Linda Fabris

ORCID: 0000-0001-5763-0052
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About
Contact & Profiles
Research Areas
  • Cancer-related molecular mechanisms research
  • RNA modifications and cancer
  • Cancer-related Molecular Pathways
  • Genetic factors in colorectal cancer
  • Circular RNAs in diseases
  • Microtubule and mitosis dynamics
  • MicroRNA in disease regulation
  • RNA Research and Splicing
  • Ubiquitin and proteasome pathways
  • Cancer Cells and Metastasis
  • Epigenetics and DNA Methylation
  • Mycobacterium research and diagnosis
  • Immune Response and Inflammation
  • Histone Deacetylase Inhibitors Research
  • Cholangiocarcinoma and Gallbladder Cancer Studies
  • Cancer Research and Treatments
  • Cancer Genomics and Diagnostics
  • Myeloproliferative Neoplasms: Diagnosis and Treatment
  • Cancer-related gene regulation
  • RNA and protein synthesis mechanisms
  • PI3K/AKT/mTOR signaling in cancer
  • Cytokine Signaling Pathways and Interactions
  • Viral-associated cancers and disorders
  • Cancer Mechanisms and Therapy
  • Hippo pathway signaling and YAP/TAZ

The University of Texas MD Anderson Cancer Center
2014-2025

Centro di Riferimento Oncologico
2010-2016

TherapeuticsMD (United States)
2016

National Cancer Institute
2014

National Institutes of Health
2014

National Cancer Institute
2012

Scripps MD Anderson Cancer Center
2012

Non-coding RNAs have been drawing increasing attention in recent years as functional data suggest that they play important roles key cellular processes. N-BLR is a primate-specific long non-coding RNA modulates the epithelial-to-mesenchymal transition, facilitates cell migration, and increases colorectal cancer invasion. We performed multivariate analyses of from two independent cohorts patients show abundance associated with tumor stage, invasion potential, overall patient survival. Through...

10.1186/s13059-017-1224-0 article EN cc-by Genome biology 2017-05-23

The cancer-risk-associated rs6983267 single nucleotide polymorphism (SNP) and the accompanying long noncoding RNA CCAT2 in highly amplified 8q24.21 region have been implicated cancer predisposition, although causality has not established. Here, using allele-specific transgenic mice, we demonstrate that overexpression leads to spontaneous myeloid malignancies. We further identified is overexpressed bone marrow peripheral blood of myelodysplastic/myeloproliferative neoplasms (MDS/MPN)...

10.1101/gr.225128.117 article EN cc-by-nc Genome Research 2018-03-22

The causes and consequences of abnormal biogenesis extracellular vesicles (EVs) are not yet well understood in malignancies, including breast cancers (BCs). Given the hormonal signaling dependence estrogen receptor-positive (ER+) BC, we hypothesized that 17β-estradiol (estrogen) might influence EV production microRNA (miRNA) loading. We report physiological doses promote secretion specifically from ER+ BC cells via inhibition miR-149-5p, hindering its regulatory activity on SP1, a...

10.1073/pnas.2122053120 article EN cc-by-nc-nd Proceedings of the National Academy of Sciences 2023-05-30

In breast cancer (BC) patients, local recurrences often arise in proximity of the surgical scar, suggesting that response to surgery may have a causative role. Radiotherapy (RT) after lumpectomy significantly reduces risk recurrence. We investigated direct effects and RT delivered intraoperatively (IORT), by collecting irradiated non-irradiated tissues from BC tumor removal. These tissue specimens been profiled for their microRNA (miR) expression, search differentially expressed miR among...

10.1038/onc.2016.23 article EN cc-by-nc-sa Oncogene 2016-02-15

p27(kip1) (p27) is an inhibitor of cyclin/cyclin-dependent kinase complexes, whose nuclear loss indicates a poor prognosis in various solid tumors. When located the cytoplasm, p27 binds Op18/stathmin (stathmin), microtubule (MT)-destabilizing protein, and restrains its activity. This leads to MT stabilization, which negatively affects cell migration. Here, we demonstrate that this function also influences morphology motility cells immersed three-dimensional (3D)matrices. Cells lacking...

10.1128/mcb.00723-09 article EN Molecular and Cellular Biology 2010-03-02

Significance Different functions have been ascribed to p27 kip1 , originally identified as a universal cyclin-dependent kinase (CDK) inhibitor, fundamental for the control of cell proliferation and tumor progression. Yet, not all can be explained by its ability bind inhibit CDKs. Here, we demonstrate that controls cycle entry also through CDK-independent function, regulating microtubule stability. Following growth factor stimulation, prevents full activation H-Ras, acting on subcellular...

10.1073/pnas.1508514112 article EN Proceedings of the National Academy of Sciences 2015-10-28

Abstract Once a patient is in septic shock, survival rates drop by 7.6% for every hour of delay antibiotic therapy. Biomarkers based on the molecular mechanism sepsis are important timely diagnosis and triage. Here, we study potential roles panel cellular viral miRNAs as biomarkers. We performed genome-wide microRNA (miRNA) expression profiling leukocytes from patients nonseptic controls, combined with quantitative RT-PCR plasmas two cohorts patients, surgical healthy volunteers....

