998 resultados para mouth cancer


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Over the last decades, technical-scientific advances of oncology have brought about an increased survival rate for cancer patients. As a result, oncologists have detected an increased number of patients presenting with other neoplasms. This research aimed to analyze factors related to demography and to the anatomic site in patients having a FPT of the mouth who developed a SPT. Medical charts of 848 patients neoplasm admitted for treatment at the Head and Neck Surgery Department of the Hospital do Cancer, Antonio Candido Camargo, Brazil, from January of 1984 to December, were analysed. of these, 12 6 developed a SPT. 49.21 % were from 51 to 65 years of age, while 83.33% were of the male gender and Caucasian. Regarding FPT site 38.89% were of the tongue, and 28.5% were of the floor of the mouth. The esophagus, excepting skin (13.49%), was more often subject to SPT (11.9%), of these 74.6% were metachronic, 15.87% simultaneous and 9.52% synchronous.

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Background: The treatment of oral cancer is complex and lengthy. Curative treatment implies a combination of surgery, radiotherapy and chemotherapy. The main goal of treatment is to guarantee long-term tumour free survival with as little functional and cosmetic damage. Despite progress in developing these strategies, cancers of the oral cavity continue to have high mortality rates that have not improved dramatically over the past ten years. Aim: The aim of this study was to uniquely explore the dynamic changes in the physical, psychological, social and existential experiences of newly diagnosed patients with oral cancer at two points across their cancer illness trajectory i.e. at the time of diagnosis and at the end of treatment. Methodology: A qualitative prospective longitudinal design was employed. Non-probability purposive sampling allowed the recruitment of 10 participants. The principal data collection method used was a digital audio taped semi-structured interview along with drawings produced by the participants. Analysis: Data was analysed using latent content analyses. Summary: Three ‘dynamic’ themes, physical, psychosocial and existential experiences were revealed that interact and influence each other in a complex and compound whole. These experiences are present at different degrees and throughout the entire trajectory of care. Patients have a number of specific concerns and challenges that cannot be compartmentalised into unitary or discrete aspects of their daily lives. Conclusion & Implications: An understanding of the patient’s experience of their illness at all stages of the disease trajectory, is essential to inform service providers’ decision making if the delivery of care is to be client centred. Dynamic and fluctuating changes in the patient’s personal experience of the cancer journey require dynamic, energetic and timely input from health care professionals.

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The knowledge of cell-cycle control has shown that the capacity of malignant growth is acquired by the stepwise accumulation of defects in specific genes regulating cell growth. Histologic diagnosis might be improved by a quantitative evaluation of more specific diagnosis biomarkers, which could help to precisely identify pre-malignant and malignant oral lesions. The aim of the present study is to evaluate whether computer-based quantitative assessment of p53, PCNA and Ki-67 immunohistochemical expression, could be used clinically to foresee the risk of oral malignant transformation. This retrospective study was carried out in ninety-five oral biopsies, 27 were classified as fibrous inflammatory hyperplasia, 40 as leukoplakia and 28 as oral squamous cell carcinoma. Sixteen out of the 40 leukoplakia were diagnosed as non-dysplastic leukoplakia, the other 24 being dysplastic leukoplakia, of which 50.0% were classified as moderate to severe dysplasia. Comparison of the four groups of oral tissues showed significant rises in p53 and Ki-67 positivity index, which increased steadily in the order benign, pre-malignant, and malignant. In contrast, it was not possible to relate higher PCNA levels with pre-malignant and malignant oral lesions. We therefore conclude that PCNA immunohistochemistry expression is probably an inappropriate marker to identify oral carcinogenesis, whereas joint quantitative evaluation of p53 and Ki-67, appears to be useful as a tumor marker, providing a pre-diagnostic estimate of the potential for cell-cycle deregulation of the oral proliferate status.

