Evidence map›Paper›PMID 35419769›Full record

ReviewCancer metastasis reviews2022

Treatment against glucose-dependent cancers through metabolic PFKFB3 targeting of glycolytic flux.

Brandon C Jones, Paula R Pohlmann, Robert Clarke, Surojeet Sengupta

Abstract readReview
PubMed Publisher
In one paragraph

Review in Cancer metastasis reviews, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
4.7field-weighted citation impact, top 3% 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

35 citing papers in PubMed, 51 citations in OpenAlex.

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  19. Emerging roles of lactate in acute and chronic inflammation.Cell communication and signaling : CCS · 2024
    Review
  20. New Insights in ATP Synthesis as Therapeutic Target in Cancer and Angiogenic Ocular Diseases.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2024
    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 at 3 institutions in 1 country.

Brandon C JonesDepartment of Oncology, Georgetown Lombardi Comprehensive Cancer Center, 3970 Reservoir Rd NW, Washington, DC, 20057, USA.
Paula R PohlmannDepartment of Breast Medical Oncology, University of Texas MD Anderson Cancer Center, 1515 Holcombe Boulevard, Unit 1354, Houston, TX, 77030, USA.
Robert ClarkeThe Hormel Institute, University of Minnesota, 801 16th Ave NE, Austin, MN, 55912, USA.
Surojeet SenguptaThe Hormel Institute, University of Minnesota, 801 16th Ave NE, Austin, MN, 55912, USA. ssengupt@umn.edu.ORCID 0000-0002-3498-9668
University of Minnesota · USGeorgetown University Medical Center · USThe University of Texas MD Anderson Cancer Center · US

Funding

TRAINING GRANT IN TUMOR BIOLOGYT32CA009686 · NCI · GEORGETOWN UNIVERSITY · PI ANNA Tate RIEGEL, DAVID J ROBBINS · 1996 to 2026
$10.8M
Collaborative Research in Integrative Cancer BiologyU01CA184902 · NCI · GEORGETOWN UNIVERSITY · PI CLARKE, ROBERT R., WANG, YUE · 2014 to 2018
$2.7M
NCI NIH HHS U01 CA184902
6 · The paper itself

Abstract

Reprogrammed metabolism and high energy demand are well-established properties of cancer cells that enable tumor growth. Glycolysis is a primary metabolic pathway that supplies this increased energy demand, leading to a high rate of glycolytic flux and a greater dependence on glucose in tumor cells. Finding safe and effective means to control glycolytic flux and curb cancer cell proliferation has gained increasing interest in recent years. A critical step in glycolysis is controlled by the enzyme 6-phosphofructo-2-kinase/fructose-2,6-biphosphatase 3 (PFKFB3), which converts fructose 6-phosphate (F6P) to fructose 2,6-bisphosphate (F2,6BP). F2,6BP allosterically activates the rate-limiting step of glycolysis catalyzed by PFK1 enzyme. PFKFB3 is often overexpressed in many human cancers including pancreatic, colon, prostate, and breast cancer. Hence, PFKFB3 has gained increased interest as a compelling therapeutic target. In this review, we summarize and discuss the current knowledge of PFKFB3 functions, its role in cellular pathways and cancer development, its transcriptional and post-translational activity regulation, and the multiple pharmacologic inhibitors that have been used to block PFKFB3 activity in cancer cells. While much remains to be learned, PFKFB3 continues to hold great promise as an important therapeutic target either as a single agent or in combination with current interventions for breast and other cancers.

Indexed as

Breast NeoplasmsPhosphofructokinase-2FructoseGlucoseGlycolysisHumansMaleFructoseGlucosePFKFB3 protein, humanPhosphofructokinase-2Aerobic glycolysisCancerGlucose metabolismPFKFB3Phosphofructo-2-kinase/fructose-2,6-biphosphatase

Identifiers

PMID35419769
OpenAlexW4223952323

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.