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Cinzia Lavarino

Researcher at Boston Children's Hospital

Publications -  15
Citations -  1102

Cinzia Lavarino is an academic researcher from Boston Children's Hospital. The author has contributed to research in topics: Carcinoma & Ovarian carcinoma. The author has an hindex of 10, co-authored 15 publications receiving 1034 citations.

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Journal Article

A Comparative Study of p53 Gene Mutations, Protein Accumulation, and Response to Cisplatin-based Chemotherapy in Advanced Ovarian Carcinoma

TL;DR: A significant correlation has been found between p53 accumulation, type of mutation, and pathological response to cisplatin-based therapy in ovarian cancer patients, consistent with a role of p53 as a determinant of chemosensitivity of ovarian carcinoma.
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Cytogenetic Prognostication Within Medulloblastoma Subgroups

David Shih, +95 more
TL;DR: A small panel of cytogenetic biomarkers is identified that reliably identifies very high-risk and very low-risk groups of patients, making it an excellent tool for selecting patients for therapy intensification and therapy de-escalation in future clinical trials.
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p53 Gene Status and Response to Platinum/Paclitaxel-Based Chemotherapy in Advanced Ovarian Carcinoma

TL;DR: Determining p53 mutational status can be useful in predicting therapeutic response to drugs effective in ovarian carcinoma, and patients with mutant p53 ovarian tumors were more responsive to paclitaxel-based chemotherapy.
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Distinct mdm2/p53 expression patterns in liposarcoma subgroups : Implications for different pathogenetic mechanisms

TL;DR: The absence of mdm2 and p53 reactivity in lipomas seems to represent a useful marker for differential diagnosis from lipoma‐like WD liposarcomas and non‐retroperitoneal WD–DD group, where the TP53 mutations appear to correlate with the dedifferentiation process.
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Rb and TP53 pathway alterations in sporadic and NF1-related malignant peripheral nerve sheath tumors.

TL;DR: The results indicate that, in MPNSTs, p16INK4A inactivation almost equally affects both groups, and TP53 mutations and loss of heterozygosity involving the TP53 locus, and p53 wild type overeexpression, related or not to mdm2 overexpression, seem to mainly be restricted to sporadic MPN STs.