A5024146693- DNA Repair Mechanisms
- Carcinogens and Genotoxicity Assessment
- Cancer therapeutics and mechanisms
- Cancer Genomics and Diagnostics
- Skin Protection and Aging
- CRISPR and Genetic Engineering
- bioluminescence and chemiluminescence research
- Cancer-related Molecular Pathways
- Mitochondrial Function and Pathology
- Endoplasmic Reticulum Stress and Disease
- Genomics and Chromatin Dynamics
- RNA modifications and cancer
- Acute Myeloid Leukemia Research
- Genetic factors in colorectal cancer
- Polar Research and Ecology
- Cancer Immunotherapy and Biomarkers
- Pesticide Exposure and Toxicity
- Protist diversity and phylogeny
- Pesticide and Herbicide Environmental Studies
- Microtubule and mitosis dynamics
- Acute Lymphoblastic Leukemia research
- Glioma Diagnosis and Treatment
- Chromosomal and Genetic Variations
- Immune cells in cancer
- Photodynamic Therapy Research Studies
Universidade de São Paulo
2017-2025
The University of Kansas Cancer Center
2025
University of Kansas Medical Center
2025
National Institutes of Health
2023-2024
Eunice Kennedy Shriver National Institute of Child Health and Human Development
2023
Universidade Estadual de Londrina
2014
Air pollution represents a considerable threat to health worldwide. The São Paulo Metropolitan area, in Brazil, has unique composition of atmospheric pollutants with population nearly 20 million people and 9 passenger cars. It is long known that exposure particulate matter less than 2.5 µm (PM2.5) can cause various effects such as DNA damage. One the most versatile defense mechanisms against accumulation damage nucleotide excision repair (NER), which includes XPC protein. However, by NER...
Base and nucleotide excision repair (BER NER) pathways are normally associated with removal of specific types DNA damage: small base modifications (such as those induced by oxidation) bulky lesions ultraviolet or chemical carcinogens), respectively. However, growing evidence indicates that this scenario is much more complex these exchange proteins cooperate each other in the lesions. In review, we highlight studies discussing involvement NER damage oxidative stress, BER participating adducts...
UVA-induced mutagenesis was investigated in human pol eta-deficient (XP-V) cells through whole-exome sequencing. In UVA-irradiated cells, the increase mutation frequency deficient included a remarkable contribution of C>T transitions, mainly at potential pyrimidine dimer sites. A strong C>A transversions, potentially due to oxidized bases, also observed non-irradiated XP-V indicating that basal caused by oxidative stress may be related internal tumours patients. The low levels mutations...
In the search for alternatives to overcome challenge imposed by drug resistance development in cancer treatment, modulation of autophagy has emerged as a promising alternative that achieved good results clinical trials. Nevertheless, most these studies have overlooked novel and selective type autophagy: chaperone-mediated (CMA). Following its discovery, research into CMA's contribution tumor progression accelerated rapidly. Therefore, we now understand stress conditions are primary signal...
The UVA component of sunlight induces DNA damage, which are basically responsible for skin cancer formation. Xeroderma Pigmentosum Variant (XP-V) patients defective in the polymerase pol eta that promotes translesion synthesis after sunlight-induced implying a clinical phenotype increased frequency cancer. However, role UVA-light carcinogenesis these is not completely understood. goal this work was to characterize UVA-induced damage and consequences XP-V cells, compared complemented cells....
Glioblastoma (GBM) is a highly aggressive brain tumor associated with poor patient survival. The current standard treatment involves invasive surgery, radiotherapy, and chemotherapy employing temozolomide (TMZ). Resistance to TMZ is, however, major challenge. Previous work from our group has identified candidate genes linked resistance, including encoding translesion synthesis (TLS) DNA polymerases iota (Polɩ) kappa (Polκ). These specialized enzymes are known for bypassing lesions tolerating...
Abstract Nucleotide excision repair (NER) is a conserved, flexible mechanism responsible for the removal of bulky, helix-distorting DNA lesions, like ultraviolet damage or cisplatin adducts, but its role in lesions generated by oxidative stress still not clear. The helicase XPD/ERCC2, one two helicases transcription complex IIH, together with XPB, participates both NER and RNA pol II-driven transcription. In this work, we investigated responses distinct XPD-mutated cell lines to...
Although active immunotherapies are effective strategies to induce activation of CD8+ T cells, advanced stage tumors require further improvements for efficient control. Concerning the burden cancer-related Human papillomavirus (HPV), particularly high incidence and mortality cervical cancer, our group developed an approach based on a DNA vaccine targeting HPV-16 E7 oncoprotein (pgDE7h). This immunotherapy is capable inducing antitumour cell response but show only partial control in more...
Abstract The crucial role of DNA polymerase eta in protecting against sunlight‐induced tumors is evidenced Xeroderma Pigmentosum Variant (XP‐V) patients, who carry mutations this protein and present increased frequency skin cancer. XP‐V cellular phenotypes may be aggravated if proteins damage response (DDR) pathway are blocked, as widely demonstrated by experiments with UVC light caffeine. However, little known about the participation DDR cells exposed to UVA light, wavelengths patients...
The Y-family DNA polymerases – Pol ι, η, κ and Rev1 are most well-known for their roles in the damage tolerance pathway of translesion synthesis (TLS). They function to overcome replication barriers by bypassing lesions that cannot be normally replicated, allowing forks continue without stalling. In this work, we demonstrate a novel interaction between each polymerase nucleotide excision repair (NER) proteins, RAD23A RAD23B. We initially focus on through series biochemical, cell-based,...
Abstract Nucleotide excision repair (NER) is one of the main pathways for genome protection against structural DNA damage caused by sunlight, which in turn extensively related to skin cancer development. The mutation spectra induced UVB were investigated whole‐exome sequencing randomly selected clones NER‐proficient and XP‐C‐deficient human fibroblasts. As a model, cell line unable recognize remove lesions (XP‐C) was used compared complemented isogenic control (COMP). expected, significant...
DNA polymerase eta (Pol η) is a Y-family translesion responsible for synthesizing new across UV-damaged templates. It recruited to replication forks following mono-ubiquitination of the PCNA clamp. This interaction mediated by PCNA-interacting protein (PIP) motifs within Pol η, as well its C-terminal ubiquitin-binding zinc finger (UBZ) domain. Previous work has suggested that η itself mono-ubiquitinated at four lysine residues, which dependent on prior UBZ Here, we show can be modified same...
Abstract XPC deficiency is associated with mitochondrial dysfunction, increased H2O2 production and sensitivity to the Complex III inhibitor antimycin A (AA), through a yet unclear mechanism. We found an imbalanced expression of several proteins that participate in important function phosphorylation tumor suppressor p53 Xeroderma pigmentosum complementation group C (XP-C) (XPC-null) cells compared isogenic line corrected locus wild-type (XPC-wt). Interestingly, inhibition nuclear import...
Abstract Translesion DNA polymerases are capable of replicating damaged DNA, without removing the lesions, performing translesion synthesis (TLS), a mechanism damage tolerance. Tumor cells use this in order to survive lesions caused by chemotherapy and, therefore, may be strategy that tumor resist treatments. Moreover, it is an error-prone process and can lead mutagenesis increasing resistance potential cells. Little known about role TLS Temozolomide (TMZ) treatment. Our aim investigate how...