Lysyl Oxidase Is a Key Player in BRAF/MAPK Pathway-Driven Thyroid Cancer Aggressiveness.


Journal

Thyroid : official journal of the American Thyroid Association
ISSN: 1557-9077
Titre abrégé: Thyroid
Pays: United States
ID NLM: 9104317

Informations de publication

Date de publication:
01 2019
Historique:
pubmed: 7 11 2018
medline: 18 12 2019
entrez: 7 11 2018
Statut: ppublish

Résumé

The BRAF The prognostic value of LOX and its association with mutated BRAF was analyzed in The Cancer Genome Atlas and an independent cohort. Inhibition of mutant BRAF and the MAPK pathway, and overexpression of mutant BRAF and mouse models of BRAF In The Cancer Genome Atlas cohort, LOX expression was higher in BRAF-mutant tumors compared to wild-type tumors (p < 0.0001). Patients with BRAF-mutant tumors with high LOX expression had a shorter disease-free survival (p = 0.03) compared to patients with a BRAF mutation and the low LOX group. In the independent cohort, a significant positive correlation between LOX and percentage of BRAF mutated cells was found. The independent cohort confirmed high LOX expression to be associated with a shorter disease-free survival (p = 0.01). Inhibition of BRAF The data suggest that BRAF

Sections du résumé

BACKGROUND
The BRAF
METHODS
The prognostic value of LOX and its association with mutated BRAF was analyzed in The Cancer Genome Atlas and an independent cohort. Inhibition of mutant BRAF and the MAPK pathway, and overexpression of mutant BRAF and mouse models of BRAF
RESULTS
In The Cancer Genome Atlas cohort, LOX expression was higher in BRAF-mutant tumors compared to wild-type tumors (p < 0.0001). Patients with BRAF-mutant tumors with high LOX expression had a shorter disease-free survival (p = 0.03) compared to patients with a BRAF mutation and the low LOX group. In the independent cohort, a significant positive correlation between LOX and percentage of BRAF mutated cells was found. The independent cohort confirmed high LOX expression to be associated with a shorter disease-free survival (p = 0.01). Inhibition of BRAF
CONCLUSIONS
The data suggest that BRAF

Identifiants

pubmed: 30398411
doi: 10.1089/thy.2018.0424
pmc: PMC6352555
doi:

Substances chimiques

Protein-Lysine 6-Oxidase EC 1.4.3.13
BRAF protein, human EC 2.7.11.1
Proto-Oncogene Proteins B-raf EC 2.7.11.1

Types de publication

Journal Article Research Support, N.I.H., Intramural

Langues

eng

Sous-ensembles de citation

IM

Pagination

79-92

Subventions

Organisme : NCI NIH HHS
ID : P30 CA008748
Pays : United States
Organisme : NCI NIH HHS
ID : P50 CA172012
Pays : United States
Organisme : Intramural NIH HHS
ID : ZIA BC011275
Pays : United States

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Auteurs

Myriem Boufraqech (M)

1 Endocrine Oncology Branch, Endocrinology, and Obesity Branch, National Institutes of Health, Bethesda, Maryland.

Dhaval Patel (D)

1 Endocrine Oncology Branch, Endocrinology, and Obesity Branch, National Institutes of Health, Bethesda, Maryland.

Naris Nilubol (N)

1 Endocrine Oncology Branch, Endocrinology, and Obesity Branch, National Institutes of Health, Bethesda, Maryland.

Astin Powers (A)

2 Laboratory of Pathology, National Institutes of Health, Bethesda, Maryland.

Timothy King (T)

1 Endocrine Oncology Branch, Endocrinology, and Obesity Branch, National Institutes of Health, Bethesda, Maryland.

Jasmine Shell (J)

1 Endocrine Oncology Branch, Endocrinology, and Obesity Branch, National Institutes of Health, Bethesda, Maryland.

Justin Lack (J)

3 NIAID Collaborative Bioinformatics Resource (NCBR), NIAID, NIH, Bethesda, Maryland.
4 Advanced Biomedical Computational Science, Frederick National Laboratory for Cancer Research, Frederick, Maryland.

Lisa Zhang (L)

1 Endocrine Oncology Branch, Endocrinology, and Obesity Branch, National Institutes of Health, Bethesda, Maryland.

Sudheer Kumar Gara (SK)

1 Endocrine Oncology Branch, Endocrinology, and Obesity Branch, National Institutes of Health, Bethesda, Maryland.

Viswanath Gunda (V)

5 Department of Surgery, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts.

Joanna Klubo-Gwiezdzinska (J)

6 Diabetes, Endocrinology, and Obesity Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland.

Suresh Kumar (S)

1 Endocrine Oncology Branch, Endocrinology, and Obesity Branch, National Institutes of Health, Bethesda, Maryland.

James Fagin (J)

7 Department of Medicine, Memorial Sloan Kettering Cancer Center and Weill Cornell Medical College, New York, New York.

Jeffrey Knauf (J)

7 Department of Medicine, Memorial Sloan Kettering Cancer Center and Weill Cornell Medical College, New York, New York.

Sareh Parangi (S)

5 Department of Surgery, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts.

David Venzon (D)

8 Biostatistics and Data Management Section, National Cancer Institute, National Institutes of Health, Bethesda, Maryland.

Martha Quezado (M)

2 Laboratory of Pathology, National Institutes of Health, Bethesda, Maryland.

Electron Kebebew (E)

9 Department of Surgery and Stanford Cancer Institute, Stanford University, Stanford, California.

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Classifications MeSH