Viví Ann Flørenes

ORCID: 0000-0003-4431-7694
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About
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Research Areas
  • Cancer-related Molecular Pathways
  • Melanoma and MAPK Pathways
  • Ovarian cancer diagnosis and treatment
  • Cancer Mechanisms and Therapy
  • Phagocytosis and Immune Regulation
  • Cancer Research and Treatments
  • Cell death mechanisms and regulation
  • Cell Adhesion Molecules Research
  • Neuroblastoma Research and Treatments
  • Occupational and environmental lung diseases
  • Cancer Genomics and Diagnostics
  • Sarcoma Diagnosis and Treatment
  • DNA Repair Mechanisms
  • Microtubule and mitosis dynamics
  • Protease and Inhibitor Mechanisms
  • Ubiquitin and proteasome pathways
  • Peptidase Inhibition and Analysis
  • Neuroendocrine Tumor Research Advances
  • Cutaneous Melanoma Detection and Management
  • Pancreatic and Hepatic Oncology Research
  • Mechanisms of cancer metastasis
  • CAR-T cell therapy research
  • Immunotherapy and Immune Responses
  • Epigenetics and DNA Methylation
  • Cancer Cells and Metastasis

Oslo University Hospital
2012-2022

Norwegian Cancer Society
2002-2020

University of Oslo
2000-2013

OsloMet – Oslo Metropolitan University
2009-2012

Med-Storm Innovation (Norway)
2007

Royal University Hospital
2006

University of Saskatchewan
2006

Sunnybrook Health Science Centre
1996-1999

University of Toronto
1996-1999

Health Sciences Centre
1999

Recent studies have demonstrated the importance of E-cadherin, a homophilic cell–cell adhesion molecule, in contact inhibition growth normal epithelial cells. Many tumor cells also maintain strong intercellular adhesion, and are growth-inhibited by cell– cell contact, especially when grown three-dimensional culture. To determine if E-cadherin could mediate contact-dependent nonadherent EMT/6 mouse mammary carcinoma that lack we transfected these with an exogenous expression vector. resulted...

10.1083/jcb.142.2.557 article EN The Journal of Cell Biology 1998-07-27

Alterations of the TP53 tumor suppressor gene appear to be implicated in tumorigenesis and progression several types human cancer, including different histologic subtypes sarcomas. The MDM2 (murine double minute-2) encodes a nuclear phosphoprotein that may interact with both mutant wild-type p 53 proteins, there by inhibiting -mediated transactivation dose-dependent manner. Recently it has been suggested mdm2 proteins are components an autoregulatory loop which is transactivated . Our...

10.1093/jnci/86.17.1297 article EN JNCI Journal of the National Cancer Institute 1994-09-07

Notoriously resistant malignant melanoma is one of the most increasing forms cancer worldwide; there thus a precarious need for new treatment options. The Wee1 kinase major regulator G2/M checkpoint, and halts cell cycle by adding negative phosphorylation on CDK1 (Tyr15). Additionally, has function in safeguarding genome integrity during DNA synthesis. To assess role development progression we examined its expression panel paraffin-embedded patient derived tissue benign nevi primary-...

10.1371/journal.pone.0038254 article EN cc-by PLoS ONE 2012-06-12

Three members of the S100 gene family, S100A2, S100A4 and S100A6, have been suggested to be associated with cancer development metastasis. To study their involvement in tumorigenesis human melanoma, we examined mRNA expression levels 3 genes 45 melanoma metastases 20 benign nevi. Interestingly, whereas none expressed S100A2 mRNA, level was low 6 cell lines established from primary melanomas, all nevi showed moderate high levels. Our results suggest that loss may an early event development. A...

10.1002/(sici)1097-0215(19970822)74:4<464::aid-ijc19>3.0.co;2-9 article EN International Journal of Cancer 1997-08-22

Protein tyrosine kinases (PTKs) have been implicated in the development of many common human tumours including melanoma. Previously we isolated PTK gene sequences expressed normal melanocytes. Here examined expression 9 these genes cell lines derived from defined stages melanoma progression, by Northern blotting and some cases immunoblotting. We also tested cells 2 animal models particular as well uncultured biopsies metastatic The receptor kinase family members found melanocytes, PTK7/CCK-4...

10.1002/(sici)1097-0215(19970611)71:6<1061::aid-ijc24>3.0.co;2-f article EN International Journal of Cancer 1997-06-11

Abstract More than half of metastatic melanoma patients receiving standard therapy fail to achieve a long-term survival due primary and/or acquired resistance. Tumor cell ability switch from epithelial more aggressive mesenchymal phenotype, attributed with AXL high molecular profile in melanoma, has been recently linked such event, limiting treatment efficacy. In the current study, we investigated therapeutic potential inhibitor (AXLi) BGB324 alone or combination clinically relevant BRAF...

10.1038/s41598-022-09078-z article EN cc-by Scientific Reports 2022-03-24

Ephrin-A1, formerly called B61, is a new melanoma growth factor; it angiogenic and chemoattractant for endothelial cells. EPH-A2, or ECK (a receptor ephrin-A1), ectopically expressed in most cell lines; the pathology where this expression first manifested possible role of tumor progression are unknown. To determine these, we studied ligand biopsies benign malignant melanocytic lesions. EPH-A2 was not detected normal melanocytes, compound nevi advanced melanomas, though found 2 9 situ....

10.1002/(sici)1097-0215(19991022)84:5<494::aid-ijc8>3.0.co;2-o article EN International Journal of Cancer 1999-10-22

Abstract Purpose: Ovarian/primary peritoneal serous carcinoma (OC/PPC) and diffuse malignant mesothelioma (DMPM) are highly aggressive tumors that closely related morphologically histogenetically. It remains unclear whether both molecularly distinct neoplasms. The current study compared global gene expression patterns in OC/PPC DMPM. Experimental Design: Ten five DMPM effusions were analyzed for profiles using the Affymetrix U133 Plus 2 arrays dCHIP analysis program. Differentially expressed...

10.1158/1078-0432.ccr-06-1059 article EN Clinical Cancer Research 2006-10-15

Our purpose was to analyze, by immunohisto-chemistry, the expression of activated serine-threonine protein kinase B (p-Akt) and phosphatase tensin homologue deleted on chromosome 10 (PTEN) in benign nevi primary metastatic melanomas correlate level with clinical variables. We observed cytoplasmic and/or nuclear p-Akt 22 (54%) 41 nevi, 112 (71.3%) 157 tumors, 50 (71%) 70 metastases. Cytoplasmic PTEN staining 0 (0%), 152 (87.7%), 64 (90%) 162 71 metastases, respectively. A significant positive...

10.1309/yt58wwmta6yr1prv article EN American Journal of Clinical Pathology 2005-10-01

Abstract BACKGROUND The granulin‐epithelin precursor (GEP) was preferentially expressed in invasive ovarian tumor epithelium specimens compared with of borderline tumors. objective the current study to evaluate anatomic site‐related and cellular expression GEP its association clinicopathologic parameters survival patients advanced‐stage carcinoma. METHODS Effusions ( n = 190), corresponding primary 64), metastatic lesions 125) were analyzed using immunohistochemistry a specific polyclonal...

10.1002/cncr.20219 article EN public-domain Cancer 2004-04-19
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