ArticleOncogene2007
Correlated break at PARK2/FRA6E and loss of AF-6/Afadin protein expression are associated with poor outcome in breast cancer.
Article in Oncogene, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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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Who cites it
43 citing papers in PubMed, 93 citations in OpenAlex.
- Post-translational modifications of selective autophagy receptors: orchestrating cellular homeostasis, disease pathogenesis, and therapeutic opportunities.Cellular & molecular biology letters · 2026Review
- Afadin loss induces breast cancer metastasis through destabilisation of E-cadherin to F-actin linkage.The Journal of pathology · 2025Article
- Selective autophagy in cancer: mechanisms, therapeutic implications, and future perspectives.Molecular cancer · 2024Review
- Targeting the Metabolic Paradigms in Cancer and Diabetes.Biomedicines · 2024Review
- Mitophagy in human health, ageing and disease.Nature metabolism · 2023Review
- Implication of alterations in Parkin gene among North Indian patients with colorectal cancer.The Turkish journal of gastroenterology : the official journal of Turkish Society of Gastroenterology · 2020Article
- Regulation of Hippo/YAP signaling and Esophageal Squamous Carcinoma progression by an E3 ubiquitin ligase PARK2.Theranostics · 2020Article
- Parkin gene mutations are not common, but its epigenetic inactivation is a frequent event and predicts poor survival in advanced breast cancer patients.BMC cancer · 2019Article
- Afadin cooperates with Claudin-2 to promote breast cancer metastasis.Genes & development · 2019Article
- Polarity protein Canoe mediates overproliferation via modulation of JNK, Ras-MAPK and Hippo signalling.Cell proliferation · 2019Article
- Mutation hotspots at CTCF binding sites coupled to chromosomal instability in gastrointestinal cancers.Nature communications · 2018Article
- A Futile Battle? Protein Quality Control and the Stress of Aging.Developmental cell · 2018Review
- Afadin Downregulation byFrontiers in microbiology · 2018Article
- Emerging role of mitophagy in human diseases and physiology.BMB reports · 2017Review
- Fragility Extraordinaire: Unsolved Mysteries of Chromosome Fragile Sites.Advances in experimental medicine and biology · 2017Review
- Tumor Suppressor Genes within Common Fragile Sites Are Active Players in the DNA Damage Response.PLoS genetics · 2016Review
- A Genome-Wide Association Study of Cutaneous Squamous Cell Carcinoma among European Descendants.Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2016Article
- Afadin is localized at cell-cell contact sites in mesangial cells and regulates migratory polarity.Laboratory investigation; a journal of technical methods and pathology · 2016Article
- Expression and clinical significance of Nectin-4 in hepatocellular carcinoma.OncoTargets and therapy · 2016Article
- Expression pattern of parkin isoforms in lung adenocarcinomas.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015Article
Corrections and comments
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Authors and funding
16 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Common fragile sites (CFSs) are regions of chromosomal break that may play a role in oncogenesis. The most frequent alteration occurs at FRA3B, within the FHIT gene, at chromosomal region 3p14. We studied a series of breast carcinomas for break of a CFS at 6q26, FRA6E, and its associated gene PARK2, using fluorescence in situ hybridization on tissue microarrays (TMA). We found break of PARK2 in 6% of cases. We studied the PARK2-encoded protein Parkin by using immunohistochemistry on the same TMA. Loss of Parkin was found in 13% of samples but was not correlated with PARK2 break. PARK2 break but not Parkin expression was correlated with prognosis. Alteration of PARK2/FRA6E may cause haplo-insufficiency of one or several telomeric potential tumor suppressor genes (TSG). The AF-6/MLLT4 gene, telomeric of PARK2, encodes the Afadin scaffold protein, which is essential for epithelial integrity. Loss of Afadin was found in 14.5% of cases, and 36% of these cases showed PARK2 break. Loss of Afadin had prognostic impact, suggesting that AF-6 may be a TSG. Loss of Afadin was correlated with loss of FHIT expression, suggesting fragility of FRA6E and FRA3B in a certain proportion of breast tumors.
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Registered trials
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