Evidence map›Paper›PMID 27074569›Full record

ArticleOncotarget2016

Targeting cancer stem cells with p53 modulators.

Zhan Zhang, Ling Liu, Roberto Gomez-Casal, Xinhui Wang, Ryo Hayashi, Ettore Appella, Levy Kopelovich, Albert B DeLeo

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.7field-weighted citation impact, top 14% 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

9 citing papers in PubMed, 21 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. The p53 Saga: Early Steps in the Development of Tumor Immunotherapy.Journal of immunology (Baltimore, Md. : 1950) · 2020
    Review
  5. Article
  6. Article
  7. Article
  8. Emerging Non-Canonical Functions and Regulation by p53: p53 and Stemness.International journal of molecular sciences · 2016
    Review
  9. 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

8 authors at 6 institutions in 2 countries.

Zhan ZhangDepartment of Obstetrics and Gynecology, The Third Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, China.
Ling LiuDepartment of Obstetrics and Gynecology, The Third Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, China.
Roberto Gomez-CasalUniversity of Pittsburgh Cancer Institute, Pittsburgh, PA, USA.
Xinhui WangDepartment of Surgery, Division of Surgical Oncology, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA.
Ryo HayashiNational Cancer Institute, Bethesda, MD, USA.
Ettore AppellaNational Cancer Institute, Bethesda, MD, USA.
Levy KopelovichDepartment of Medicine, Weill Cornell Medical College, New York, NY, USA.
Albert B DeLeoUniversity of Pittsburgh Cancer Institute, Pittsburgh, PA, USA.
National Cancer Institute · USUniversity of Pittsburgh · USCornell University · USHarvard University · USMassachusetts General Hospital · USThird Affiliated Hospital of Zhengzhou University · CN

Funding

Tumor Suppressor Protein, p53ZIABC005599 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI APPELLA, ETTORE · 2009 to 2025
$8.1M
Improving Radiation Therapy For Pancreatic CancerR21CA181851 · NCI · MASSACHUSETTS GENERAL HOSPITAL · PI WANG, XINHUI · 2015 to 2016
$407k
NCI NIH HHS R21 CA181851
6 · The paper itself

Abstract

Cancer stem cells (CSC) typically over-express aldehyde dehydrogenase (ALDH). Thus, ALDHbright tumor cells represent targets for developing novel cancer prevention/treatment interventions. Loss of p53 function is a common genetic event during cancer development wherein small molecular weight compounds (SMWC) that restore p53 function and reverse tumor growth have been identified. Here, we focused on two widely studied p53 SMWC, CP-31398 and PRIMA-1, to target ALDHbright CSC in human breast, endometrial and pancreas carcinoma cell lines expressing mutant or wild type (WT) p53. CP-31398 and PRIMA-1 significantly reduced CSC content and sphere formation by these cell lines in vitro. In addition, these agents were more effective in vitro against CSC compared to cisplatin and gemcitabine, two often-used chemotherapeutic agents. We also tested a combinatorial treatment in methylcholantrene (MCA)-treated mice consisting of p53 SMWC and p53-based vaccines. Yet using survival end-point analysis, no increased efficacy in the presence of either p53 SMWC alone or with vaccine compared to vaccine alone was observed. These results may be due, in part, to the presence of immune cells, such as activated lymphocytes expressing WT p53 at levels comparable to some tumor cells, wherein further increase of p53 expression by p53 SMWC may alter survival of these immune cells and negatively impact an effective immune response. Continuous exposure of mice to MCA may have also interfered with the action of these p53 SMWC, including potential direct interaction with MCA. Nonetheless, the effect of p53 SMWC on CSC and cancer treatment remains of great interest.

Indexed as

AnimalsAntineoplastic AgentsAza CompoundsBridged Bicyclo Compounds, HeterocyclicCancer VaccinesCell Line, TumorCell ProliferationHumansMiceMice, Inbred C57BLNeoplastic Stem CellsPyrimidinesTumor Suppressor Protein p532,2-bis(hydroxymethyl)-1-azabicyclo(2,2,2,)octan-3-oneAntineoplastic AgentsAza CompoundsBridged Bicyclo Compounds, HeterocyclicCancer VaccinesCP 31398PyrimidinesTumor Suppressor Protein p53cancer stem cellsCP-31398P53 vaccinePRIMA-1T cells

Identifiers

PMID27074569
PMCPMC5216707
OpenAlexW2329885691

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.