Evidence map›Paper›PMID 42421031›Full record

ReviewJournal of translational medicine2026

Regulated cell death plasticity in cancer: thresholds, reversibility, and therapeutic failure.

Tooba Jawwad, Sadaf Khursheed Baba, Anju Surendranath, Elena Chaudhary, Ghulam Jeelani, Ammira S Al-Shabeeb Akil, Asma Al Menhali, Ajaz A Bhat, Sameer Mirza

Abstract readReview
In one paragraph

Review in Journal of translational medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
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

2 citing papers in PubMed.

  1. Review
  2. 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

9 authors.

Tooba JawwadDepartment of Chemistry, College of Science (COS), United Arab Emirates University (UAEU), P.O. Box 15551, Al Ain, United Arab Emirates.
Sadaf Khursheed BabaDepartment of Chemistry, College of Science (COS), United Arab Emirates University (UAEU), P.O. Box 15551, Al Ain, United Arab Emirates.
Anju SurendranathMetabolic and Mendelian Disorders Clinical Research Program, Precision Genomics and Translational Omics Lab, Sidra Medicine, Doha, 26999, Qatar.
Elena ChaudharyMohammed Bin Rashid University of Medicine and Health Sciences, Dubai, United Arab Emirates.
Ghulam JeelaniDepartment of Biomedical Chemistry, Graduate School of Medicine, The University of Tokyo, Bunkyo, Tokyo, Japan.
Ammira S Al-Shabeeb AkilMetabolic and Mendelian Disorders Clinical Research Program, Precision Genomics and Translational Omics Lab, Sidra Medicine, Doha, 26999, Qatar.
Asma Al MenhaliDepartment of Biology, College of Science, United Arab Emirates University (UAEU), P.O. Box 15551, Al Ain, United Arab Emirates.
Ajaz A BhatMetabolic and Mendelian Disorders Clinical Research Program, Precision Genomics and Translational Omics Lab, Sidra Medicine, Doha, 26999, Qatar.
Sameer MirzaDepartment of Chemistry, College of Science (COS), United Arab Emirates University (UAEU), P.O. Box 15551, Al Ain, United Arab Emirates. sameermirza@uaeu.ac.ae.ORCID http://orcid.org/0000-0002-9394-2421

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Therapy resistance and disease recurrence remain major challenges across cancer types despite substantial advances in targeted therapy, chemotherapy, and immunotherapy. In many clinical settings, treatments successfully engage stress and death signaling pathways and produce rapid tumor regression, yet complete and durable eradication is uncommon. A consistent pattern emerges in which most tumor cells are eliminated while a small fraction survives, persists as residual disease, and later drives relapse. These observations suggest that failure is not always due to the absence of death pathways, but rather to incomplete execution. Here, we synthesize emerging evidence supporting the view that regulated cell death operates as a threshold-governed, highly plastic process. Apoptosis, ferroptosis, and inflammatory death programs remain largely intact in many tumors but are tightly controlled by buffering networks that regulate mitochondrial commitment, redox balance, metabolic state, and inflammatory signaling. Under therapeutic pressure, cancer cells frequently activate proximal death signaling without progressing to irreversible collapse. Sublethal engagement can generate stressed but viable cell states that contribute to drug tolerance, minimal residual disease, and later resistance evolution. Clinical data across hematologic and solid malignancies reinforce this framework. Biomarkers of pathway activation often correlate with early response but do not reliably predict long-term benefit. Dose limitations, treatment interruptions, and adaptive rewiring further allow surviving populations to recover and expand. We propose that execution depth, rather than pathway activation alone, represents a critical determinant of durable response. This perspective supports therapeutic strategies that simultaneously drive death signaling while disabling buffering systems, prevent adaptive state transitions, and incorporate immune-mediated clearance to achieve sustained tumor elimination.

Indexed as

Cell PlasticityNeoplasmsRegulated Cell DeathAnimalsCell DeathHumansSignal TransductionTreatment FailureCancer stem cellsDeath plasticityDrug-tolerant persistersFractional killingMetabolic bufferingMinimal residual diseaseRegulated cell deathTumor heterogeneity

Identifiers

PMID42421031
PMCPMC13640099

What Socratic 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 Socratic graph.