Evidence map›Paper›PMID 35975971›Full record

ReviewEndocrine-related cancer2022

Molecular mechanisms of resistance to kinase inhibitors and redifferentiation in thyroid cancers.

Marie-Claude Hofmann, Muthusamy Kunnimalaiyaan, Jennifer R Wang, Naifa L Busaidy, Steven I Sherman, Stephen Y Lai, Mark Zafereo, Maria E Cabanillas

Open access · bronzeAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Endocrine-related cancer, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
3.3field-weighted citation impact, top 6% of its field
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

30 citing papers in PubMed, 29 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Review
  5. Genomics and Multi-Omics to Guide Clinical Management in Thyroid Cancer.International journal of molecular sciences · 2026
    Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Review
  13. Article
  14. Review
  15. Article
  16. Review
  17. Review
  18. Systemic therapies for medullary thyroid carcinoma: state of the art.Therapeutic advances in endocrinology and metabolism · 2025
    Review
  19. Review
  20. Review
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

8 authors at 1 institution in 1 country.

Marie-Claude HofmannDepartment of Endocrine Neoplasia and Hormonal Disorders, University of Texas MD Anderson Cancer Center, Houston, Texas, USA.ORCID 0000-0002-4899-8039
Muthusamy KunnimalaiyaanDepartment of Endocrine Neoplasia and Hormonal Disorders, University of Texas MD Anderson Cancer Center, Houston, Texas, USA.
Jennifer R WangDepartment of Head and Neck Surgery, University of Texas MD Anderson Cancer Center, Houston, Texas, USA.
Naifa L BusaidyDepartment of Endocrine Neoplasia and Hormonal Disorders, University of Texas MD Anderson Cancer Center, Houston, Texas, USA.
Steven I ShermanDepartment of Endocrine Neoplasia and Hormonal Disorders, University of Texas MD Anderson Cancer Center, Houston, Texas, USA.
Stephen Y LaiDepartment of Head and Neck Surgery, University of Texas MD Anderson Cancer Center, Houston, Texas, USA.
Mark ZafereoDepartment of Head and Neck Surgery, University of Texas MD Anderson Cancer Center, Houston, Texas, USA.
Maria E CabanillasDepartment of Endocrine Neoplasia and Hormonal Disorders, University of Texas MD Anderson Cancer Center, Houston, Texas, USA.
The University of Texas MD Anderson Cancer Center · US

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI DIANE BODURKA · 1985 to 2026
$290.8M
Role of p21-activated kinases in thyroid cancerR01CA227847 · NCI · OHIO STATE UNIVERSITY · PI RINGEL, MATTHEW D · 2018 to 2022
$1.9M
Radiosensitization of thyroid cancer by cancer cell specific reduction of gold ionsR21CA259839 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI LAI, STEPHEN Y, SOKOLOV, KONSTANTIN V · 2022 to 2023
$412k
NCI NIH HHS P30 CA016672NCI NIH HHS R01 CA227847NCI NIH HHS R21 CA259839
6 · The paper itself

Abstract

Protein kinases play critical roles in cell survival, proliferation, and motility. Their dysregulation is therefore a common feature in the pathogenesis of a number of solid tumors, including thyroid cancers. Inhibiting activated protein kinases has revolutionized thyroid cancer therapy, offering a promising strategy in treating tumors refractory to radioactive iodine treatment or cytotoxic chemotherapies. However, despite satisfactory early responses, these drugs are not curative and most patients inevitably progress due to drug resistance. This review summarizes up-to-date knowledge on various mechanisms that thyroid cancer cells develop to bypass protein kinase inhibition and outlines strategies that are being explored to overcome drug resistance. Understanding how cancer cells respond to drugs and identifying novel molecular targets for therapy still represents a major challenge for the treatment of these patients.

Indexed as

Antineoplastic AgentsThyroid NeoplasmsHumansIodine RadioisotopesProtein Kinase InhibitorsProtein KinasesAntineoplastic AgentsIodine RadioisotopesProtein Kinase InhibitorsProtein Kinasesanaplastic thyroid carcinomaBRAFdifferentiated thyroid cancersdrug resistancekinase inhibitorsNISRAS

Identifiers

PMID35975971
PMCPMC9534048
OpenAlexW4292261975

What OpenQuestion 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 OpenQuestion graph.