Human MRE11 is inactivated in mismatch repair‐deficient cancers
- G. Giannini, E. Ristori, A. Gulino
- BiologyEMBO Reports
- 1 March 2002
MRE11 is identified as a novel and major target for inactivation in mismatch repair‐defective cells and suggest its impairment may contribute to the development of colorectal cancer.
Association of type and location of BRCA1 and BRCA2 mutations with risk of breast and ovarian cancer.
- T. Rebbeck, N. Mitra, I. Andrulis
- Biology, MedicineJAMA
- 7 April 2015
To identify mutation-specific cancer risks for carriers of BRCA1/2, an Observational study of women who were ascertained between 1937 and 2011 and found to carry disease-associated BRCa1 or BRC a2 mutations is conducted.
Multiple independent variants at the TERT locus are associated with telomere length and risks of breast and ovarian cancer
- S. Bojesen, K. Pooley, A. Dunning
- BiologyNature Genetics
- 27 March 2013
Using the Illumina custom genotyping array iCOGs, SNPs at the TERT locus in breast, ovarian and BRCA1 mutation carrier cancer cases and controls and leukocyte telomere measurements are analyzed to find associations cluster into three independent peaks.
Numb is a suppressor of Hedgehog signalling and targets Gli1 for Itch-dependent ubiquitination
- L. Marcotullio, E. Ferretti, A. Gulino
- BiologyNature Cell Biology
- 19 November 2006
This work identifies Numb as a Hedgehog-pathway inhibitor that is downregulated in early GCPs and GCP-derived cancer cells and demonstrates that the Hedgehog transcription factor Gli1 is targeted by Numb for Itch-dependent ubiquitination, which suppresses Hedgehog signals, thus arresting growth and promoting cell differentiation.
Mutational spectrum in a worldwide study of 29,700 families with BRCA1 or BRCA2 mutations
- T. Rebbeck, T. Friebel, K. Nathanson
- BiologyHuman Mutation
- 1 May 2018
In addition to known founder mutations, mutations of relatively high frequency were identified in specific racial/ethnic or geographic groups that may reflect founder mutations and which could be used in targeted (panel) first pass genotyping for specific populations.
Modulation of the Heparanase-inhibiting Activity of Heparin through Selective Desulfation, Graded N-Acetylation, and Glycol Splitting*
- A. Naggi, B. Casu, I. Vlodavsky
- Biology, ChemistryJournal of Biological Chemistry
- 1 April 2005
The combination of high inhibition of heparanase and low release/potentiation of ECM-bound growth factor indicates that N-acetylated, glycol-split heparins are potential antiangiogenic and antimetastatic agents that are more effective than their counterparts with unmodified backbones.
retSDR1, a short-chain retinol dehydrogenase/reductase, is retinoic acid-inducible and frequently deleted in human neuroblastoma cell lines.
- F. Cerignoli, Xiaojia Guo, G. Giannini
- BiologyCancer Research
- 15 February 2002
The observations suggest that retSDR1 is a novel regulator of vitamin A metabolism and that its frequent deletion in NB cells bearing MYCN amplification could compromise the sensitivity of those cells to retinol, thereby contributing to cancer development and progression.
Heparanase: a rainbow pharmacological target associated to multiple pathologies including rare diseases.
- S. Rivara, F. Milazzo, G. Giannini
- Biology, MedicineFuture Medicinal Chemistry
- 8 April 2016
An overview on heparanase, its biological role, inhibitors and possible clinical applications, covering the latest findings in these areas is provided.
The role of peroxiredoxins in cancer
- A. Nicolussi, S. D’Inzeo, C. Capalbo, G. Giannini, A. Coppa
- Biology, ChemistryMolecular and clinical oncology
- 10 January 2017
The present review focuses on the complex association between oxidant balance and cancer, and provides a brief account of the involvement of PRDXs in tumorigenesis and in the development of chemoresistance.
EGF‐ and cell‐cycle–regulated STAG1/PMEPA1/ERG1.2 belongs to a conserved gene family and is overexpressed and amplified in breast and ovarian cancer
- G. Giannini, M. Ambrosini, A. Gulino
- BiologyMolecular Carcinogenesis
- 1 December 2003
Although in most cases STAG1 overexpression is probably due to the abnormal activation of the EGF pathway, the demonstrated genetic amplification and rearrangement of its locus in one breast cancer cell line and one primary ovarian cancer, suggesting that STAG 1 might be a direct molecular target in the carcinogenetic process.
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