Karen Cherubini

Prof. Karen Cherubini

orcid

Research Focus & Metrics

Academic Career Length

23Years (2004-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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1 September 2013 in Archives of Oral Biology
Verified
Journal Article
Closed access
MPMárcia Rodrigues Payeras
Márcia Rodrigues Payeras
KCKaren Cherubini
Karen Cherubini
MFMaria Antonia Figueiredo
Maria Antonia Figueiredo
FSFernanda Gonçalves Salum
Fernanda Gonçalves Salum

1 February 2015 in Archives of Oral Biology
Verified
Journal Article
Closed access
JSJamil Saleh
Jamil Saleh
MFMaria Antonia Zancanaro Figueiredo
Maria Antonia Zancanaro Figueiredo
KCKaren Cherubini
Karen Cherubini
Fernanda Gonçalves SalumFernanda Gonçalves Salum
Fernanda Gonçalves Salum

13 October 2010 in Cancer
Verified
Journal Article
Open access
PDF file
FDFilipe Ivan Daniel
Filipe Ivan Daniel
KCKaren Cherubini
Karen Cherubini
LYLiliane Soares Yurgel
Liliane Soares Yurgel
MFMaria Antonia Zancanaro de Figueiredo
Maria Antonia Zancanaro de Figueiredo
FSFernanda Gonçalves Salum
Fernanda Gonçalves Salum
Epigenetic alterations such as DNA methylation have been implicated in the development and progression of various cancers. DNA methylation consists of the reversible addition of a methyl group to the carbon 5 position of cytosine in CpG dinucleotides and is considered essential for normal embryonic development. However, global genomic hypomethylation and aberrant hypermethylation of regulatory regions of tumor suppressor genes have been associated with chromosomal instability and transcription repression, respectively, providing neoplastic cells with a selective advantage. DNA methyltransferases are the enzymes responsible for the addition of methyl groups to CpG dinucleotides, which, together with histone modifiers, initiate the events necessary for transcription repression to occur. It has been demonstrated that increased expression of DNA methyltransferases may contribute to tumor progression through methylation‐mediated gene inactivation in various human cancers. Given their importance, this article reviews the main epigenetic mechanisms for regulating transcription and its implications in cancer development. Cancer 2011. © 2010 American Cancer Society.

14 January 2011 in Head & Neck
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Journal Article
Closed access
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MMMarcia P. Maahs
Marcia P. Maahs
AAAlan A. Azambuja
Alan A. Azambuja
MCMaria Campos
Maria Campos
FSFernanda G. Salum
Fernanda G. Salum
KCKaren Cherubini
Karen Cherubini

1 October 2014 in Photomedicine and Laser Surgery
Verified
Journal Article
Closed access
JSJamil Saleh
Jamil Saleh
MFMaria Antonia Zancanaro Figueiredo
Maria Antonia Zancanaro Figueiredo
KCKaren Cherubini
Karen Cherubini
ABAroldo Braga-Filho
Aroldo Braga-Filho
FSFernanda Gonçalves Salum
Fernanda Gonçalves Salum
Objective: The present pilot study aimed to assess the effect of low-level laser therapy (LLLT) on hyposalivation and xerostomia as a consequence of head and neck radiotherapy. Background data: The benefits of LLLT in salivary flow have been shown; however, there are no studies investigating its effects on patients who have already undergone radiotherapy and present hyposalivation and xerostomia as a sequela. Methods: Twenty-three patients with a history of head and neck malignancy, who were treated by fractioned teletherapy (dosimetry ranging from 45 to 70 Gy) in the cervicofacial region were selected. They all presented with xerostomia and severe hyposalivation. Patients were randomly distributed into a laser group ( n =12) and a control group ( n =11). A GaAlAs laser (830 nm, 100 mW, illuminated area 0.028 cm 2 , 3.57 W/cm 2 , 20 sec, 2.0 J, 71 J/cm 2 ) was used punctually in the major salivary glands, twice a week for 6 weeks, with a 12 session total. Stimulated and unstimulated salivary flow rate (SFR) were assessed, as well as the xerostomia and quality of life related to oral health (QLROH). Results: The analysis did not show any significant difference between the groups with regards to the SFR and xerostomia, and the QLROH. However, at the end of the treatment, the xerostomia and the QLROH showed significant improvement in both groups compared with assessments performed at baseline, highlighting the importance of advice given to the irradiated patients, and their follow-up. Conclusions: With the parameters used, LLLT was not able to increase SFR or decrease xerostomia. The results may be associated with the late effects of radiotherapy on glandular structure, such as fibrosis and acinar atrophy.

5 April 2017 in Diagnostic Pathology
Verified
Journal Article
Open access
PDF file
MPMaria Noel Marzano Rodrigues Petruzzi
Maria Noel Marzano Rodrigues Petruzzi
KCKaren Cherubini
Karen Cherubini
Fernanda Gonçalves SalumFernanda Gonçalves Salum
Fernanda Gonçalves Salum
MFMaria Antonia Zancanaro de Figueiredo
Maria Antonia Zancanaro de Figueiredo
Oral squamous cell carcinoma (OSCC) accounts over 90% of malignant neoplasms of the oral cavity. This pathological entity is associated to a high mortality rate that has remained unchanged over the past decades. Tumour-associated macrophages (TAMs) are believed to have potential involvement in OSCC progression. However, the molecular networks involved in communication between stroma and cancer cells have not yet been fully elucidated. The role of M2 polarized cells in oral carcinogenesis is supported by a correlation between TAMs accumulation into OSCC stroma and poor clinical outcome. Signalling pathways such as the NF-κB and cytokines released in the tumour microenvironment promote a bidirectional cross-talk between M2 and OSCC cells. These interactions consequently result in an increased proliferation of malignant cells and enhances aggressiveness, thus reducing patients’ survival time. Here, we present a comprehensive review of the role of interleukin (IL)-1, IL-4, IL-6, IL-8, IL-10 and the receptor tyrosine kinase Axl in macrophage polarization to an M2 phenotype and OSCC progression. Understanding the molecular basis of oral carcinogenesis and metastatic spread of OSCC would promote the development of targeted treatment contributing to a more favourable prognosis.