Evidence map›Paper›PMID 19737977›Full record

ArticleMolecular cancer research : MCR2009

Bcl-2 modulation to activate apoptosis in prostate cancer.

Kevin Bray, Hsin-Yi Chen, Cristina M Karp, Michael May, Shridar Ganesan, Vassiliki Karantza-Wadsworth, Robert S DiPaola, Eileen White

Open access · bronzeAbstract read
In one paragraph

Article in Molecular cancer research : MCR, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

26 citing papers in PubMed, 50 citations in OpenAlex.

  1. Trial
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  6. Harnessing the Utility ofFrontiers in oncology · 2022
    Review
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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 2 institutions in 1 country.

Kevin BrayThe Cancer Institute of New Jersey, New Brunswick, NJ 08903-2681, USA.
Hsin-Yi Chen
Cristina M Karp
Michael May
Shridar Ganesan
Vassiliki Karantza-Wadsworth
Robert S DiPaola
Eileen White
Rutgers, The State University of New Jersey · USCancer Institute of Florida · US

Funding

Role of Autophagy in CancerR01CA130893 · NCI · RUTGERS, THE STATE UNIV OF N.J. · PI WHITE, EILEEN P. · 2008 to 2017
$3.4M
Function of the Adenovirus E1B OncogeneR37CA053370 · NCI · RUTGERS THE ST UNIV OF NJ NEW BRUNSWICK · PI WHITE, EILEEN P. · 2001 to 2009
$3.1M
VIRUS-HOST INTERACTIONS IN EUKARYOTIC CELLST32AI007403 · NIAID · UNIV OF MED/DENT NJ-R W JOHNSON MED SCH · PI BREWER, GARY A. · 1991 to 2014
$1.7M
Role of Autophagy in Breast CancerR00CA133181 · NCI · UNIV OF MED/DENT NJ-R W JOHNSON MED SCH · PI KARANTZA, VASSILIKI · 2009 to 2011
$734k
NCI NIH HHS R00 CA133181NCI NIH HHS R01 CA130893NCI NIH HHS R01CA130893NCI NIH HHS R37 CA053370NCI NIH HHS R37CA53370NIAID NIH HHS 2T32 AI007403NIAID NIH HHS T32 AI007403
6 · The paper itself

Abstract

Apoptosis resistance is a hallmark of cancer linked to disease progression and treatment resistance, which has led to the development of anticancer therapeutics that restore apoptotic function. Antiapoptotic Bcl-2 is frequently overexpressed in refractory prostate cancer and increased following standard hormonal therapy and chemotherapy; however, the rationally designed Bcl-2 antagonist, ABT-737, has not shown single agent apoptosis-promoting activity against human prostate cancer cell lines. This is likely due to the coordinate expression of antiapoptotic, Bcl-2-related Mcl-1 that is not targeted by ABT-737. We developed a mouse model for prostate cancer in which apoptosis resistance and tumorigenesis were conferred by Bcl-2 expression. Combining ABT-737 with agents that target Mcl-1 sensitized prostate cancer cell lines with an apoptotic block to cell death in vitro. In mice in vivo, ABT-737 showed single agent efficacy in prostate tumor allografts in which tumor cells are under hypoxic stress. In human prostate cancer tissue, examined using a novel tumor explant system designated Tumor Tissue Assessment for Response to Chemotherapy, combination chemotherapy promoted efficient apoptosis. Thus, rational targeting of both the Bcl-2 and Mcl-1 mechanisms of apoptosis resistance may be therapeutically advantageous for advanced prostate cancer.

Indexed as

AnimalsAntineoplastic Combined Chemotherapy ProtocolsApoptosisBiphenyl CompoundsCisplatinDrug SynergismHumansImmunohistochemistryMaleMiceMice, Inbred C57BLMice, NudeMyeloid Cell Leukemia Sequence 1 ProteinNitrophenolsPaclitaxelPiperazinesABT-737Biphenyl CompoundsCisplatinMcl1 protein, mouseMyeloid Cell Leukemia Sequence 1 ProteinNitrophenolsPaclitaxelPiperazinesProto-Oncogene Proteins c-bcl-2SulfonamidesTumor Suppressor Protein p53

Identifiers

PMID19737977
PMCPMC2855683
OpenAlexW2137271899

What OpenQuestion holds

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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.