Evidence map›Paper›PMID 36675817›Full record

ReviewJournal of personalized medicine2023

Potential Therapies Targeting the Metabolic Reprogramming of Diabetes-Associated Breast Cancer.

Hang Chee Erin Shum, Ke Wu, Jaydutt Vadgama, Yong Wu

Abstract readReview
In one paragraph

Review in Journal of personalized medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
7citing 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

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

  1. Pooled it
  2. Review
  3. Review
  4. Review
  5. Review
  6. Article
  7. 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

4 authors.

Hang Chee Erin ShumLi Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong, China.
Ke WuDavid Geffen UCLA School of Medicine and UCLA Jonsson Comprehensive Cancer Center, Division of Cancer Research and Training, Department of Internal Medicine, Charles R. Drew University of Medicine and Science, 1748 E. 118th Street, Los Angeles, CA 90095, USA.
Jaydutt VadgamaDavid Geffen UCLA School of Medicine and UCLA Jonsson Comprehensive Cancer Center, Division of Cancer Research and Training, Department of Internal Medicine, Charles R. Drew University of Medicine and Science, 1748 E. 118th Street, Los Angeles, CA 90095, USA.ORCID 0000-0002-0019-8622
Yong WuDavid Geffen UCLA School of Medicine and UCLA Jonsson Comprehensive Cancer Center, Division of Cancer Research and Training, Department of Internal Medicine, Charles R. Drew University of Medicine and Science, 1748 E. 118th Street, Los Angeles, CA 90095, USA.

Funding

Workshop for Junior Biostatisticians in Health ResearchU54MD007598 · NIMHD · CHARLES R. DREW UNIVERSITY OF MED & SCI · PI Ali Andalibi, Jose A Torres-Ruiz · 2012 to 2026
$60.0M
Mechanisms behind hyperglycemia-associated breast cancer risk and progressionSC1CA200517 · NCI · CHARLES R. DREW UNIVERSITY OF MED & SCI · PI WU, YONG · 2015 to 2018
$1.4M
A novel metabolic reprograming strategy for the treatment of diabetes-associated breast cancerSC1GM135050 · NIGMS · CHARLES R. DREW UNIVERSITY OF MED & SCI · PI WU, YONG · 2020 to 2023
$1.4M
Drew/UCLA Cancer Partnership ProgramU56CA101599 · NCI · CHARLES R. DREW UNIVERSITY OF MED &SCI · PI VADGAMA, JAYDUTT V. · 2003 to 2009
$1.3M
NIGMS NIH HHS SC1 GM135050NIH HHS CTSI UL1TR000124NIH HHS NIH/NCI1U54CA14393NIH HHS SC1CA200517NIH HHS SC1 GM135050-05NIH HHS U54MD007598NIH HHS U56 CA101599-01NIMHD NIH HHS U54 MD007598
6 · The paper itself

Abstract

In recent years, diabetes-associated breast cancer has become a significant clinical challenge. Diabetes is not only a risk factor for breast cancer but also worsens its prognosis. Patients with diabetes usually show hyperglycemia and hyperinsulinemia, which are accompanied by different glucose, protein, and lipid metabolism disorders. Metabolic abnormalities observed in diabetes can induce the occurrence and development of breast cancer. The changes in substrate availability and hormone environment not only create a favorable metabolic environment for tumorigenesis but also induce metabolic reprogramming events required for breast cancer cell transformation. Metabolic reprogramming is the basis for the development, swift proliferation, and survival of cancer cells. Metabolism must also be reprogrammed to support the energy requirements of the biosynthetic processes in cancer cells. In addition, metabolic reprogramming is essential to enable cancer cells to overcome apoptosis signals and promote invasion and metastasis. This review aims to describe the major metabolic changes in diabetes and outline how cancer cells can use cellular metabolic changes to drive abnormal growth and proliferation. We will specifically examine the mechanism of metabolic reprogramming by which diabetes may promote the development of breast cancer, focusing on the role of glucose metabolism, amino acid metabolism, and lipid metabolism in this process and potential therapeutic targets. Although diabetes-associated breast cancer has always been a common health problem, research focused on finding treatments suitable for the specific needs of patients with concurrent conditions is still limited. Most studies are still currently in the pre-clinical stage and mainly focus on reprogramming the glucose metabolism. More research targeting the amino acid and lipid metabolism is needed.

Indexed as

breast cancercancer metabolismdiabeteshyperglycemiametabolic reprogramming

Identifiers

PMID36675817
PMCPMC9861470

What OpenQuestion holds

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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.