Advanced search
Start date
(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

DNA repair genes in astrocytoma tumorigenesis, progression and therapy resistance

Full text
de Sousa, Juliana Ferreira [1] ; Serafim, Rodolfo Bortolozo [2] ; de Freitas, Laura Marise [3] ; Fontana, Carla Raquel [4] ; Valente, Valeria [2, 4, 5]
Total Authors: 5
[1] NCI, Radiat Oncol Branch, NIH, Bldg 10, Bethesda, MD 20892 - USA
[2] Univ Sao Paulo, Dept Biol Celular & Mol & Bioagentes Patogen, Fac Med Ribeirao Preto, Ribeirao Preto, SP - Brazil
[3] Univ Sao Paulo, Inst Quim, Dept Bioquim, Sao Paulo, SP - Brazil
[4] Univ Estadual Paulista, Fac Ciencias Fatmaceut, Dept Anal Clin, UNESP, Rodovia Araraquara Jau, Km 01, BR-14800901 Araraquara, SP - Brazil
[5] Ctr Terapia Celular CEPID FAPESP, Ribeirao Preto, SP - Brazil
Total Affiliations: 5
Document type: Review article
Source: GENETICS AND MOLECULAR BIOLOGY; v. 43, n. 1, 1 2020.
Web of Science Citations: 0

Glioblastoma (GBM) is the most common and malignant type of primary brain tumor, showing rapid development and resistance to therapies. On average, patients survive 14.6 months after diagnosis and less than 5% survive five years or more. Several pieces of evidence have suggested that the DNA damage signaling and repair activities are directly correlated with GBM phenotype and exhibit opposite functions in cancer establishment and progression. The functions of these pathways appear to present a dual role in tumorigenesis and cancer progression. Activation and/or overexpression of ATRX, ATM and RAD51 genes were extensively characterized as barriers for GBM initiation, but paradoxically the exacerbated activity of these genes was further associated with cancer progression to more aggressive stages. Excessive amounts of other DNA repair proteins, namely HJURP, EXO1 , NEIL3, BRCA2, and BRIP, have also been connected to proliferative competence, resistance and poor prognosis. This scenario suggests that these networks help tumor cells to manage replicative stress and treatment-induced damage, diminishing genome instability and conferring therapy resistance. Finally, in this review we address promising new drugs and therapeutic approaches with potential to improve patient survival. However, despite all technological advances, the prognosis is still dismal and further research is needed to dissect such complex mechanisms. (AU)

FAPESP's process: 16/05345-4 - Improving antimicrobial photodynamic therapy for infectious disease associating peptide aurein 1.2
Grantee:Carla Raquel Fontana Mendonça
Support type: Regular Research Grants
FAPESP's process: 13/13465-1 - Functional characterization of HJURP (Holliday junction recognizing protein) in glioblastoma multiforme cells
Grantee:Valeria Valente
Support type: Regular Research Grants
FAPESP's process: 14/24581-5 - Evaluation of the role of photodynamic therapy combined with antimicrobial peptides against bacterial resistance
Grantee:Laura Marise de Freitas
Support type: Scholarships in Brazil - Doctorate
FAPESP's process: 18/05018-9 - Investigation of HJURP action (Holliday Junction Recognizing Protein) in DNA repair activity of glioblastoma cells
Grantee:Valeria Valente
Support type: Regular Research Grants
FAPESP's process: 13/08135-2 - CTC - Center for Cell-Based Therapy
Grantee:Dimas Tadeu Covas
Support type: Research Grants - Research, Innovation and Dissemination Centers - RIDC