Evidence map›Paper›PMID 38539200›Full record

ReviewCell communication and signaling : CCS2024

Polyploidy and mTOR signaling: a possible molecular link.

Debopriya Choudhury, Dhruba Ghosh, Meghna Mondal, Didhiti Singha, Ramesh Pothuraju, Pushkar Malakar

Open access · goldAbstract readReview
In one paragraph

Review in Cell communication and signaling : CCS, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
3.3field-weighted citation impact, top 8% 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

11 citing papers in PubMed, 14 citations in OpenAlex.

  1. Article
  2. Polyploidy: A macromutational force pushing bioeconomic developments.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Review
  3. Article
  4. Review
  5. Cell Fusion in Reprogramming and Regeneration.Advances in experimental medicine and biology · 2026
    Review
  6. Review
  7. Article
  8. Review
  9. Review
  10. Article
  11. 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

6 authors at 2 institutions in 1 country.

Debopriya ChoudhuryDepartment of Biomedical Science and Technology, School of Biological Sciences, Ramakrishna Mission Vivekananda Educational Research Institute (RKMVERI), Kolkata, India.
Dhruba GhoshDepartment of Biomedical Science and Technology, School of Biological Sciences, Ramakrishna Mission Vivekananda Educational Research Institute (RKMVERI), Kolkata, India.
Meghna MondalDepartment of Biomedical Science and Technology, School of Biological Sciences, Ramakrishna Mission Vivekananda Educational Research Institute (RKMVERI), Kolkata, India.
Didhiti SinghaDepartment of Biomedical Science and Technology, School of Biological Sciences, Ramakrishna Mission Vivekananda Educational Research Institute (RKMVERI), Kolkata, India.
Ramesh PothurajuCancer Research Program, Rajiv Gandhi Center for Biotechnology (RGCB), Thiruvananthapuram, 695014, Kerala, India.
Pushkar MalakarDepartment of Biomedical Science and Technology, School of Biological Sciences, Ramakrishna Mission Vivekananda Educational Research Institute (RKMVERI), Kolkata, India. pushkarbt@gm.rkmvu.ac.in.
Ramakrishna Mission Vivekananda Educational and Research Institute · INRajiv Gandhi Centre for Biotechnology · IN

Funding

Science and Engineering Research Board RJF/2021/000123
6 · The paper itself

Abstract

Polyploidy is typically described as the condition wherein a cell or organism has more than two complete sets of chromosomes. Occurrence of polyploidy is a naturally occurring phenomenon in the body's development and differentiation processes under normal physiological conditions. However, in pathological conditions, the occurrence of polyploidy is documented in numerous disorders, including cancer, aging and diabetes. Due to the frequent association that the polyploidy has with these pathologies and physiological process, understanding the cause and consequences of polyploidy would be beneficial to develop potential therapeutic applications. Many of the genetic and epigenetic alterations leading to cancer, diabetes and aging are linked to signaling pathways. Nonetheless, the specific signaling pathway associated with the cause and consequences of polyploidy still remains largely unknown. Mammalian/mechanistic target of rapamycin (mTOR) plays a key role in the coordination between eukaryotic cell growth and metabolism, thereby simultaneously respond to various environmental inputs including nutrients and growth factors. Extensive research over the past two decades has established a central role for mTOR in the regulation of many fundamental cellular processes that range from protein synthesis to autophagy. Dysregulated mTOR signaling has been found to be implicated in various disease progressions. Importantly, there is a strong correlation between the hallmarks of polyploidy and dysregulated mTOR signaling. In this review, we explore and discuss the molecular connection between mTOR signaling and polyploidy along with its association with cancer, diabetes and aging. Additionally, we address some unanswered questions and provide recommendations to further advance our understanding of the intricate relationship between mTOR signaling and polyploidy.

Indexed as

Diabetes MellitusNeoplasmsAnimalsHumansMammalsMechanistic Target of Rapamycin Complex 1Mechanistic Target of Rapamycin Complex 2PolyploidySignal TransductionTOR Serine-Threonine KinasesMechanistic Target of Rapamycin Complex 1Mechanistic Target of Rapamycin Complex 2TOR Serine-Threonine KinasesAgingCancerDiabetesmTORC1mTORC2mTOR signalingPolyploidy

Identifiers

PMID38539200
PMCPMC10976710
OpenAlexW4393221394

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.