10.1038/cddis.2014.515 article EN cc-by Cell Death and Disease 2014-12-04

The transcribed ultraconserved regions (T-UCRs) encode long non-coding RNAs implicated in human carcinogenesis. Their mechanisms of action and the factors regulating their expression cancers are poorly understood. Here we show that high uc.339 correlates with lower survival 210 non-small cell lung cancer (NSCLC) patients. We provide evidence from lines primary samples TP53 directly regulates uc.339. find is upregulated archival NSCLC samples, functioning as a decoy RNA for miR-339-3p,...

10.1038/s41467-017-01562-9 article EN cc-by Nature Communications 2017-11-21

The tumor suppressor gene p27Kip1 plays a fundamental role in human cancer progression. Its expression and/or functions are altered almost all the different histotype analyzed so far. Recently, it has been demonstrated that suppression function of p27 resides not only ability to inhibit Cyclins/CDKs complexes through its N-terminal domain but also capacity modulate cell motility C-terminal portion. Particular interest raised by last amino-acid, (Threonine 198) regulation both protein...

10.1371/journal.pone.0017673 article EN cc-by PLoS ONE 2011-03-14

The CDK inhibitor p27kip1 is a critical regulator of cell cycle progression, but the mechanisms by which controls proliferation in vivo are still not fully elucidated. We recently demonstrated that microtubule destabilizing protein stathmin relevant binding partner. To get more insights into significance this interaction, we generated and double knock-out (DKO) mice. Interestingly, thorough characterization DKO mice most phenotypes null linked to hyper-proliferative behavior, such as...

10.4161/15384101.2014.949512 article EN Cell Cycle 2014-10-01

In early breast cancer, local relapses represent a determinant and not simply an indicator of risk for distant relapse death. Notably, 90% recurrences occur at or close to the same quadrant primary cancer. Relevance PI3K/mTOR/p70S6K signaling in tumorigenesis is very well documented. However, pathway/s involved process cancer are understood. The ribosomal protein p70S6K has been implicated cell response post‐surgical inflammation, supporting hypothesis that it may be crucial also recurrence....

10.1016/j.molonc.2014.02.006 article EN cc-by-nc-nd Molecular Oncology 2014-03-12

The mutational landscape of phylogenetically ultraconserved elements (UCEs), especially those in noncoding DNAs (ncUCEs), and their functional relevance cancers remain poorly characterized. Here, we perform a systematic analysis whole-genome in-house targeted UCE sequencing datasets from more than 3000 patients with cancer 13,736 UCEs demonstrate that ncUCE somatic alterations are common. Using multiplexed CRISPR knockout screen colorectal cells, show the loss several altered ncUCEs...

10.1126/sciadv.ado2830 article EN cc-by-nc Science Advances 2025-02-19

// Carmela De Marco 1, 2 , Donatella Malanga Nicola Rinaldo Fernanda Vita Marianna Scrima Sara Lovisa 3 Linda Fabris Maria Vincenza Carriero 4 Renato Franco Antonia Rizzuto 5 Gustavo Baldassarre Giuseppe Viglietto 1 Department of Experimental and Clinical Medicine, University "Magna Graecia", Catanzaro, Italy BIOGEM-Institute Genetic Research, Ariano Irpino (AV), Oncology 2, Centro di Riferimento Oncologico, Aviano (PN), Oncology, IRCCS Fondazione Pascale, Napoli, Medical Surgical Sciences,...

10.18632/oncotarget.4022 article EN Oncotarget 2015-05-25

Myelofibrosis (MF) is a myeloproliferative neoplasm characterized by cytopenia and extramedullary hematopoiesis, resulting in splenomegaly. Multiple pathological mechanisms (e.g., circulating cytokines genetic alterations, such as JAKV617F mutation) have been implicated the etiology of MF, but molecular mechanism causing resistance to JAK2V617F inhibitor therapy remains unknown. Among MF patients who were treated with JAK ruxolitinib, we compared noncoding RNA profiles ruxolitinib responders...

10.1172/jci.insight.121781 article EN cc-by JCI Insight 2020-01-15

// Joshua Armenia 1 , Linda Fabris Francesca Lovat 2 Stefania Berton Ilenia Segatto Sara D'Andrea Cristina Ivan 3 Luciano Cascione George A. Calin Carlo M. Croce Alfonso Colombatti 1,4 Andrea Vecchione 2,5 Barbara Belletti and Gustavo Baldassarre Division of Experimental Oncology 2, CRO, National Cancer Institute, Aviano, Italy. Department Molecular Virology, Immunology Medical Genetics Comprehensive Center, Ohio State University, Columbus, OH, USA. Therapeutics, The University Texas MD...

10.18632/oncotarget.1803 article EN Oncotarget 2014-03-04

The microtubule-destabilizing protein stathmin is highly expressed in several types of tumor, thus deserving the name oncoprotein 18. High levels expression and/or activity favor metastatic spreading and mark most aggressive tumors, representing a realistic marker poor prognosis. Stathmin downstream target many signaling pathways, including Ras-MAPK, PI3K p53, involved both tumor onset progression. We hypothesized that could also play role during early stages tumorigenesis, an issue...

10.1371/journal.pone.0045561 article EN cc-by PLoS ONE 2012-09-20
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