Evidence map›Paper›PMID 24787239›Full record

ReviewCancer gene therapy2014

Epithelial-to-mesenchymal transition and the cancer stem cell phenotype: insights from cancer biology with therapeutic implications for colorectal cancer.

V J Findlay, C Wang, D K Watson, E R Camp

Open access · bronzeAbstract readReview
In one paragraph

Review in Cancer gene therapy, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.

0numbers the graph read from it
0cells of the map it votes in
62citing papers in PubMed
8.5field-weighted citation impact, top 1% 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

62 citing papers in PubMed, 112 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. ACancer research communications · 2023
    Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Review
  10. Is Curcumin the Answer to Future Chemotherapy Cocktail?Molecules (Basel, Switzerland) · 2021
    Review
  11. Review
  12. Article
  13. Article
  14. Article
  15. RBBP4 promotes colon cancer malignant progressionWorld journal of gastroenterology · 2020
    Article
  16. Article
  17. Article
  18. Cholangiocarcinoma 2020: the next horizon in mechanisms and management.Nature reviews. Gastroenterology & hepatology · 2020
    Review
  19. Article
  20. Review

2 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

4 authors at 1 institution in 1 country.

V J FindlayDepartment of Pathology and Laboratory Medicine, Medical University of South Carolina, Charleston, SC, USA.
C WangDivision of Surgical Oncology, Department of Surgery, Medical University of South Carolina, Charleston, SC, USA.
D K Watson1] Department of Pathology and Laboratory Medicine, Medical University of South Carolina, Charleston, SC, USA [2] Department of Biochemistry and Molecular Biology, Medical University of South Carolina, Charleston, SC, USA [3] Hollings Cancer Center, Medical University of South Carolina, Charleston, SC, USA.
E R Camp1] Division of Surgical Oncology, Department of Surgery, Medical University of South Carolina, Charleston, SC, USA [2] Hollings Cancer Center, Medical University of South Carolina, Charleston, SC, USA [3] Ralph H. Johnson VA Medical Center, Medical University of South Carolina, Charleston, SC, USA.
Medical University of South Carolina · US

Funding

Innovative Delivery Strategy for CaSm Gene Therapy in Pancreatic CancerK08CA142904 · NCI · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI CAMP, ERNEST RAMSAY · 2010 to 2014
$867k
NCI NIH HHS 5R 1K08CA142904NCI NIH HHS K08 CA142904
6 · The paper itself

Abstract

Although mortality from colorectal cancer (CRC) is decreasing, CRC is still the second highest cause of cancer-related deaths in America. Chemotherapy and radiation therapy now have central roles in our strategies to fight cancer, although we continue to lack novel strategies overcoming therapeutic resistance. Molecular mechanisms of therapeutic resistance in CRC continue to be under intense investigation. In this review, we highlight the recent evidence linking epithelial-to-mesenchymal transition (EMT) with aggressive tumor biology as well as with the cancer stem cells (CSCs) across multiple organ systems including colon cancer. Furthermore, in the era of neo-adjuvant treatment, the clinical implications are concerning that our treatments may have the potential to induce more aggressive cancer cells through EMT, perhaps even generating CSCs more capable of metastasis and further resistant to treatment. This concern and potential reality highlights the critical need for further understanding the impact of clinical therapy on the pathobiology of cancer and further supports the need to therapeutically target the CSC. Besides serving as potential biomarkers for aggressive tumor biology and therapeutic resistance, EMT and CSC molecular pathways may highlight novel therapeutic targets as strategies for improving the response to conventional anti-neoplastic agents translating into improved oncologic outcomes.

Indexed as

Epithelial-Mesenchymal TransitionColorectal NeoplasmsDrug Resistance, NeoplasmHumansMicroRNAsNeoplastic Stem CellsPhenotypeMicroRNAs

Identifiers

PMID24787239
PMCPMC4041800
OpenAlexW2113207478

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.