Evidence map›Paper›PMID 10408709›Full record

ArticleBritish journal of cancer1999

Absence of mutation of the p73 gene localized at chromosome 1p36.3 in hepatocellular carcinoma.

M Mihara, Y Nimura, S Ichimiya, S Sakiyama, S Kajikawa, W Adachi, J Amano, A Nakagawara

Open access · hybridAbstract read
In one paragraph

Article in British journal of cancer, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

12 citing papers in PubMed, 37 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

8 authors at 2 institutions in 1 country.

M MiharaDivision of Biochemistry, Chiba Cancer Center Research Institute, Japan.
Y Nimura
S Ichimiya
S Sakiyama
S Kajikawa
W Adachi
J Amano
A Nakagawara
Chiba Cancer Center · JPShinshu University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Accumulating evidence has demonstrated that aberration of the p53 tumour-suppressor gene is one of the pivotal genetic events in hepatocellular carcinogenesis. Recent reports suggest that the product of hepatitis B virus (HBV) interacts with p53 and that the hepatitis C virus (HCV) core protein reduces p53 expression. A novel p73 gene, which is related to p53, has recently been identified and mapped to chromosome 1p36.3, which is a locus of multiple tumour-suppressor genes for many cancers, including hepatocellular carcinoma (HCC) and neuroblastoma. Here, we investigated mRNA expression, allelotype and mutation of p73 in 48 HCCs obtained from untreated patients. Reverse transcriptase polymerase chain reaction (RT-PCR) revealed that p73 mRNA was expressed ubiquitously at low levels in all the tumour tissues, as well as in the adjacent normal liver tissues. The frequency of p73 loss of heterozygosity was observed in 20% of HCCs, but PCR-single strand conformation polymorphism (SSCP) analysis showed no mutations in the 48 tumours except for three types of polymorphisms. These results suggest that p73 may play a role in hepatocellular carcinogenesis in a different manner from a Knudson two-hit model. The regulatory mechanism of interaction between p73 and hepatitis viruses remains to be determined.

Indexed as

Chromosomes, Human, Pair 1Genes, Tumor SuppressorMutationBase SequenceCarcinoma, HepatocellularDNA-Binding ProteinsDNA PrimersHumansLiver NeoplasmsLoss of HeterozygosityNuclear ProteinsReverse Transcriptase Polymerase Chain ReactionRNA, MessengerTumor Protein p73Tumor Suppressor ProteinsDNA-Binding ProteinsDNA PrimersNuclear ProteinsRNA, MessengerTP73 protein, humanTumor Protein p73Tumor Suppressor Proteins

Identifiers

PMID10408709
PMCPMC2362167
OpenAlexW1989337156

What OpenQuestion holds

Textmetadata
LicenceCC BY
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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.