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UNIVERSITÀ DEGLI STUDI
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Massimo Pancione

Contatti

Massimo Pancione
Ricercatore
BIO/11 - Biologia Molecolare
0824305116
Molecular Oncology Pancione

Attività di ricerca

Parole chiave: 
cell division
centrosome
Argomenti di ricerca: 

The laboratory of Massimo Pancione, PhD is interested in the molecular basis of human cancer. Dr. Pancione’s approach is to study normal and malignant functions of genes implicated in human cancer at the level of the cell and macromolecular intracellular structures.

Focus research areas

  • Centrosome cohesion function and chromosome stability.  Already 120 years ago the biologist T. Boveri noted that centrosome aberrations are a hallmark of cancer cells suggesting a direct participation of centrosomes in cell transformation.  The centrosome is the main microtubule (MT) organizing center (MTOC) of human cells and metazoans. Centrosome cohesion, the joining of the two centrosomes of a cell, is increasingly appreciated as major regulator of cell functions such as Golgi organization, cilia positioning and chromosome segregation in mitosis. One major element of centrosome cohesion is the centrosome linker. We don’t know the reason for this tethering and its benefits for the cell are unknown. Therefore,  we study the molecular mechanisms at the base of this machinery and its functional consequences on cell division in healthy and cancer cells.
  • Tumour microenvironment and metastatic cascade.  Cancer mortality is mainly caused by metastasis, a process in which cancer cells escape the site of the primary tumor invading normal tissue at distant organs. Abnormality of chromosome number known as chromosomal instability (CIN) is a hallmark of the vast majority of human cancers. CIN promotes  phenotypic plasticity and intratumoral heterogeneity resulting in drug resistance. Abnormal mitosis also imparts specific vulnerabilities involving tumour microenvironment (TME). The major objective of work in this area is to understand the role of critical genes in normal and neoplastic growth acting at the crossroads of CIN, inflammation and immune evasion.