Evidence map›Paper›PMID 24747769›Full record

ReviewBiochimica et biophysica acta2014

Cellular prostatic acid phosphatase, a PTEN-functional homologue in prostate epithelia, functions as a prostate-specific tumor suppressor.

Sakthivel Muniyan, Matthew A Ingersoll, Surinder K Batra, Ming-Fong Lin

Open access · greenAbstract readReview
In one paragraph

Review in Biochimica et biophysica acta, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing 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

17 citing papers in PubMed, 33 citations in OpenAlex.

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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

4 authors at 1 institution in 2 countries.

Sakthivel MuniyanDepartment of Biochemistry and Molecular Biology, University of Nebraska Medical Center, Omaha, NE, USA.
Matthew A IngersollDepartment of Biochemistry and Molecular Biology, University of Nebraska Medical Center, Omaha, NE, USA.
Surinder K BatraDepartment of Biochemistry and Molecular Biology, University of Nebraska Medical Center, Omaha, NE, USA; Eppley Institute for Research in Cancer and Allied Diseases, University of Nebraska Medical Center, Omaha, NE, USA.
Ming-Fong LinDepartment of Biochemistry and Molecular Biology, University of Nebraska Medical Center, Omaha, NE, USA; Eppley Institute for Research in Cancer and Allied Diseases, University of Nebraska Medical Center, Omaha, NE, USA; Department of Surgery/Urology, University of Nebraska Medical Center, Omaha, NE, USA; College of Pharmacy, Kaohsiung Medical University, Kaohsiung, Taiwan, ROC. Electronic address: mlin@unmc.edu.
University of Nebraska Medical Center · US

Funding

SIGNALING IN ANDROGEN REFRACTORY PROSTATE CANCERR01CA088184 · NCI · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI LIN, MING-FONG · 2000 to 2010
$2.6M
Novel deregulated genes in the etiology and progression of human prostate cancerR01CA138791 · NCI · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI BATRA, SURINDER K. · 2010 to 2014
$1.9M
NCI NIH HHS R01 CA088184NCI NIH HHS R01 CA138791NCI NIH HHS R01 CA88184
6 · The paper itself

Abstract

The inactivation of tumor suppressor genes (TSGs) plays a vital role in the progression of human cancers. Nevertheless, those ubiquitous TSGs have been shown with limited roles in various stages of diverse carcinogenesis. Investigation on identifying unique TSG, especially for early stage of carcinogenesis, is imperative. As such, the search for organ-specific TSGs has emerged as a major strategy in cancer research. Prostate cancer (PCa) has the highest incidence in solid tumors in US males. Cellular prostatic acid phosphatase (cPAcP) is a prostate-specific differentiation antigen. Despite intensive studies over the past several decades on PAcP as a PCa biomarker, the role of cPAcP as a PCa-specific tumor suppressor has only recently been emerged and validated. The mechanism underlying the pivotal role of cPAcP as a prostate-specific TSG is, in part, due to its function as a protein tyrosine phosphatase (PTP) as well as a phosphoinositide phosphatase (PIP), an apparent functional homologue to phosphatase and tensin homolog (PTEN) in PCa cells. This review is focused on discussing the function of this authentic prostate-specific tumor suppressor and the mechanism behind the loss of cPAcP expression leading to prostate carcinogenesis. We review other phosphatases' roles as TSGs which regulate oncogenic PI3K signaling in PCa and discuss the functional similarity between cPAcP and PTEN in prostate carcinogenesis.

Indexed as

Genes, Tumor SuppressorAcid PhosphataseAnimalsCarcinogenesisEpitheliumHumansMaleProstateProstatic NeoplasmsProtein Tyrosine PhosphatasesPTEN PhosphohydrolaseSequence HomologyAcid Phosphataseprostatic acid phosphataseProtein Tyrosine PhosphatasesPTEN PhosphohydrolasePTEN protein, humancPAcPErbB-2Phosphoinositide phosphataseProstate cancerProtein tyrosine phosphataseTumor suppressor

Identifiers

PMID24747769
PMCPMC4140952
OpenAlexW2083035689

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.