Evidence map›Paper›PMID 33970362›Full record

ReviewClinical & experimental metastasis2022

Cancer microenvironment and genomics: evolution in process.

Stanley P Leong, Isaac P Witz, Orit Sagi-Assif, Sivan Izraely, Jonathan Sleeman, Brian Piening, Bernard A Fox, Carlo B Bifulco, Rachel Martini, Lisa Newman and 5 more

Abstract readReview
In one paragraph

Review in Clinical & experimental metastasis, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
–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

8 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Article
  6. Review
  7. Article
  8. Introduction: Novel Frontiers in Cancer Metastasis.Clinical & experimental metastasis · 2022
    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

15 authors.

Stanley P LeongCalifornia Pacific Medical Center and Research Institute, San Francisco, USA.ORCID 0000-0002-0047-0112
Isaac P WitzThe Shmunis School of Biomedicine and Cancer Research, School of Molecular Cell Biology & Biotechnology, George S. Wise Faculty of Life Science, Tel Aviv University, Tel Aviv, Israel.
Orit Sagi-AssifThe Shmunis School of Biomedicine and Cancer Research, School of Molecular Cell Biology & Biotechnology, George S. Wise Faculty of Life Science, Tel Aviv University, Tel Aviv, Israel.
Sivan IzraelyThe Shmunis School of Biomedicine and Cancer Research, School of Molecular Cell Biology & Biotechnology, George S. Wise Faculty of Life Science, Tel Aviv University, Tel Aviv, Israel.
Jonathan SleemanEuropean Center for Angioscience, Medizinische Fakultät Mannheim der Universität Heidelberg, Heidelberg, Germany.
Brian PieningProvidence Portland Medical Center, Portland, USA.
Bernard A FoxProvidence Portland Medical Center, Portland, USA.
Carlo B BifulcoProvidence Portland Medical Center, Portland, USA.
Rachel MartiniDepartment of Surgery, Weill Cornell Medical College, New York City, NY, USA.
Lisa NewmanDepartment of Surgery, Weill Cornell Medical College, New York City, NY, USA.
Melissa DavisDepartment of Surgery, Weill Cornell Medical College, New York City, NY, USA. mbd4001@med.cornell.edu.
Lauren M SandersDepartment of Molecular, Cell and Developmental Biology, University of California Santa Cruz and UC Santa Cruz Genomics Institute, Santa Cruz, USA.
David HausslerUC Santa Cruz Genomics Institute and Howard Hughes Medical Institute, University of California Santa Cruz, Santa Cruz, USA. haussler@ucsc.edu.
Olena M VaskeDepartment of Molecular, Cell and Developmental Biology, University of California Santa Cruz and UC Santa Cruz Genomics Institute, Santa Cruz, USA.
Marlys WitteDepartment of Surgery, Neurosurgery and Pediatrics, University of Arizona College of Medicine-Tucson, Tucson, AZ, USA.

Funding

The DARC side of Breast CancerR21CA210237 · NCI · UNIVERSITY OF GEORGIA · PI DAVIS, MELISSA B · 2017 to 2018
$386k
NCI NIH HHS R21 CA210237NIMHD NIH HHS L60 MD011128
6 · The paper itself

Abstract

Cancer heterogeneity is a result of genetic mutations within the cancer cells. Their proliferation is not only driven by autocrine functions but also under the influence of cancer microenvironment, which consists of normal stromal cells such as infiltrating immune cells, cancer-associated fibroblasts, endothelial cells, pericytes, vascular and lymphatic channels. The relationship between cancer cells and cancer microenvironment is a critical one and we are just on the verge to understand it on a molecular level. Cancer microenvironment may serve as a selective force to modulate cancer cells to allow them to evolve into more aggressive clones with ability to invade the lymphatic or vascular channels to spread to regional lymph nodes and distant sites. It is important to understand these steps of cancer evolution within the cancer microenvironment towards invasion so that therapeutic strategies can be developed to control or stop these processes.

Indexed as

NeoplasmsTumor MicroenvironmentEndothelial CellsGenomicsHumansLymph NodesCancer evolutionCancer heterogeneityCancer metastasisCancer microenvironment

Identifiers

PMID33970362
PMCPMC13508170

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.