c-src structure in human cancers with elevated pp60c-src activity.

P Wang, F Fromowitz, M Koslow, N Hagag, B Johnson, M Viola

Open access · bronzeAbstract read

In one paragraph

Article in British journal of cancer, 1991. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it

0cells of the map it votes in

0citing papers in PubMed

0.9field-weighted citation impact, top 27% 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

0 citing papers in PubMed, 15 citations in OpenAlex.

No citing paper in PubMed yet.

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

6 authors at 2 institutions in 1 country.

P WangDepartment of Medicine, State University of New York, Stony Brook 11794.

F Fromowitz

M Koslow

N Hagag

B Johnson

M Viola

State University of New York · USStony Brook University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We used RNAase protection and restriction fragment length polymorphism assays to detect activating mutations of c-src in a spectrum of human tumours. No mutations were detected at codons 98, 381, 444, and 530. We conclude that mutational activation is not the mechanism of enhancement of pp60c-src-specific kinase activity found in a number of human cancer types.

Indexed as

Genes, srcMutationBase SequenceCodonHumansMolecular Sequence DataMutagenesis, Site-DirectedNeoplasmsOligodeoxyribonucleotidesPolymorphism, Restriction Fragment LengthProtein-Tyrosine KinasesProto-Oncogene Proteins pp60(c-src)RNA, MessengerCodonOligodeoxyribonucleotidesProtein-Tyrosine KinasesProto-Oncogene Proteins pp60(c-src)RNA, Messenger

Identifiers

PMID1716952

DOI10.1038/bjc.1991.344

PMCPMC1977675

OpenAlexW2022919182

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.