Search

Your search keyword '"PATRICIA LORENA BERZAVA"' showing total 4 results
Start Over Author "PATRICIA LORENA BERZAVA"
4 results on '"PATRICIA LORENA BERZAVA"'

1. VEGF Pathway Gene Expression Profile of Proliferating versus Involuting Infantile Hemangiomas: Preliminary Evidence and Review of the Literature

Author

Rodica Elena Heredea, Eugen Melnic, Laura Elena Cirligeriu, Patricia Lorena Berzava, Maria Corina Stănciulescu, Călin Marius Popoiu, and Anca Maria Cimpean

Subjects
VEGF pathway, involuting hemangioma, proliferating hemangioma, gene expression profile, Pediatrics, RJ1-570
Abstract

Background. Infantile hemangiomas may have unexpected behavior. Initial regression (spontaneously or drug-induced) may be followed by unexplained recurrences. At this moment, there are no well-established criteria to predict infantile hemangioma reccurrences. Methods. We compared the VEGF pathway gene expression profile for one case of involuting infantile hemangioma versus one case of recurrent proliferative infantile hemangioma using TaqMan Array. Results. We found ten genes upregulated for both involuting and recurrent proliferative hemangiomas: ACTB, KRAS, MAP2K1, HRAS, NOS3, BAD, HSPB1, HPRT1, GUSB, and CASP9. Thirteen genes were downregulated for both involuting and proliferative hemangiomas: FIGF, ACTG1, GRB2, MAPKAPK2, ACTG2, MAP2K2, MAPK3, HSP90AA1, MAP2K6, NRAS, ACTA1, KDR, and MAPK1. Three genes showed divergent expression between proliferating and involuting hemangiomas. Proliferating hemangioma had MAPK14 and AKT1 gene upregulation and ACTA2 downregulation. Involuting infantile hemangioma was characterized by ACTA2 upregulation and AKT1 and MAPK14 downregulation. Conclusions. Three genes, AKT1, p38/MAPK14, and ACTA2, were found to have divergent expression in proliferating and involuting infantile hemangiomas. Excepting AKT1, which was mentioned in the last ISSVA classification (strictly related to Proteus Syndrome), none of the other genes were reported. An accurate gene expression profile mapping of infantile hemangiomas together with a gene expression-based hemangioma classification is stringently needed.

Published
2022
Full Text
View/download PDF

3. Heterogeneity of Platelet Derived Growth Factor Pathway Gene Expression Profile Defines Three Distinct Subgroups of Renal Cell Carcinomas

Author

ADELA MARIA FERICIAN, OVIDIU CATALIN FERICIAN, ANDREI DRAGOS CUMPANAS, PATRICIA LORENA BERZAVA, ALEXANDRU NESIU, ARIANA BARMAYOUN, and ANCA MARIA CIMPEAN

Subjects
Platelet-Derived Growth Factor, Vascular Endothelial Growth Factor A, Cancer Research, Genetics, Humans, Transcriptome, Molecular Biology, Biochemistry, Carcinoma, Renal Cell, Kidney Neoplasms, Research Article
Abstract

Background/Aim: We previously described four different vascular patterns (reticular, diffuse, fasciculate, and trabecular) in renal cell carcinoma (RCC) suggesting an early and heterogeneous acquisition of perivascular cells most probably due to a particular PDGF pathway gene expression profile. The aim of the study was to study PDGF pathway gene expression profiles, separately for each vascular pattern. Materials and Methods: TaqMan assay for the PDGF pathway was performed on twelve cases of ccRCC previously evaluated by histopathology, immunohistochemistry, and RNAscope. Gene expression profile was correlated with grade, invasion, vascular patterns, and VEGF. Results: PIK3C3 and SLC9A3 genes were overexpressed in all vascular patterns, but they were significantly correlated with high VEGF mRNA in the reticular and diffuse pattern. STAT1, JAK2, SHC2, SRF and CHUK (IKK) were exclusively overexpressed in cases with diffuse vascular pattern. SLC9A3, CHUK and STAT3 were overexpressed in G2 tumors. Conclusion: Three ccRCC subgroups were defined: 1) PIK3C3 (VSP34)/SLC9A3 which may be proper for anti PIK3C3 inhibitors; 2) VEGF(high) subgroup where association of anti VEGF may be a benefit and 3) JAK2/STAT1 subgroup, potentially being eligible for anti JAK/STAT therapy associated with IKK inhibitors.

Published
2022

4. Anti-chloride Intracellular Channel Protein 1 (CLIC1) Antibodies Induce Tumour Necrosis and Angiogenesis Inhibition on

Author

Andrei Dan, Radu-Cosnita, Alexandru, Nesiu, Patricia Lorena, Berzava, Simona, Cerbu, Andrei, Cosma, Serban, Comsa, Simona, Sarb, Adela Maria, Ferician, Ovidiu Catalin, Ferician, and Anca Maria, Cimpean

Subjects
Male, Time Factors, Neovascularization, Pathologic, Angiogenesis Inhibitors, Chick Embryo, Xenograft Model Antitumor Assays, Kidney Neoplasms, Tumor Burden, Necrosis, Antineoplastic Agents, Immunological, Chloride Channels, Animals, Molecular Targeted Therapy, Rabbits, Carcinoma, Renal Cell, Cell Proliferation, Signal Transduction
Abstract

Chloride intracellular channel protein 1 (CLIC1) is known as a promoter of cancer progression, metastasis, and angiogenesis. Thus, CLIC1 could be a future therapeutic target. This study aimed to evaluate the effect of anti-CLIC1 antibodies on tumour cells and vessels of human renal cell carcinoma (RCC) in rabbit cornea and chick embryo chorioallantoic membrane (CAM) models.Human cc-RCC xenografts on rabbit cornea and CAM surface were performed. Anti-CLIC1 antibodies were applied for 5 consecutive days on both tumor models. We comparatively evaluated treated and untreated tumors by combining ultrasonography with microscopic techniques.RCC implants rapidly recruited blood vessels and had an exponential growth rate on both tumor models. Anti-CLIC1 antibodies suppressed tumor growth by inducing tumor cell necrosis. Tumor vessels regressed rapidly but not completely during anti-CLIC1 antibodies based therapy.Anti-CLIC1 antibodies induced tumor necrosis and tumor vasculature regression in human cc-RCC xenografts in both in vivo experimental models.

Published
2021

Catalog

Books, media, physical & digital resources
See catalog results