Evidence map›Paper›PMID 29560608›Full record

ReviewMolecular diagnosis & therapy2018

Programmed Cell Death, from a Cancer Perspective: An Overview.

Abhay P Mishra, Bahare Salehi, Mehdi Sharifi-Rad, Raffaele Pezzani, Farzad Kobarfard, Javad Sharifi-Rad, Manisha Nigam

Abstract readReview
PubMed Publisher
In one paragraph

Review in Molecular diagnosis & therapy, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 104 papers.

0numbers the graph read from it
0cells of the map it votes in
104citing papers in PubMed
10.5field-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

104 citing papers in PubMed, 185 citations in OpenAlex.

  1. Review
  2. A β‑1,3‑1,6‑glucan fromMolecular medicine reports · 2026
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44 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

7 authors at 4 institutions in 4 countries.

Abhay P MishraDepartment of Pharmaceutical Chemistry, H. N. B. Garhwal (A Central) University, Srinagar Garhwal, Uttarakhand, 246174, India.
Bahare SalehiMedical Ethics and Law Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Mehdi Sharifi-RadDepartment of Medical Parasitology, Zabol University of Medical Sciences, Zabol, 61663335, Iran.
Raffaele PezzaniOU Endocrinology, Dept. Medicine (DIMED), University of Padova, via Ospedale 105, 35128, Padua, Italy.
Farzad KobarfardPhytochemistry Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Javad Sharifi-RadPhytochemistry Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran. javad.sharifirad@gmail.com.ORCID http://orcid.org/0000-0002-7301-8151
Manisha NigamDepartment of Biochemistry, H. N. B. Garhwal (A Central) University, Srinagar Garhwal, Uttarakhand, 246174, India. m.nigam@hnbgu.ac.in.
Shahid Beheshti University of Medical Sciences · IRHemwati Nandan Bahuguna Garhwal University · INUniversity of Padua · ITZabol University of Medical Sciences · IR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Programmed cell death (PCD) is probably the most widely discussed subject among the topics of cancer therapy. Over the last 2 decades an astonishing boost in our perception of cell death has been seen, and its role in cancer and cancer therapy has been thoroughly investigated. A number of discoveries have clarified the molecular mechanism of PCD, thus expounding the link between PCD and therapeutic tools. Even though PCD is assumed to play a major role in anticancer therapy, the clinical relevance of its induction remains uncertain. Since PCD involves multiple death programs including programmed necrosis and autophagic cell death, it has contributed to our better understanding of cancer pathogenesis and therapeutics. In this review, we discuss a brief outline of PCD types as well as their role in cancer therapeutics. Since irregularities in the cell death process are frequently found in various cancers, key proteins governing cell death type could be used as therapeutic targets for a wide range of cancer.

Indexed as

Gene Expression Regulation, NeoplasticAntineoplastic AgentsApoptosisApoptosis Regulatory ProteinsAutophagyAutophagy-Related ProteinsHumansMolecular Targeted TherapyNecrosisNeoplasm ProteinsNeoplasmsProtein KinasesSignal TransductionTumor Suppressor Protein p53Antineoplastic AgentsApoptosis Regulatory ProteinsAutophagy-Related ProteinsMLKL protein, humanNeoplasm ProteinsProtein KinasesTumor Suppressor Protein p53

Identifiers

PMID29560608
OpenAlexW2790388852

What OpenQuestion holds

Textmetadata
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.