Evidence map›Paper›PMID 37170010›Full record

ReviewMedical oncology (Northwood, London, England)2023

Oncogenic metabolic reprogramming in breast cancer: focus on signaling pathways and mitochondrial genes.

Rhuthuparna Malayil, Yogita Chhichholiya, Kanika Vasudeva, Harsh Vikram Singh, Tashvinder Singh, Sandeep Singh, Anjana Munshi

Abstract readReview
PubMed Publisher
In one paragraph

Review in Medical oncology (Northwood, London, England), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
4.1field-weighted citation impact, top 6% 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

10 citing papers in PubMed, 17 citations in OpenAlex.

  1. Review
  2. Translational cancer research · 2025
    Article
  3. Article
  4. Review
  5. Article
  6. Review
  7. Review
  8. Article
  9. Review
  10. 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

7 authors at 3 institutions in 1 country.

Rhuthuparna MalayilDepartment of Human Genetics and Molecular Medicine, Central University of Punjab Bathinda, Punjab, India.
Yogita ChhichholiyaDepartment of Human Genetics and Molecular Medicine, Central University of Punjab Bathinda, Punjab, India.
Kanika VasudevaIndian Council of Medical Research, New Delhi, India.
Harsh Vikram SinghDepartment of Orthopedics, All India Institute of Medical Sciences, Bathinda, India.
Tashvinder SinghDepartment of Human Genetics and Molecular Medicine, Central University of Punjab Bathinda, Punjab, India.
Sandeep SinghDepartment of Human Genetics and Molecular Medicine, Central University of Punjab Bathinda, Punjab, India. sandeepsingh82@cup.edu.in.
Anjana MunshiDepartment of Human Genetics and Molecular Medicine, Central University of Punjab Bathinda, Punjab, India. anjana.munshi@cup.edu.in.ORCID http://orcid.org/0000-0002-7657-8592
Central University of Punjab · INAll India Institute of Medical Sciences · INIndian Council of Medical Research · IN

Funding

Council for Scientific and Industrial Research India 09/1051(0038)/2019-EMR-1Council for Scientific and Industrial Research, India 09/1051(0042)/2019-EMR-1Science and Engineering Research Board SRG/2021/001806University Grants Commission, India KL1216200313
6 · The paper itself

Abstract

Oncogenic metabolic reprogramming impacts the abundance of key metabolites that regulate signaling and epigenetics. Metabolic vulnerability in the cancer cell is evident from the Warburg effect. The research on metabolism in the progression and survival of breast cancer (BC) is under focus. Oncogenic signal activation and loss of tumor suppressor are important regulators of tumor cell metabolism. Several intrinsic and extrinsic factors contribute to metabolic reprogramming. The molecular mechanisms underpinning metabolic reprogramming in BC are extensive and only partially defined. Various signaling pathways involved in the metabolism play a significant role in the modulation of BC. Notably, PI3K/AKT/mTOR pathway, lactate-ERK/STAT3 signaling, loss of the tumor suppressor Ras, Myc, oxidative stress, activation of the cellular hypoxic response and acidosis contribute to different metabolic reprogramming phenotypes linked to enhanced glycolysis. The alterations in mitochondrial genes have also been elaborated upon along with their functional implications. The outcome of these active research areas might contribute to the development of novel therapeutic interventions and the remodeling of known drugs.

Indexed as

NeoplasmsPhosphatidylinositol 3-KinasesGenes, MitochondrialGlycolysisHumansSignal TransductionPhosphatidylinositol 3-KinasesBCMetabolic reprogrammingMitochondriaSignaling

Identifiers

PMID37170010
OpenAlexW4376129178

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.