Evidence map›Paper›PMID 33602906›Full record

ReviewCell death & disease2021

Cell death in head and neck cancer pathogenesis and treatment.

Martina Raudenská, Jan Balvan, Michal Masařík

Open access · goldAbstract readReview
In one paragraph

Review in Cell death & disease, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed, 3 pooled it
4.6field-weighted citation impact, top 4% 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

54 citing papers in PubMed, 3 syntheses or guidelines pooled it, 76 citations in OpenAlex.

  1. Pooled it
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  11. Ferroptosis and cancer: when iron turns against tumors.Cellular and molecular life sciences : CMLS · 2025
    Review
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  14. USP14 targets FABP5-mediated ferroptosis to promote proliferation and cisplatin resistance of HNSCC.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2025
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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

3 authors at 2 institutions in 1 country.

Martina RaudenskáDepartment of Physiology, Faculty of Medicine, Masaryk University / Kamenice 5, CZ-625 00, Brno, Czech Republic.
Jan BalvanDepartment of Pathological Physiology, Faculty of Medicine, Masaryk University / Kamenice 5, CZ-625 00, Brno, Czech Republic.
Michal MasaříkDepartment of Physiology, Faculty of Medicine, Masaryk University / Kamenice 5, CZ-625 00, Brno, Czech Republic. masarik@med.muni.cz.
Mendel University in Brno · CZMasaryk University · CZ

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Many cancer therapies aim to trigger apoptosis in cancer cells. Nevertheless, the presence of oncogenic alterations in these cells and distorted composition of tumour microenvironment largely limit the clinical efficacy of this type of therapy. Luckily, scientific consensus describes about 10 different cell death subroutines with different regulatory pathways and cancer cells are probably not able to avoid all of cell death types at once. Therefore, a focused and individualised therapy is needed to address the specific advantages and disadvantages of individual tumours. Although much is known about apoptosis, therapeutic opportunities of other cell death pathways are often neglected. Molecular heterogeneity of head and neck squamous cell carcinomas (HNSCC) causing unpredictability of the clinical response represents a grave challenge for oncologists and seems to be a critical component of treatment response. The large proportion of this clinical heterogeneity probably lies in alterations of cell death pathways. How exactly cells die is very important because the predominant type of cell death can have multiple impacts on the therapeutic response as cell death itself acts as a second messenger. In this review, we discuss the different types of programmed cell death (PCD), their connection with HNSCC pathogenesis and possible therapeutic windows that result from specific sensitivity to some form of PCD in some clinically relevant subgroups of HNSCC.

Indexed as

AnimalsAntineoplastic AgentsApoptosisAutophagyDrug Resistance, NeoplasmFerroptosisGenetic HeterogeneityHead and Neck NeoplasmsHumansNecroptosisPyroptosisRegulated Cell DeathSignal TransductionSquamous Cell Carcinoma of Head and NeckTumor MicroenvironmentAntineoplastic Agents

Identifiers

PMID33602906
PMCPMC7893032
OpenAlexW3130233413

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.