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- Campus Samambaia, Campus Colemar Natal e Silva, Campus Aparecida de Goiânia.
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Bacterial vaginosis and inflammatory response showed association with severity of cervical neoplasia in HPV-positive women
(2016) Castro Sobrinho, Juçara Maria de; Santos, Silvia Helena Rabelo dos; Alves, Rosane Ribeiro Figueiredo; Derchain, Sophie Françoise Mauricette; Sarian, Luis Otávio Zanatta; Moraes, Denise da Rocha Pitta Lima de; Campos, Elisabete A.; Zeferino, Luiz Carlos
Vaginal infections may affect susceptibility to and clearance of human papillomavirus (HPV) infection and chronic inflammation has been linked to carcinogenesis. This study aimed to evaluate the association between bacterial vaginosis (BV) and inflammatory response (IR) with the severity of cervical neoplasia in HPV-infected women. HPV DNA was amplified using PGMY09/11 primers and genotyping was performed using a reverse line blot hybridization assay in 211 cervical samples from women submitted to excision of the transformation zone. The bacterial flora was assessed in Papanicolaou stained smears, and positivity for BV was defined as ≥20% of clue cells. Present inflammatory response was defined as ≥30 neutrophils per field at 1000× magnification. Age higher than 29 years (OR:1.91 95% CI 1.06–3.45), infections by the types 16 and/or 18 (OR:1.92 95% CI 1.06–3.47), single or multiple infections associated with types 16 and/or 18 (OR: 1.92 CI 95% 1.06–3.47), BV (OR: 3.54 95% CI 1.62–7.73) and IR (OR: 6.33 95% CI 3.06–13.07) were associated with severity of cervical neoplasia (CIN 2 or worse diagnoses), while not smoking showed a protective effect (OR: 0.51 95% CI 0.26–0.98). After controlling for confounding factors, BV(OR: 3.90 95% CI 1.64–9.29) and IR (OR: 6.43 95% CI 2.92–14.15) maintained their association with the severity of cervical neoplasia. Bacterial vaginosis and inflammatory response were independently associated with severity of cervical neoplasia in HPV-positive women, which seems to suggest that the microenvironment would relate to the natural history of cervical neoplasia.
Human papillomavirus in oral cavity and oropharynx carcinomas in the central region of Brazil
(2017) Petito, Guilherme; Carneiro, Megmar Aparecida dos Santos; Santos, Silvia Helena Rabelo dos; Silva, Antonio Márcio Teodoro Cordeiro; Alencar, Rita de Cássia Gonçalves de; Gontijo, Antonio Paulo Machado; Saddi, Vera Aparecida
Introduction: Molecular studies about carcinomas of the oral cavity and oropharynx demon strate the presence of human papilomavirus genome in these tumors, reinforcing the
participation of human papilomavirus in oral carcinogenesis.
Objectives: This study aimed to determine the prevalence of human papilomavirus and geno type distribution of HPV16 and HPV18 in oral cavity and oropharynx carcinomas, as well as their
association with clinical characteristics of the tumors.
Methods: This is a retrospective study, with clinical data collected from 82 patients. Human
papilomavirus detection was conducted on specimens of oral cavity and oropharynx carcinomas
included in paraffin blocks. Patients were assisted in a cancer reference center, in the central
region of Brazil, between 2005 and 2007. Polymerase chain reaction was used for the detection
and genotyping of human papilomavirus.
Results: Among the patients evaluated, 78% were male. The average age of the group was about
58 years. Risk factors, such as smoking (78%) and alcohol consumption (70.8%) were recorded
for the group. HPV DNA was detected in 21 cases (25.6%; 95% confidence interval 16.9---36.6)
of which 33.3% were HPV16 and 14.3% were HPV18. The presence of lymph node metastases
and registered deaths were less frequent in human papilomavirus positive tumors, suggesting
a better prognosis for these cases; however, the differences between the groups were not
statistically significant.
