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Biomedical subjects

A Zerbini

Publications and source records attributed to A Zerbini.

5 recordsLinked to original sources
PubMed2006

Is there a role for immunotherapy in hepatocellular carcinoma?

Incidence of hepatocellular carcinoma has been rising in the last two decades because of the wide exposure to hepatitis C virus during 1960s and 1970s. Improvement in treatment has been achieved by local ablative therapies, however because of early recurrence and lack of effective chemotherapies, alternative treatments based on stimulation of the anti-tumour immune response could represent new strategies to control hepatocellular carcinoma spread and recurrence. Proof of principle of an effective immunotherapy has been achieved for other solid tumours such as melanoma and several results could be transferred to the immunotherapy of hepatocellular carcinoma. Specific tumour antigens have been identified in hepatocellular carcinoma, such as cancer testis antigens expressed in a large part of hepatocellular carcinomas and alpha-fetoprotein that has been already employed in clinical trials demonstrating immunogenicity without however significant clinical efficacy. Better results have been achieved by non-antigen-specific immunotherapies that demonstrated improvement in recurrence and recurrence-free survival in patients undergoing surgical resection for hepatocellular carcinoma. Passive immunotherapy and targeted therapies blocking tumour cell receptors or enzymatic pathways are already in the clinic for other malignancies and the near future will see these new treatments applied to hepatocellular carcinoma patients along with the development of efficacious active immunotherapies aimed at reducing disease recurrence and improving survival.

Animals↗
PubMed2001

Glutamine deprivation-mediated cell shrinkage induces ligand-independent CD95 receptor signaling and apoptosis.

Cell shrinkage and loss of cell viability by apoptosis have been examined in cultured CD95(Fas/Apo-1)-expressing leukemia-derived CEM and HL-60 cells subjected to acute deprivation of glutamine, a major compatible osmolyte engaged in cell volume control. Glutamine deprivation-mediated cell shrinkage promoted a ligand-independent activation of the CD95-mediated apoptotic pathway. Cell transfection with plasmids expressing FADD-DN or v-Flip viral proteins pointed to a functional clustering of CD95 receptors at the cell surface with activation of the 'extrinsic pathway' caspase cascade. Accordingly, cell shrinkage did not induce apoptosis in CD95 receptor-negative lymphoma L1210 cells. Replacement of glutamine with surrogate compatible osmolytes counteracted cell volume decrement and protected the CD95-expressing cells from apoptosis. A glutamine deprivation-dependent cell shrinkage with activation of the CD95-mediated pathway was also observed when asparaginase was added to the medium. Asparagine depletion had no role in this process. The cell-size shrinkage-dependent apoptosis induced by glutamine restriction in CD95-expressing leukemic cells may therefore be of clinical relevance in amidohydrolase enzyme therapies.

Adaptor Proteins, Signal Transducing↗
PubMedDate not supplied

[Dyslalia and orofacial dysmorphism].

In the light of reported data and personal experience, relations between malocclusions and dyslalias are examined. Although the coexistence of malocclusions and dyslalia is a frequent clinical observation, correlations between the two conditions do not appear to be closely linked by any clearly identifiable cause-effect relationship. Considering the high number of aetiological factors involved, stress is laid on the need for a multidisciplinary approach to cases that present contemporaneously malocclusions and dyslalias in the interests of correct diagnosis and rational therapeutic orientation.

Cleft Palate↗