Evidence map›Paper›PMID 29455653›Full record

ReviewMolecular cancer2018

Novel targeted therapies and immunotherapy for advanced thyroid cancers.

George E Naoum, Michael Morkos, Brian Kim, Waleed Arafat

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

Review in Molecular cancer, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 138 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
138citing papers in PubMed, 2 pooled it
16.6field-weighted citation impact, top 1% 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

138 citing papers in PubMed, 2 syntheses or guidelines pooled it, 235 citations in OpenAlex.

  1. Pooled it
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  18. CTHRC1 is associated withBiomolecules & biomedicine · 2024
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78 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

4 authors at 2 institutions in 1 country.

George E NaoumDepartment of Radiation Oncology, Harvard Medical School, Massachusetts General Hospital, 55 Fruit St, Boston, MA, 02114, USA.
Michael MorkosDepartment of Endocrinology, Rush University, 1900 W Polk St, Room 801, Chicago, IL, USA.
Brian KimDepartment of Endocrinology, Thyroid Cancer Program, Rush University, Jelke Building, Room 604, 1735 W Harrison St, Chicago, IL, 60612, UK.
Waleed ArafatAlexandria Comprehensive Cancer center, Alexandria, Egypt. w.o.arafaat@gmail.com.
Rush University · USMassachusetts General Hospital · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Thyroid cancer is a frequently encountered endocrine malignancy. Despite the favorable prognosis of this disease, 15-20% of differentiated thyroid cancer (DTC) cases and most anaplastic types, remain resistant to standard treatment options, including radioactive iodine (RAI). In addition, around 30% of medullary thyroid cancer (MTC) cases show resistance after surgery. The evolving understanding of disease-specific molecular therapeutic targets has led to the approval of two targeted therapies (Sorafenib and Lenvatinib) for RAI refractory DTC and another two drugs (Vandetanib and Cabozantinib) for MTC. These advanced therapies exert their effects by blocking the MAPK pathway, which has been widely correlated to different types of thyroid cancers. While these drugs remain reserved for thyroid cancer patients who failed all treatment options, their ability to improve patients' overall survival remain hindered by their low efficacy and other molecular factors. Among these factors is the tumor's ability to activate parallel proliferative signaling pathways other than the cascades blocked by these drugs, along with overexpression of some tyrosine kinase receptors (TKR). These facts urge the search for novel different treatment strategies for advanced thyroid cases beyond these drugs. Furthermore, the growing knowledge of the dynamic immune system interaction with tumor microenvironment has revolutionized the cancer immune therapy field. In this review, we aim to discuss the molecular escape mechanisms of thyroid tumors from these drugs. We also highlight novel therapeutic options targeting other pathways than MAPK, including PI3K pathway, ALK translocations and HER2/3 receptors and their clinical impact. We also aim to discuss the usage of targeted therapy in restoring thyroid tumor sensitivity to RAI, and finally turn to extensively discuss the role of immunotherapy as a potential alternative treatment option for advanced thyroid diseases.

Indexed as

ImmunotherapyMolecular Targeted TherapyAnimalsBiomarkersCombined Modality TherapyGene Expression Regulation, NeoplasticHumansImmune SystemIodine RadioisotopesMutationNeoplasm StagingSignal TransductionThyroid NeoplasmsTumor EscapeBiomarkersIodine Radioisotopes

Identifiers

PMID29455653
PMCPMC5817719
OpenAlexW2788935695

What Socratic holds

Textmetadata
LicenceCC BY
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.