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The purpose of this study was to analyse the oral cancer mortality trends in Brazil by geographic region, age and sex, from 1996 to 2001. The Brazilian Ministry of Health database DATASUS and the Brazilian Institute of Geography and Statistics were used as the source of data. Oral cancer mortality rates per 100,000 population were estimated. Statistical analyses comprised estimates of oral cancer mortality rates, grouped according to the study variables, in 1996, 1997, 1998, 1999, 2000 and 2001; also, the three-year periods 1996-1998 and 1999-2001 were analysed, allowing the oral cancer mortality trends between these two periods to be calculated. For comparison, in each geographical region, the ratio between two death rates (related to period or sex) was calculated. In the period 1996-2001, a total of 25,972 deaths due to oral cancer were reported, giving a mortality rate of 2.67. The rates for the periods 1996-1998 and 1999-2001 were 2.53 and 2.73, respectively, showing a slight increase in the rate. There was a predominance of oral cancer in males with a male/female ratio of approximately 4. All regions exhibited an increase in mortality rates, with the exception of the Southeast region. From 1996 to 2001, the average mortality rates were 3.55 and 3.58 for the Southeast and South regions, and 1.94, 1.41, and 0.86 for the Mid-West, Northeast, and North regions, respectively. Over the age of 40, oral cancer mortality rates were seen to increase rapidly with age. Oral cancer mortality increased in all regions, except in the Southeast, and was considerably higher among males and older individuals.

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Background: Macrophage migration inhibitory factor (MIF) is a pleiotropic cytokine with pro-inflammatory functions and involved in tumorigenesis. The aim of this study was to evaluate the expression and localization of the macrophage MIF in oral squamous carcinoma (OSC). In addition, the relationship between MIF expression and clinicopathological parameters such as survival data, tobacco use, alcohol habits, TNM stage, tumor graduation, and peritumoral inflammatory infiltrate were evaluated. Methods: Using immunohistochemistry, expression and localization of MIF was detected in 44 specimens of OSC. The absolute number and relative proportions of MIF-positive cells detected were also determined separately for tumor parenchyma vs. stroma. All counts were determined from 10 consecutive high-power fields using an integration graticule. Moreover, some parameters were analyzed separately for lip and intra-oral cancers. Results: Migration inhibitory factor-positive cells were observed in both the tumor parenchyma and in inflammatory cells of all specimens. In contrast, MIF expression was not detected in tumoral nests associated with poorly differentiated tumors. In specimens of lip cancer, a greater number of MIF-positive stromal immune cells were detected than in intra-oral cancer specimens (Mann-Whitney test, P = 0.049). Conclusions: Oral squamous carcinoma cells consistently express MIF independent of their location. Lip tumors presented more MIF-positive peritumoral inflammatory cells, similar to control, suggesting that immunological differences in leukocyte activation exist between in lip and intra-oral cancers. © 2012 John Wiley & Sons A/S.

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Genomic instability underlies the transformation of host cells toward malignancy, promotes development of invasion and metastasis and shapes the response of established cancer to treatment. In this review, we discuss recent advances in our understanding of genomic stability in squamous cell carcinoma of the head and neck (HNSCC), with an emphasis on DNA repair pathways. HNSCC is characterized by distinct profiles in genome stability between similarly staged cancers that are reflected in risk, treatment response and outcomes. Defective DNA repair generates chromosomal derangement that can cause subsequent alterations in gene expression, and is a hallmark of progression toward carcinoma. Variable functionality of an increasing spectrum of repair gene polymorphisms is associated with increased cancer risk, while aetiological factors such as human papillomavirus, tobacco and alcohol induce significantly different behaviour in induced malignancy, underpinned by differences in genomic stability. Targeted inhibition of signalling receptors has proven to be a clinically-validated therapy, and protein expression of other DNA repair and signalling molecules associated with cancer behaviour could potentially provide a more refined clinical model for prognosis and treatment prediction. Development and expansion of current genomic stability models is furthering our understanding of HNSCC pathophysiology and uncovering new, promising treatment strategies. © 2013 Glenn Jenkins et al.

