Evidence map›Paper›PMID 27207748›Full record

ArticleOncology2016

Comprehensive Genomic Profiling of Clinically Advanced Medullary Thyroid Carcinoma.

Andreas M Heilmann, Vivek Subbiah, Kai Wang, James X Sun, Julia A Elvin, Juliann Chmielecki, Steven I Sherman, Ravi Murthy, Naifa L Busaidy, Ishwaria Subbiah and 11 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Oncology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
4.2field-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

34 citing papers in PubMed, 60 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Familial Clinical Heterogeneity of Medullary Thyroid Cancer with GermlineJournal of clinical research in pediatric endocrinology · 2025
    Article
  6. Long-Term Follow-Up in Medullary Thyroid Carcinoma Patients.Recent results in cancer research. Fortschritte der Krebsforschung. Progres dans les recherches sur le cancer · 2025
    Review
  7. Review
  8. Review
  9. Review
  10. Article
  11. Not OnlyJournal of the Endocrine Society · 2024
    Article
  12. Review
  13. Article
  14. Review
  15. Review
  16. Article
  17. Review
  18. Article
  19. Precision oncology forFrontiers in oncology · 2022
    Review
  20. RET kinase inhibitors forTherapeutic advances in medical oncology · 2022
    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

21 authors at 8 institutions in 1 country.

Andreas M HeilmannFoundation Medicine, Inc., Cambridge, Mass., USA.
Vivek Subbiah
Kai Wang
James X Sun
Julia A Elvin
Juliann Chmielecki
Steven I Sherman
Ravi Murthy
Naifa L Busaidy
Ishwaria Subbiah
Roman Yelensky
Chaitali Nangia
Jo-Anne Vergilio
Saad A Khan
Rachel L Erlich
Doron Lipson
Jeffrey S Ross
Vincent A Miller
Manisha H Shah
Siraj M Ali
Philip J Stephens
Foundation Medicine (United States)Advanced Cancer Therapeutics · USEndocrine Society · USTech Foundation · USThe Ohio State University Comprehensive Cancer Center – Arthur G. James Cancer Hospital and Richard J. Solove Research Institute · USThe University of Texas MD Anderson Cancer Center · USThe University of Texas Southwestern Medical Center · USUniversity of California, Irvine · US

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Scott Kopetz · 1985 to 2026
$290.8M
NCI NIH HHS P30 CA016672
6 · The paper itself

Abstract

objectiveThe aim of this study was to determine the genomic alterations of cancer-related genes in advanced medullary thyroid carcinoma during the course of clinical care.

methodsHybrid-capture-based comprehensive genomic profiling was performed on 34 consecutive medullary thyroid carcinoma cases to identify all four classes of genomic alterations, and outcome for an index patient was collected.

resultsRET was mutated in 88% (30/34) of cases, with RET M918T being responsible for 70% (21/30) of the RET alterations. The other RET alterations were RET E632_L633del, C634R, C620R, C618G/R/S, V804M, and RET amplification. Two of the four RET wild-type patients harbored mutations in KRAS or HRAS (1/34 each). The next most frequent genomic alterations were amplifications of CCND1, FGF3, and FGF19 and alterations in CDKN2A (3/34 each). One case with a RET M918T mutation developed acquired resistance to progressively dose-escalated vandetanib. When the mTOR inhibitor everolimus was added to continued vandetanib treatment, the patient achieved a second 25% reduction of tumor volume (RECIST 1.1) for 8 months.

conclusionsComprehensive genomic profiling identified the full breadth of RET alterations in metastatic medullary thyroid carcinoma and possible cooperating oncogenic driver alterations. This approach may refine the use of targeted therapy for these patients.

Indexed as

Gene Expression ProfilingMutationAgedAnilidesAntineoplastic Combined Chemotherapy ProtocolsCarcinoma, NeuroendocrineCyclin D1Cyclin-Dependent Kinase Inhibitor p16Drug Resistance, NeoplasmEverolimusFemaleFibroblast Growth Factor 3Fibroblast Growth FactorsGene AmplificationGene Expression Regulation, NeoplasticHumansAnilidescabozantinibCCND1 protein, humanCyclin D1Cyclin-Dependent Kinase Inhibitor p16EverolimusFGF19 protein, humanFGF3 protein, humanFibroblast Growth Factor 3Fibroblast Growth FactorsHRAS protein, humanKRAS protein, humanMethioninePiperidinesProto-Oncogene Proteins c-retProto-Oncogene Proteins p21(ras)PyridinesQuinazolinesRET protein, humanThreoninevandetanib

Identifiers

PMID27207748
PMCPMC4909575
OpenAlexW2403869272

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.