Strong SOD2 expression and HPV-16/18 positivity are independent events in cervical cancer
(2018) Santos, Silvia Helena Rabelo dos; Termini, Lara; Pierulivo, Enrique Mario Boccardo; Derchain, Sophie Françoise Mauricette; Longatto Filho, Adhemar; Andreoli, Maria Antonieta Avilla; Costa, Maria Cecília; Nunes, Rafaella Almeida Lima; Andrade, Liliana Aparecida Lucci de Angelo; Villa, Luisa Lina
Human papillomavirus and anal cancer: prevalence, genotype distribution, and prognosis aspects from midwestern region of Brazil
(2019) Libera, Larisse Silva Dalla; Carvalho, Keila Patrícia Almeida de; Ramos, Jessica Enocencio Porto; Cabral, Lázara Alyne Oliveira; Alencar, Rita de Cássia Gonçalves de; Villa, Luísa Lina; Alves, Rosane Ribeiro Figueiredo; Santos, Silvia Helena Rabelo dos; Carneiro, Megmar Aparecida dos Santos; Saddi, Vera Aparecida
d. Approximately 90% of all anal cancers are associated with human papillomavirus (HPV), especially high-risk
genotypes such as HPVs 16 and 18. Objective. To investigate the clinical and prognostic aspects of anal cancers associated
with the presence, as well as the genotypic distribution of human papillomavirus (HPV). Methods. A retrospective study
carried out over a 10-year period, using clinical and molecular data, with PCR analysis and reverse hybridization (INNO LIPA kit), in anal cancers. ,e data analysis was done using descriptive univariate statistics, and the survival curves were
made using the Kaplan–Meier and log-rank methods. Results. Of the 81 formalin-fixed and paraffin-embedded specimens,
HPV prevalence was 69% and was significantly higher in squamous cell carcinomas (SCC) than in other anal tumors
(p � 0.0001). Female patients had a higher prevalence of HPV (p � 0.01). Multiple infections were detected in 14.3% of cases.
,e most prevalent genotypes were HPVs 16, 33, and 18. ,e overall survival at 60 months was 44.3%, and the prognostic
factors included gender (p � 0.008) with greater survival for men (52.9%) in comparison to women (29.6%), histological
type (p � 0.01), SCC (54.4%), adenocarcinomas (37.5%), other carcinomas (14.2%), and the presence of distant metastasis
(p � 0.01). Survival was not influenced by the presence of HPV (p � 0.54). Conclusions. ,e association of HPV to anal
cancer was found in this study, especially in SCC. However, the presence of HPV did not influence the prognosis of patients
with anal cancer.
Swainsonine, an alpha-mannosidase inhibitor, may worsen cervical cancer progression through the increase in myeloid derived suppressor cells population
(2019) Silveira, Caio Raony Farina; Manzine, Marcella Cipelli Carolina; Santos, Silvia Helena Rabelo dos; Zeferino, Luiz Carlos; Rodríguez Rodríguez, Gretel; Assis, Josiane Betim de; Herbster, Suellen da Silva Gomes; Bernadinelli, Isabel; Laginha, Fábio Martins
Cervical cancer, caused by high oncogenic risk Human Papillomavirus (HPV) infection, con tinues to be a public health problem, mainly in developing countries. Using peptide phage
display as a tool to identify potential molecular targets in HPV associated tumors, we identi fied α-mannosidase, among other enriched sequences. This enzyme is expressed in both
tumor and inflammatory compartment of the tumor microenvironment. Several studies in
experimental models have shown that its inhibition by swainsonine (SW) led to inhibition of
tumor growth and metastasis directly and indirectly, through activation of macrophages and
NK cells, promoting anti-tumor activity. Therefore, the aim of this work was to test if swainso nine treatment could modulate anti-tumor immune responses and therefore interfere in HPV
associated tumor growth. Validation of our biopanning results showed that cervical tumors,
both tumor cells and leukocytes, expressed α-mannosidase. Ex vivo experiments with
tumor associated macrophages showed that SW could partially modulate macrophage phe notype, decreasing CCL2 secretion and impairing IL-10 and IL-6 upregulation, which
prompted us to proceed to in vivo tests. However, in vivo, SW treatment increased tumor
growth. Investigation of the mechanisms leading to this result showed that SW treatment
significantly induced the accumulation of myeloid derived suppressor cells in the spleen of
tumor bearing mice, which inhibited T cell activation. Our results suggested that SW contrib utes to cervical cancer progression by favoring proliferation and accumulation of myeloid
cells in the spleen, thus exacerbating these tumors systemic effects on the immune system,
therefore facilitating tumor growth.