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Over the past 10 years, the use of saliva as a diagnostic fluid has gained attention and has become a translational research success story. Some of the current nanotechnologies have been demonstrated to have the analytical sensitivity required for the use of saliva as a diagnostic medium to detect and predict disease progression. However, these technologies have not yet been integrated into current clinical practice and work flow. As a diagnostic fluid, saliva offers advantages over serum because it can be collected noninvasively by individuals with modest training, and it offers a cost-effective approach for the screening of large populations. Gland-specific saliva can also be used for diagnosis of pathology specific to one of the major salivary glands. There is minimal risk of contracting infections during saliva collection, and saliva can be used in clinically challenging situations, such as obtaining samples from children or handicapped or anxious patients, in whom blood sampling could be a difficult act to perform. In this review we highlight the production of and secretion of saliva, the salivary proteome, transportation of biomolecules from blood capillaries to salivary glands, and the diagnostic potential of saliva for use in detection of cardiovascular disease and oral and breast cancers. We also highlight the barriers to application of saliva testing and its advancement in clinical settings. Saliva has the potential to become a first-line diagnostic sample of choice owing to the advancements in detection technologies coupled with combinations of biomolecules with clinical relevance.

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Human saliva mirrors body’s health and well-being and many of the biomolecules present in blood or urine can also be found in salivary secretions. However, biomolecular concentrations in saliva are usually one tenth to one thousandth of the levels in blood (Pfaffe et al., 2011). Sensitive detection technology platforms are therefore required to detect biomolecules in saliva. Another road block to the advancement of salivary diagnostics is the lack of information related to healthy state saliva vs. a diseased saliva, baseline levels and reference ranges and diurnal variations. Saliva has numerous advantages over blood or urine as a diagnostic fluid: (a) the non-invasive nature of sample collection and the simple, safe, painless and cost-effective methods to collect it; (b) unskilled personnel can collect saliva samples at multiple time points; and (c) the total protein concentration is approximately a quarter of that is present in plasma, which makes it easier to investigate low abundance proteins (Pfaffe et al., 2011). Currently, saliva assays are routinely used to determine, diseases such as HIV, drugs and substances of abuse to provide information on exposure and give qualitative information on the type of illicit drug used (Kintz et al., 2009), cortisol levels for diagnosing Cushing’s syndrome (Doi et al., 2008), and use for biomonitoring of exposure to chemicals (Caporossi et al., 2010) to measure hormones (Gröschl, 2009)....

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Introduction: Mouth cancer is classified as having one of the ten highest cancer incidences in the world. In Brazil, the incidence and mortality rates of oral cancer are among the highest in the world. Intraoral cancer (tongue, gum, floor of the mouth, and other non-specified parts of the mouth), the accumulated survival rate after five years is less than 50%. Objectives: Estimate the accumulated survival probability after five years and adjust the Cox regression model for mouth and oropharyngeal cancers, according to age range, sex, morphology, and location, for the city of Natal. Describe the mortality and incidence coefficients of oral and oropharyngeal cancer and their tendencies in the city of Natal, between 1980 and 2001 and between 1997 and 2001, respectively. Methods: Survival data of patients registered between 1997 and 2001 was obtained from the Population-based Cancer Record of Natal. Differences between the survival curves were tested using the log-rank test. The Cox proportional risk model was used to estimate risk ratios. The simple linear regression model was used for tendency analyses of the mortality and incidence coefficients. Results: The probability after five years was 22.9%. The patients with undifferentiated malignant neoplasia were 4.7 times more at risk of dying than those with epidermoid carcinoma, whereas the patients with oropharyngeal cancer had 2.0 times more at risk of dying than those with mouth cancer. The mouth cancer mortality and incidence coefficients for Natal were 4.3 and 2.9 per 100 000 inhabitants, respectively. The oropharyngeal cancer mortality and incidence coefficients were, respectively, 1.1 and 0.7 per 100 000 87 inhabitants. Conclusions: A low survival rate after five years was identified. Patients with oropharyngeal cancer had a greater risk of dying, independent of the factors considered in this study. Also independent of other factors, undifferentiated malignant neoplasia posed a greater risk of death. The magnitudes of the incidence coefficients found are not considered elevated, whereas the magnitudes of the mortality coefficients are high

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Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)

