Evidence map›Paper›PMID 36935322›Full record

ReviewTrends in cancer2023

Reprogramming of tissue metabolism during cancer metastasis.

Koelina Ganguly, Alec C Kimmelman

Open access · greenAbstract readReview
In one paragraph

Review in Trends in cancer, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
6.5field-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

22 citing papers in PubMed, 27 citations in OpenAlex.

  1. Review
  2. Article
  3. Cancer cachexia: molecular basis and therapeutic advances.Signal transduction and targeted therapy · 2026
    Review
  4. Review
  5. Review
  6. Article
  7. Long noncoding RNAs regulating enzymatic reactions in cancer.Experimental & molecular medicine · 2025
    Review
  8. Review
  9. Review
  10. Article
  11. Article
  12. Deciphering organotropism reveals therapeutic targets in metastasis.Frontiers in cell and developmental biology · 2025
    Review
  13. Review
  14. Article
  15. Review
  16. Review
  17. Article
  18. Review
  19. Review
  20. 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

2 authors at 1 institution in 1 country.

Koelina GangulyPerlmutter Cancer Center, New York University School of Medicine, New York, NY, USA; Department of Radiation Oncology, New York University Grossman School of Medicine, New York, NY, USA.
Alec C KimmelmanPerlmutter Cancer Center, New York University School of Medicine, New York, NY, USA; Department of Radiation Oncology, New York University Grossman School of Medicine, New York, NY, USA. Electronic address: alec.kimmelman@nyulangone.org.
New York University · US

Funding

Vaccine FacilityP30CA016087 · NCI · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI ANIRBAN MAITRA · 1985 to 2026
$83.1M
The RAS and P13K Pathways in Pancreatic AdenocarcinomaP01CA117969 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI DEPINHO, RONALD ANTHONY · 2006 to 2025
$41.7M
Identifying Metabolic Dependencies of Pancreatic CancersR35CA232124 · NCI · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI KIMMELMAN, ALEC · 2018 to 2024
$6.5M
Targeting the autophagy-lysosome system to block pancreatic cancerR01CA251726 · NCI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI PERERA, RUSHIKA MIRIAM · 2021 to 2025
$1.8M
NCI NIH HHS P01 CA117969NCI NIH HHS P30 CA016087NCI NIH HHS R01 CA251726NCI NIH HHS R35 CA232124
6 · The paper itself

Abstract

Cancer is a systemic disease that involves malignant cell-intrinsic and -extrinsic metabolic adaptations. Most studies have tended to focus on elucidating the metabolic vulnerabilities in the primary tumor microenvironment, leaving the metastatic microenvironment less explored. In this opinion article, we discuss the current understanding of the metabolic crosstalk between the cancer cells and the tumor microenvironment, both at local and systemic levels. We explore the possible influence of the primary tumor secretome to metabolically and epigenetically rewire the nonmalignant distant organs during prometastatic niche formation and successful metastatic colonization by the cancer cells. In an attempt to understand the process of prometastatic niche formation, we have speculated how cancer may hijack the inherent regenerative propensity of tissue parenchyma during metastatic colonization.

Indexed as

NeoplasmsHumansTumor Microenvironmentmetabolismmetastasisprometastatic nichestromatissue regenerationwound response

Identifiers

PMID36935322
PMCPMC10192089
OpenAlexW4327725894

What OpenQuestion holds

Textmetadata
LicenceTDM
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.