Evidence map›Paper›PMID 24145349›Full record

ArticleCancer research2013

BCCIP suppresses tumor initiation but is required for tumor progression.

Yi-Yuan Huang, Li Dai, Dakim Gaines, Roberto Droz-Rosario, Huimei Lu, Jingmei Liu, Zhiyuan Shen

Open access · bronzeAbstract read
In one paragraph

Article in Cancer research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

25 citing papers in PubMed, 30 citations in OpenAlex.

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  12. Roles of BCCIP deficiency in mammary tumorigenesis.Breast cancer research : BCR · 2017
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  18. Expression pattern of BCCIP in hepatocellular carcinoma is correlated with poor prognosis and enhanced cell proliferation.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
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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

7 authors at 1 institution in 1 country.

Yi-Yuan HuangAuthors' Affiliation: Rutgers Cancer Institute of New Jersey, Department of Radiation Oncology, Rutgers Robert Wood Johnson Medical School, Rutgers, The State University of New Jersey, New Brunswick, New Jersey.
Li Dai
Dakim Gaines
Roberto Droz-Rosario
Huimei Lu
Jingmei Liu
Zhiyuan Shen
Rutgers, The State University of New Jersey · US

Funding

TRANSCRIPTIONAL PROFILINGP30CA072720 · NCI · UNIV OF MED/DENT NJ-R W JOHNSON MED SCH · PI Chang S Chan · 1997 to 2026
$94.5M
Alternative Mechanisms to Inactivate p53 During OncogenesisR01CA156706 · NCI · UNIV OF MED/DENT NJ-R W JOHNSON MED SCH · PI SHEN, ZHIYUAN · 2011 to 2015
$1.9M
NCI NIH HHS P30 CA072720NCI NIH HHS P30CA072720NCI NIH HHS R01 CA156706NCI NIH HHS R01CA156706
6 · The paper itself

Abstract

Dysfunctions of genome caretaker genes contribute to genomic instability and tumor initiation. Because many of the caretaker genes are also essential for cell viability, permanent loss of function of these genes would prohibit further tumor progression. How essential caretaker genes contribute to tumorigenesis is not fully understood. Here, we report a "hit-and-run" mode of action for an essential caretaker gene in tumorigenesis. Using a BRCA2-interacting protein BCCIP as the platform, we found that a conditional BCCIP knockdown and concomitant p53 deletion caused rapid development of medulloblastomas, which bear a wide spectrum of alterations involving the Sonic Hedgehog (Shh) pathway, consistent with a caretaker responsibility of BCCIP on genomic integrity. Surprisingly, the progressed tumors have spontaneously lost the transgenic BCCIP knockdown cassette and restored BCCIP expression. Thus, a transient downregulation of BCCIP, but not necessarily a permanent mutation, is sufficient to initiate tumorigenesis. After the malignant transformation has been accomplished and autonomous cancer growth has been established, BCCIP reverses its role from a tumor-initiation suppressor to become a requisite for progression. This exemplifies a new type of tumor suppressor, which is distinct from the classical tumor suppressors that are often permanently abrogated during tumorigenesis. It has major implications on how a nonmutagenic or transient regulation of essential caretaker gene contributes to tumorigenesis. We further suggest that BCCIP represents a paradoxical class of modulators for tumorigenesis as a suppressor for initiation but a requisite for progression (SIRP).

Indexed as

AnimalsCalcium-Binding ProteinsCarcinogenesisCell Cycle ProteinsCerebellar NeoplasmsDisease ProgressionGenes, Tumor SuppressorHedgehog ProteinsMaleMedulloblastomaMiceMice, Inbred C57BLMice, TransgenicNeoplasmsNeurogenesisNuclear ProteinsBCCIP protein, humanCalcium-Binding ProteinsCell Cycle ProteinsHedgehog ProteinsNuclear Proteins

Identifiers

PMID24145349
PMCPMC3918420
OpenAlexW2039047093

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.