ArticleOncogene2003
HBX causes cyclin D1 overexpression and development of breast cancer in transgenic animals that are heterozygous for p53.
Article in Oncogene, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.
What it found
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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.
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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.
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Who cites it
21 citing papers in PubMed, 1 synthesis or guideline pooled it, 42 citations in OpenAlex.
- The prevalence and clinicopathological features of breast cancer patients with hepatitis B virus infection in China.Oncotarget · 2017Pooled it
- The Role of HBx Protein in Diseases Beyond the Liver.Infection and drug resistance · 2023Review
- ER stress regulating protein phosphatase 2A-B56γ, targeted by hepatitis B virus X protein, induces cell cycle arrest and apoptosis of hepatocytes.Cell death & disease · 2018Article
- Hepatitis B Virus X and Regulation of Viral Gene Expression.Cold Spring Harbor perspectives in medicine · 2016Review
- Hepatitis B virus molecular biology and pathogenesis.Hepatoma research · 2016Article
- Distinctive pharmacological differences between liver cancer cell lines HepG2 and Hep3B.Cytotechnology · 2015Article
- Hepatitis B virus infection and intrahepatic cholangiocarcinoma.World journal of gastroenterology · 2014Review
- Review
- miR-338-3p is down-regulated by hepatitis B virus X and inhibits cell proliferation by targeting the 3'-UTR region of CyclinD1.International journal of molecular sciences · 2012Article
- The effect of miR-338-3p on HBx deletion-mutant (HBx-d382) mediated liver-cell proliferation through CyclinD1 regulation.PloS one · 2012Article
- The elements of human cyclin D1 promoter and regulation involved.Clinical epigenetics · 2011Article
- Hepatitis B virus X protein downregulates expression of the miR-16 family in malignant hepatocytes in vitro.British journal of cancer · 2011Article
- Viral manipulation of DNA repair and cell cycle checkpoints.DNA repair · 2009Review
- c-Jun/AP-1 pathway-mediated cyclin D1 expression participates in low dose arsenite-induced transformation in mouse epidermal JB6 Cl41 cells.Toxicology and applied pharmacology · 2009Article
- Molecular Pathogenesis of Hepatitis-B-virus-associated Hepatocellular Carcinoma.Gut and liver · 2007Article
- Chronic hepatitis B in hepatocarcinogenesis.Postgraduate medical journal · 2006Review
- Involvement of nuclear factor of activated T cells 3 (NFAT3) in cyclin D1 induction by B[a]PDE or B[a]PDE and ionizing radiation in mouse epidermal Cl 41 cells.Molecular and cellular biochemistry · 2006Article
- Activation of focal adhesion kinase by hepatitis B virus HBx protein: multiple functions in viral replication.Journal of virology · 2006Article
- Gene expression profiling: cell cycle deregulation and aneuploidy do not cause breast cancer formation in WAP-SVT/t transgenic animals.Journal of molecular medicine (Berlin, Germany) · 2005Article
- The enigmatic X gene of hepatitis B virus.Journal of virology · 2004Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Transgenic mice, which selectively express the WAP-HBX transgene in mammary gland epithelial cells (ME-cells), were established in order to elucidate the consequences of HBX gene expression on organ differentiation, cell death program and tumor development. Transgene expression was demonstrable by RT-PCR, Northern and Western blot analysis during pregnancy, lactation and after weaning. HBX synthesis neither affect mammary gland differentiation nor apoptosis in ME-cells. Although breast cancer formation was rare in WAP-HBX animals (<1%), WAP-HBX*p53+/- hybrid animals developed breast tumors at an increased rate (12/85) after a latency period of 8-18 months. We also show here for the first time that HBX can immortalize ME-cells generated from mammary gland tissue segments in a p53-independent fashion. HBX causes cyclin D1 gene overexpression during early pregnancy, and this is maintained in ME-cells isolated either from mammary gland or from breast tumors. Intranuclear cyclin D1 accumulation also occurs in the absence of external growth factors and the BrdU incorporation rate remains high under serum starvation conditions. Finally, both cyclin D1 induction and HBX mitotic activity are dependent on p38 and c-Jun N-terminal kinase, but not on MEK-1 kinase activity.
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Registered trials
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.