Evidence map›Paper›PMID 24723911›Full record

ReviewFrontiers in endocrinology2014

Mechanisms of therapeutic resistance in cancer (stem) cells with emphasis on thyroid cancer cells.

Sabine Hombach-Klonisch, Suchitra Natarajan, Thatchawan Thanasupawat, Manoj Medapati, Alok Pathak, Saeid Ghavami, Thomas Klonisch

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in endocrinology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

19 citing papers in PubMed, 37 citations in OpenAlex.

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  15. Combined Treatments with Photodynamic Therapy for Non-Melanoma Skin Cancer.International journal of molecular sciences · 2015
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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

7 authors at 2 institutions in 1 country.

Sabine Hombach-KlonischDepartment of Human Anatomy and Cell Science, University of Manitoba , Winnipeg, MB , Canada ; Department of Obstetrics, Gynecology and Reproductive Sciences, University of Manitoba , Winnipeg, MB , Canada.
Suchitra NatarajanDepartment of Human Anatomy and Cell Science, University of Manitoba , Winnipeg, MB , Canada.
Thatchawan ThanasupawatDepartment of Human Anatomy and Cell Science, University of Manitoba , Winnipeg, MB , Canada.
Manoj MedapatiDepartment of Human Anatomy and Cell Science, University of Manitoba , Winnipeg, MB , Canada.
Alok PathakDepartment of Human Anatomy and Cell Science, University of Manitoba , Winnipeg, MB , Canada ; Department of Surgery, University of Manitoba , Winnipeg, MB , Canada.
Saeid GhavamiDepartment of Human Anatomy and Cell Science, University of Manitoba , Winnipeg, MB , Canada ; Manitoba Institute of Child Health, University of Manitoba , Winnipeg, MB , Canada.
Thomas KlonischDepartment of Human Anatomy and Cell Science, University of Manitoba , Winnipeg, MB , Canada ; Department of Surgery, University of Manitoba , Winnipeg, MB , Canada ; Manitoba Institute of Child Health, University of Manitoba , Winnipeg, MB , Canada ; Department of Medical Microbiology and Infectious Diseases, University of Manitoba , Winnipeg, MB , Canada.
University of Manitoba · CAChildren's Hospital Research Institute of Manitoba · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The two main reasons for death of cancer patients, tumor recurrence and metastasis, are multi-stage cellular processes that involve increased cell plasticity and coincide with elevated resistance to anti-cancer treatments. Epithelial-to-mesenchymal transition (EMT) is a key contributor to metastasis in many cancer types, including thyroid cancer and is known to confer stem cell-like properties onto cancer cells. This review provides an overview of molecular mechanisms and factors known to contribute to cancer cell plasticity and capable of enhancing cancer cell resistance to radio- and chemotherapy. We elucidate the role of DNA repair mechanisms in contributing to therapeutic resistance, with a special emphasis on thyroid cancer. Next, we explore the emerging roles of autophagy and damage-associated molecular pattern responses in EMT and chemoresistance in tumor cells. Finally, we demonstrate how cancer cells, including thyroid cancer cells, can highjack the oncofetal nucleoprotein high-mobility group A2 to gain increased transformative cell plasticity, prevent apoptosis, and enhance metastasis of chemoresistant tumor cells.

Indexed as

autophagyDAMPDNA repairER stressHMGA2stem cellstherapeutic resistancethyroid cancer

Identifiers

PMID24723911
PMCPMC3971176
OpenAlexW2041877446

What OpenQuestion 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 OpenQuestion graph.