Evidence map›Paper›PMID 35521962›Full record

ArticleExperimental biology and medicine (Maywood, N.J.)2022

Tumor cell anabolism and host tissue catabolism-energetic inefficiency during cancer cachexia.

Mangala Hegde, Uzini Devi Daimary, Sosmitha Girisa, Aviral Kumar, Ajaikumar B Kunnumakkara

Abstract read
In one paragraph

Article in Experimental biology and medicine (Maywood, N.J.), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed, 1 pooled it
–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

14 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. SEOM clinical guidelines for cancer anorexia-cachexia syndrome (2023).Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2024
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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

5 authors.

Mangala HegdeCancer Biology Laboratory, Department of Biosciences and Bioengineering, Indian Institute of Technology-Guwahati, Guwahati 781039, Assam, India.
Uzini Devi DaimaryCancer Biology Laboratory, Department of Biosciences and Bioengineering, Indian Institute of Technology-Guwahati, Guwahati 781039, Assam, India.
Sosmitha GirisaCancer Biology Laboratory, Department of Biosciences and Bioengineering, Indian Institute of Technology-Guwahati, Guwahati 781039, Assam, India.
Aviral KumarCancer Biology Laboratory, Department of Biosciences and Bioengineering, Indian Institute of Technology-Guwahati, Guwahati 781039, Assam, India.
Ajaikumar B KunnumakkaraCancer Biology Laboratory, Department of Biosciences and Bioengineering, Indian Institute of Technology-Guwahati, Guwahati 781039, Assam, India.ORCID 0000-0001-9121-6816

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cancer-associated cachexia (CC) is a pathological condition characterized by sarcopenia, adipose tissue depletion, and progressive weight loss. CC is driven by multiple factors such as anorexia, excessive catabolism, elevated energy expenditure by growing tumor mass, and inflammatory mediators released by cancer cells and surrounding tissues. In addition, endocrine system, systemic metabolism, and central nervous system (CNS) perturbations in combination with cachexia mediators elicit exponential elevation in catabolism and reduced anabolism in skeletal muscle, adipose tissue, and cardiac muscle. At the molecular level, mechanisms of CC include inflammation, reduced protein synthesis, and lipogenesis, elevated proteolysis and lipolysis along with aggravated toxicity and complications of chemotherapy. Furthermore, CC is remarkably associated with intolerance to anti-neoplastic therapy, poor prognosis, and increased mortality with no established standard therapy. In this context, we discuss the spatio-temporal changes occurring in the various stages of CC and highlight the imbalance of host metabolism. We provide how multiple factors such as proteasomal pathways, inflammatory mediators, lipid and protein catabolism, glucocorticoids, and in-depth mechanisms of interplay between inflammatory molecules and CNS can trigger and amplify the cachectic processes. Finally, we highlight current diagnostic approaches and promising therapeutic interventions for CC.

Indexed as

CachexiaNeoplasmsAdipose TissueAnorexiaHumansInflammation MediatorsMuscle, SkeletalInflammation MediatorsanabolismanorexiacachexiacatabolismgluconeogenesisGlycolysis

Identifiers

PMID35521962
PMCPMC9134760

What OpenQuestion holds

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Registered trials

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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.