archives of pharmacology · 2026
    Article
  4. Article
  5. Generation of actionable, cancer-specific neoantigens from KRAS(G12C) with adagrasib.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  6. Article
  7. Biological Activity of Peptide Fraction Derived fromInternational journal of molecular sciences · 2025
    Article
  8. Article
  9. Resistance to TOP-1 Inhibitors: Good Old Drugs Still Can Surprise Us.International journal of molecular sciences · 2023
    Review
  10. Article
  11. Article
  12. Review
  13. Article
  14. Targeting Mutated KRAS Genes to Treat Solid Tumours.Molecular diagnosis & therapy · 2022
    Review
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. Article
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.

Leanne G AhronianMassachusetts General Hospital Cancer Center, Boston, MA, 02129, USA.
Ryan B CorcoranMassachusetts General Hospital Cancer Center, Boston, MA, 02129, USA. rbcorcoran@partners.org.

Funding

Tissue and Pathology ResourcesP50CA127003 · NCI · DANA-FARBER CANCER INST · PI EL-BARDEESY, NABEEL, SELLERS, WILLIAM R · 2007 to 2023
$33.2M
Therapeutic resistance and tumor heterogeneity in BRAF mutant colorectal cancerR01CA208437 · NCI · MASSACHUSETTS GENERAL HOSPITAL · PI CORCORAN, RYAN BRUCE · 2016 to 2020
$2.0M
Combination Therapy to Improve MAPK Pathway Inhibitor Efficacy in BRAF and KRAS MK08CA166510 · NCI · MASSACHUSETTS GENERAL HOSPITAL · PI CORCORAN, RYAN BRUCE · 2013 to 2017
$896k
NCI NIH HHS K08 CA166510NCI NIH HHS P50 CA127003NCI NIH HHS R01 CA208437
6 · The paper itself

Abstract

Targeted therapies such as kinase inhibitors and monoclonal antibodies have dramatically altered cancer care in recent decades. Although these targeted therapies have improved patient outcomes in several cancer types, resistance ultimately develops to these agents. One potential strategy proposed to overcome acquired resistance involves taking repeat tumor biopsies at the time of disease progression, to identify the specific molecular mechanism driving resistance in an individual patient and to select a new agent or combination of agents capable of surmounting that specific resistance mechanism. However, recent studies sampling multiple metastatic lesions upon acquired resistance, or employing "liquid biopsy" analyses of circulating tumor DNA, have revealed that multiple, heterogeneous resistance mechanisms can emerge in distinct tumor subclones in the same patient. This heterogeneity represents a major clinical challenge for devising therapeutic strategies to overcome resistance. In many cancers, multiple drug resistance mechanisms often converge to reactivate the original pathway targeted by the drug. This convergent evolution creates an opportunity to target a common signaling node to overcome resistance. Furthermore, integration of liquid biopsy approaches into clinical practice may allow real-time monitoring of emerging resistance alterations, allowing intervention prior to standard detection of radiographic progression. In this review, we discuss recent advances in understanding tumor heterogeneity and resistance to targeted therapies, focusing on combination kinase inhibitors, and we discuss approaches to address these issues in the clinic.

Indexed as

Drug Resistance, NeoplasmAntineoplastic AgentsHumansNeoplasmsProtein Kinase InhibitorsAntineoplastic AgentsProtein Kinase Inhibitors

Identifiers

PMID28431544
PMCPMC5399860

What OpenQuestion holds

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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 OpenQuestion graph.