Evidence map›Paper›PMID 26493492›Full record

Trial reportThe Prostate2016

Saracatinib as a metastasis inhibitor in metastatic castration-resistant prostate cancer: A University of Chicago Phase 2 Consortium and DOD/PCF Prostate Cancer Clinical Trials Consortium Study.

Edwin M Posadas, Rafi S Ahmed, Theodore Karrison, Russell Z Szmulewitz, Peter H O'Donnell, James L Wade, James Shen, Murali Gururajan, Margarit Sievert, Walter M Stadler

Abstract readClinical Trial, Phase IIMulticenter StudyRandomized Controlled Trial
In one paragraph

Trial report in The Prostate, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.2field-weighted citation impact, top 12% 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

22 citing papers in PubMed, 42 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

10 authors at 4 institutions in 1 country.

Edwin M PosadasUrologic Oncology Program, Samuel Oschin Comprehensive Cancer Institute, Cedars-Sinai Medical Center, Los Angeles, California.
Rafi S AhmedUrologic Oncology Program, Samuel Oschin Comprehensive Cancer Institute, Cedars-Sinai Medical Center, Los Angeles, California.
Theodore KarrisonBiostatistics, Department of Health Service, University of Chicago, Chicago, Illinois.
Russell Z SzmulewitzGenitourinary Oncology Program, Section of Hematology/Oncology, Department of Medicine, University of Chicago, Chicago, Illinois.
Peter H O'DonnellGenitourinary Oncology Program, Section of Hematology/Oncology, Department of Medicine, University of Chicago, Chicago, Illinois.
James L WadeCancer Care Specialists of Central Illinois, S.C, Decatur, Illinois.
James ShenUrologic Oncology Program, Samuel Oschin Comprehensive Cancer Institute, Cedars-Sinai Medical Center, Los Angeles, California.
Murali GururajanUrologic Oncology Program, Samuel Oschin Comprehensive Cancer Institute, Cedars-Sinai Medical Center, Los Angeles, California.
Margarit SievertUrologic Oncology Program, Samuel Oschin Comprehensive Cancer Institute, Cedars-Sinai Medical Center, Los Angeles, California.
Walter M StadlerGenitourinary Oncology Program, Section of Hematology/Oncology, Department of Medicine, University of Chicago, Chicago, Illinois.
Cedars-Sinai Medical Center · USUniversity of Chicago · USCancer Care Specialists of Illinois · USChicago Department of Public Health · US

Funding

NCI NIH HHS HHSN261201100071CNCI NIH HHS N01-CM-2011-00071C
6 · The paper itself

Abstract

backgroundFyn is a kinase that is upregulated in a subset of metastatic castration-resistant prostate cancer. Saracatinib potently inhibits Fyn activation. We have noted a relationship between Fyn expression and directional motility, a cellular process related to metastasis. As such we hypothesized that treatment with saracatinib would increase the time required to develop new metastatic lesions.

methodsPatients with metastatic castration-resistant prostate cancer that had progressed after docetaxel were eligible for enrollment. This study was executed as a randomized discontinuation trial. During a lead-in phase of two 28-Day cycles, all patients received saracatinib. Afterward, patients with radiographically stable disease were randomized to either saracatinib or placebo. Patients continued treatment until evidence of new metastasis.

resultsThirty-one patients were treated. Only 26% of patients had stable disease after 8 weeks and thus proceeded to randomization. This required early termination of the study for futility. The 70% of patients who progressed after the lead-in phase exhibited expansion of existing lesions or decompensation due to clinical progression without new metastatic lesions. Fatigue was reported in more than 25% of patients (all grades) with only two patients experiencing grade 3 toxicity. Other grade 3 adverse events included dehydration, thrombocytopenia, and weakness.

conclusionsThis study was unable to determine if saracatinib had potential as metastasis inhibitor. Metastasis inhibition by saracatinib may still be viable in an earlier time in the disease history.

Indexed as

Academic Medical CentersAgedAged, 80 and overAntineoplastic AgentsBenzodioxolesChicagoHumansMaleMiddle AgedNeoplasm MetastasisProstatic Neoplasms, Castration-ResistantQuinazolinesAntineoplastic AgentsBenzodioxolesQuinazolinessaracatinibazd0530castration-resistantFynprostate cancersaracatinib

Identifiers

PMID26493492
PMCPMC4904773
OpenAlexW2142064431

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.