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OBJECTIVE: To carry out a retrospective study to determine whether human papillomavirus (HPV) infection and immunohistochemical expression of p53 and proliferating cell nuclear antigen (PCNA) are related to the risk of oral cancer. STUDY DESIGN: Fifty-seven oral biopsies, consisting of 30 oral squamous papillomas (OSPs) and 27 oral squamous cell carcinomas (OSCCs) were tested for the presence of HPV 6/11 and 16/18 by in situ hybridization using catalyzed signal amplification and in situ hybridization. p53 And PCNA expression was analyzed by immunohistochemistry and evaluated quantitatively by image analysis. RESULTS: Nineteen of the 57 oral lesions (33.3%) were positive for HPV. HPV 6/11 was found in 6 of 30 (20%) OSPs and 1 of 27 (3.7%) OSCCs. HPV 16/18 was found in 10 of 27 (37%) OSCCs and 2 of 30 (6.7%) OSPs. Sixteen of the 19 HPV-positive cases (84.2%) were p53 negative; 5 (9%) were HPV 6/11 and 11 (19%) HPV 16/18, with an inverse correlation between the presence of HPV DNA and p53 expression (P=.017, P < .05). PCNA expression appeared in 18 (94.7%) of HPV positive cases, showing that HPV 16/18 was associated with intensity of PCNA expression and with OSCCs (P=.037, P < .05). CONCLUSION: Quantitative evaluation of p53 by image analysis showed an inverse correlation between p53 expression and HPV presence, suggesting protein degradation. Image analysis also demonstrated that PCNA expression was more intense in HPV DNA 16/18 OSCCs. These findings suggest involvement of high-risk HPV types in oral carcinogenesis.

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Human papillomavirus (HPV) is believed to promote the oncogenic process, and the correlation between viral oncoproteins and dysfunction of p16 INK4A tumor suppressor protein in oral lesions is controversial. To test the hypothesis that anogenital HPV types participate in disruption of the regulation of p16INK4A suppressor protein in oral lesions, we analyzed 46 oral biopsy specimens for the presence of HPV 6/11 and 16/18 by in situ hybridization (ISH) and for p16INK4A expression by immunohistochemistry (IHC). Eighteen (39%) of the 46 oral lesions were HPV-positive and 28 (61%) were HPV-negative. HPV 6/11 DNA was found in 5 (11%) and HPV 16/18 in 13 (28%) of 46 biopsies. Nine of the 18 HPV-positive oral lesions (50%), assessed by catalyzed signal amplification coupled to ISH (CSA-ISH), gave high-intensity p16INK4A immunostaining. Focal and diffuse patterns were observed in 11/13 (77%) lesions with HPV 16/18, focal immunopositivity in 3/5 (80%) with HPV 6/11, and negative or sporadic p16-labeling in 18/28 (64%) without the presence of HPV DNA. These results showed a strong association between overexpression of p16 protein and malignant oral lesions, mainly those infected by HPV 16/18. We can conclude that high-risk HPV types are associated with p16 overexpression, and p16 may serve as a biomarker in oral cancer related to high-risk HPV infection.

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Introduction: much studies regarding risk factors associated with oral cancer. Factors such as smoking and alcohol and solar radiation are well established, but others, such as bacterial influence in the development or progression of a tumor still remain unexplained. Interest in the possible relationship between bacteria and different stages of cancer development has increased since the classification of H. pylori by the WHO as a definite carcinogen. Subsequently, links between infection and the onset of cancer in various sites in the body were discovered. Review of literature: this literature review attempts to show the influence of poor oral hygiene, with consequent bacterial accumulation as a possible important risk factor for the initiation and development of mouth cancer, and correlate the possible mechanisms by which bacteria can initiate or promote carcinogenesis. Conclusion: there is much evidence that bacteria in the oral cavity and periodontopathic are present in tumor tissue, however, still can not affirm that these bacteria initiate or promote carcinogenesis.

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Introduction: much studies regarding risk factors associated with oral cancer. Factors such as smoking and alcohol and solar radiation are well established, but others, such as bacterial influence in the development or progression of a tumor still remain unexplained. Interest in the possible relationship between bacteria and different stages of cancer development has increased since the classification of H. pylori by the WHO as a definite carcinogen. Subsequently, links between infection and the onset of cancer in various sites in the body were discovered. Review of literature: this literature review attempts to show the influence of poor oral hygiene, with consequent bacterial accumulation as a possible important risk factor for the initiation and development of mouth cancer, and correlate the possible mechanisms by which bacteria can initiate or promote carcinogenesis. Conclusion: there is much evidence that bacteria in the oral cavity and periodontopathic are present in tumor tissue, however, still can not affirm that these bacteria initiate or promote carcinogenesis.