Elisa Giovannetti

Publications (111) View all

• Article: Gender, Cytidine Deaminase, and 5-Aza/Decitabine--Letter.

  Joseph Ciccolini, Godefridus J Peters, Elisa Giovannetti
  Clinical Cancer Research 05/2013; · 7.74 Impact Factor
• Article: Distinct miRNA profiles are associated with malignant transformation of pancreatic cystic tumors revealing potential biomarkers for clinical use.

  Adam E Frampton, Tamara Mh Gall, Elisa Giovannetti, Justin Stebbing, Leandro Castellano, Long R Jiao, Jonathan Krell
  [show abstract] [hide abstract]
  ABSTRACT: Evaluation of: Lubezky N, Loewenstein S, Ben-Haim M et al. MicroRNA expression signatures in intraductal papillary mucinous neoplasm of the pancreas. Surgery doi:10.1016/j.surg.2012.11.016 (2013) (Epub ahead of print). Pancreatic cysts are now being detected more frequently owing to increased recognition and the liberal use of cross-sectional imaging. There is a spectrum of pancreatic cystic lesions ranging from the completely benign inflammatory to the highly malignant. Pancreatic cystic tumors, especially those with a mucinous epithelial lining such as the intraductal papillary mucinous neoplasms (IPMNs), have the potential to become malignant. The evaluated paper provides further evidence for miRNAs as diagnostic biomarkers for detecting dysplastic and malignant change in IPMNs, which may be useful for future clinical decision making. IPMNs of varying degrees of dysplasia, as well as IPMN with carcinoma, pancreatic ductal adenocarcinoma and normal pancreas samples were examined by microarray. Upregulation of miR-21, miR-155 and miR-708 was found to occur during IPMN malignant transformation. Here, the authors evaluate the published miRNA profiles of premalignant pancreatic lesions in order to consolidate these data.
  Expert Review of Molecular Diagnostics 05/2013; 13(4):325-9. · 4.86 Impact Factor
• Article: An analysis of human equilibrative nucleoside transporter-1, ribonucleoside reductase subunit M1, ribonucleoside reductase subunit M2, and excision repair cross-complementing gene-1 expression in patients with resected pancreas adenocarcinoma: Implications for adjuvant treatment.

  Amir Avan, Mina Maftouh, Elisa Giovannetti
  Cancer 04/2013; · 4.77 Impact Factor
• Article: An analysis of human equilibrative nucleoside transporter-1, ribonucleoside reductase subunit M1, ribonucleoside reductase subunit M2, and excision repair cross-complementing gene-1 expression in patients with resected pancreas adenocarcinoma: Implications for adjuvant treatment.

  Amir Avan, Mina Maftouh, Elisa Giovannetti
  Cancer 04/2013; · 4.77 Impact Factor
• Article: MAPK p38 and JNK have opposing activities on TRAIL-induced apoptosis activation in NSCLC H460 cells that involves RIP1 and caspase-8 and is mediated by Mcl-1.

  Kaamar Azijli, Saravanan Yuvaraj, Ingrid van Roosmalen, Koen Flach, Elisa Giovannetti, Godefridus J Peters, Steven de Jong, Frank A E Kruyt
  [show abstract] [hide abstract]
  ABSTRACT: Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) can induce both caspase-dependent apoptosis and kinase activation in tumor cells. Here, we examined the consequences and mechanisms of TRAIL-induced MAPKs p38 and JNK in non-small cell lung cancer (NSCLC) cells. In apoptosis sensitive H460 cells, these kinases were phosphorylated, but not in resistant A549 cells. Time course experiments in H460 cells showed that induction of p38 phosphorylation preceded that of JNK. To explore the function of these kinases in apoptosis activation by TRAIL, chemical inhibitors or siRNAs were employed to impair JNK or p38 functioning. JNK activation counteracted TRAIL-induced apoptosis whereas activation of p38 stimulated apoptosis. Notably, the serine/threonine kinase RIP1 was cleaved following TRAIL treatment, concomitant with detectable JNK phosphorylation. Further examination of the role of RIP1 by short hairpin (sh)RNA-dependent knockdown or inhibition by necrostatin-1 showed that p38 can be phosphorylated in both RIP1-dependent and -independent manner, whereas JNK phosphorylation occurred independent of RIP1. On the other hand JNK appeared to suppress RIP1 cleavage via an unknown mechanism. In addition, only the activation of JNK by TRAIL was caspase-8-dependent. Finally, we identified Mcl-1, a known substrate for p38 and JNK, as a downstream modulator of JNK or p38 activity. Collectively, our data suggest in a subset of NSCLC cells a model in which TRAIL-induced activation of p38 and JNK have counteracting effects on Mcl-1 expression leading to pro- or anti-apoptotic effects, respectively. Strategies aiming to stimulate p38 and inhibit JNK may have benefit for TRAIL-based therapies in NSCLC.
  Apoptosis 03/2013; · 4.07 Impact Factor