Evidence map›Paper›PMID 9387095›Full record

ReviewJournal of bioenergetics and biomembranes1997

Oncogenes in tumor metabolism, tumorigenesis, and apoptosis.

C V Dang, B C Lewis, C Dolde, G Dang, H Shim

Abstract readReview
PubMed Publisher
In one paragraph

Review in Journal of bioenergetics and biomembranes, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
2.5field-weighted citation impact, top 10% 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

45 citing papers in PubMed, 121 citations in OpenAlex.

  1. Targeting MYC-Driven Cancers: From Oncogenic Addiction to Therapeutic Vulnerability.BioDrugs : clinical immunotherapeutics, biopharmaceuticals and gene therapy · 2026
    Review
  2. Review
  3. Review
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Dysregulation of Glucose Metabolism by Oncogenes and Tumor Suppressors in Cancer CellsAsian Pacific journal of cancer prevention : APJCP · 2018
    Review
  11. Article
  12. Review
  13. Review
  14. Pheochromocytoma: The First Metabolic Endocrine Cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2016
    Review
  15. Review
  16. Hypothesis: solid tumours behave as systemic metabolic dictators.Journal of cellular and molecular medicine · 2016
    Article
  17. Article
  18. Article
  19. Article
  20. Article
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 at 2 institutions in 1 country.

C V DangDepartment of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA.
B C Lewis
C Dolde
G Dang
H Shim
Johns Hopkins Medicine · USJohns Hopkins University · US

Funding

C-MYC TARGETS IN THE PATHOGENESIS OF HUMAN CANCERSR01CA057341 · NCI · WISTAR INSTITUTE · PI DANG, CHI V. · 1992 to 2021
$8.3M
TRAINING PROGRAM IN HEMATOLOGYT32HL007525 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI ROBERT A BRODSKY · 1985 to 2026
$6.2M
NCI NIH HHS CA57341NHLBI NIH HHS T32HL07525
6 · The paper itself

Abstract

The ability of cancer cells to overproduce lactic acid aerobically was recognized by Warburg about seven decades ago, although its molecular basis has been elusive. Increases in glucose transport and hexokinase activity in cancer cells appear to account for the increased flux of glucose through the cancer cells. Herein we review current findings indicating that the c-Myc oncogenic transcription factor and hypoxia-inducible factor 1 (HIF-1) are able to bind the lactate dehydrogenase A promoter cis acting elements, which resemble the core carbohydrate response element (ChoRE), CACGTG. These and other observations suggest that the normal cell responds physiologically to changes in oxygen tension or the availability of glucose by altering glycolysis through the ChoRE, which hypothetically binds c-Myc, HIF-1, or related factors. The neoplastic cell is hypothesized to augment glycolysis by activation of ChoRE/ HIF-1 sites through direct interaction with c-Myc or through activation of HIF-1 or HIF-1-like activity. We hypothesize that oncogene products either stimulate HIF-1 and related factors or, in the case of c-Myc, directly activate hypoxia/glucose responsive elements in glycolytic enzyme genes to increase the ability of cancer cells to undergo aerobic glycolysis.

Indexed as

ApoptosisCell Transformation, NeoplasticOncogenesAnimalsHumansNeoplasms

Identifiers

PMID9387095
OpenAlexW1537539007

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.