TY  - JOUR
A1  - Ascierto, Maria Libera
A1  - Worschech, Andrea
A1  - Yu, Zhiya
A1  - Adams, Sharon
A1  - Reinboth, Jennifer
A1  - Chen, Nanhai G
A1  - Pos, Zoltan
A1  - Roychoudhuri, Rahul
A1  - Di Pasquale, Giovanni
A1  - Bedognetti, Davide
A1  - Uccellini, Lorenzo
A1  - Rossano, Fabio
A1  - Ascierto, Paolo A
A1  - Stroncek, David F
A1  - Restifo, Nicholas P
A1  - Wang, Ena
A1  - Szalay, Aladar A
A1  - Marincola, Francesco M
T1  - Permissivity of the NCI-60 cancer cell lines to oncolytic Vaccinia Virus GLV-1h68
JF  - BMC Cancer
N2  - Background: 

Oncolytic viral therapy represents an alternative therapeutic strategy for the treatment of cancer. We previously described GLV-1h68, a modified Vaccinia Virus with exclusive tropism for tumor cells, and we observed a cell line-specific relationship between the ability of GLV-1h68 to replicate in vitro and its ability to colonize and eliminate tumor in vivo. 

Methods: 

In the current study we surveyed the in vitro permissivity to GLV-1h68 replication of the NCI-60 panel of cell lines. Selected cell lines were also tested for permissivity to another Vaccinia Virus and a vesicular stomatitis virus (VSV) strain. In order to identify correlates of permissity to viral infection, we measured transcriptional profiles of the cell lines prior infection. 

Results: 

We observed highly heterogeneous permissivity to VACV infection amongst the cell lines. The heterogeneity of permissivity was independent of tissue with the exception of B cell derivation. Cell lines were also tested for permissivity to another Vaccinia Virus and a vesicular stomatitis virus (VSV) strain and a significant correlation was found suggesting a common permissive phenotype. While no clear transcriptional pattern could be identified as predictor of permissivity to infection, some associations were observed suggesting multifactorial basis permissivity to viral infection. 

Conclusions: 

Our findings have implications for the design of oncolytic therapies for cancer and offer insights into the nature of permissivity of tumor cells to viral infection.
KW  - gene-therapy
KW  - adenovirus
KW  - receptor
KW  - identification
KW  - infection
KW  - CD9
KW  - panel
Y1  - 2011
U6  - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-141503
VL  - 11
IS  - 451
ER  - 
TY  - JOUR
A1  - Tomei, Sara
A1  - Adams, Sharon
A1  - Uccellini, Lorenzo
A1  - Bedognetti, Davide
A1  - De Giorgi, Valeria
A1  - Erdenebileg, Narnygerel
A1  - Libera Ascierto, Maria
A1  - Reinboth, Jennifer
A1  - Liu, Qiuzhen
A1  - Bevilacqua, Generoso
A1  - Wang, Ena
A1  - Mazzanti, Chiara
A1  - Marincola, Francesco M.
T1  - Association between HRAS rs12628 and rs112587690 polymorphisms with the risk of melanoma in the North American population
JF  - Medical Oncology
N2  - HRAS belongs to the RAS genes superfamily. RAS genes are important players in several human tumors and the single-nucleotide polymorphism rs12628 has been shown to contribute to the risk of bladder, colon, gastrointestinal, oral, and thyroid carcinoma. We hypothesized that this SNP may affect the risk of cutaneous melanoma as well. HRAS gene contains a polymorphic region (rs112587690), a repeated hexanucleotide -GGGCCT- located in intron 1. Three alleles of this region, P1, P2, and P3, have been identified that contain two, three, and four repeats of the hexanucleotide, respectively. We investigated the clinical impact of these polymorphisms in a case–control study. A total of 141 melanoma patients and 118 healthy donors from the North America Caucasian population were screened for rs12628 and rs112587690 polymorphisms. Genotypes were assessed by capillary sequencing or fragment analysis, respectively, and rs12628 CC and rs112587690 P1P1 genotypes significantly associated with increased melanoma risk (OR = 3.83, p = 0.003; OR = 11.3, p = 0.033, respectively), while rs112587690 P1P3 frequency resulted significantly higher in the control group (OR = 0.5, p = 0.017). These results suggest that rs12628 C homozygosis may be considered a potential risk factor for melanoma development in the North American population possibly through the linkage to rs112587690.
KW  - HRAS
KW  - polymorphism
KW  - melanoma
KW  - rs12628
KW  - rs112587690
Y1  - 2012
U6  - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-126834
VL  - 29
IS  - 5
ER  -