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Applications of Chaos Theory Methods in Clinical Digital Pathology
Published in Christos H. Skiadas, Charilaos Skiadas, Handbook of Applications of Chaos Theory, 2017
For the ILF method, image segmentation is not necessary. For validation of this method, we used it to differentiate clinical cases of three grades of anal intraepithelial neoplasia (AIN) [15] for which today adequate quantitative and nonsubjective screening techniques have not turned out to be satisfactory. AIN is a disease that is characterized by epithelial dysplasia and can lead to anal carcinoma. The presence of dysplastic cells and an abnormal epithelial texture in the anal tissue strongly depends on the presence of human papilloma viruses (HPVs). The number of abnormal cells or abnormal nuclei as well as their distribution throughout the epithelium yields three grades of dysplasia—AIN1, AIN2, and AIN3. AIN3 is the highest grade with the highest risk for invasive anal carcinoma. This classification is widely used but there is considerable interobserver variation in staging of AIN.
Shape of epithelia
Published in A. Šiber, P. Ziherl, Cellular Patterns, 2018
On long time scales, the assumption that stroma is an elastic solid no longer holds and replacing it by a viscous material is more appropriate. In the viscous‐stroma model of epithelial dysplasia, the necessary condition for instability analogous to Eq. (4.28) is simply that at the interface the epithelium grows, i.e., that k - k0 > 0. This is of course not sufficient and the typical dependence of the exact ω on the wavevector is qualitatively similar to Figure 4.19, peaking at a finite q. At a given profile of the net cell production, instability can be prevented by increasing the epithelium‐stroma tension much like in the case of a solid stroma.
Neural Networks for the Estimation of Prognosis in Lung Cancer
Published in Raouf N.G. Naguib, Gajanan V. Sherbet, Artificial Neural Networks in Cancer Diagnosis, Prognosis, and Patient Management, 2001
H. Esteva, M. Bellotti, A.M. Marchevsky
The oncoprotein p53 is a suppressor gene functioning during the development and progression of tumours. It controls cell proliferation. The product of the p53 gene is a phosphoprotein of 53000 daltons, located at chromosome 17p13. It is indeed when there is DNA damage that it stops the cells from entering the S-phase until such damage is repaired. Disturbance of the p53 function may occur by somatic mutations. Mutations of p53 have been described in cigarette smokers with bronchial epithelial dysplasia. They probably play a role in early lung carcinoma and could be associated with poor prognosis in patients with nonsmall cells lung cancer [13, 25, 26].
Bioimpedance spectroscopy and spectral camera techniques in detection of oral mucosal diseases: a narrative review of the state-of-the-art
Published in Journal of Medical Engineering & Technology, 2019
Shekh Emran, Miia Hurskainen, Laura Tomppo, Reijo Lappalainen, Arja M. Kullaa, Sami Myllymaa
Fournier and Darier first introduced the name erythroplasia to describe a malignant dyskeratosis with the obscure aetiology in 1893 and termed it as épithéliome papillaire [15]. This rare lesion is typically asymptomatic, but a few patients may complain of a burning sensation in the mouth [15]. The most common locations of oral erythroplakia are the lateral surface of the tongue, the retromolar area, and the soft palate [17]. On biopsy and histopathologic assessment, oral erythroplakia regularly displays signs of severe epithelial dysplasia, carcinoma in situ, or micro invasive carcinoma [15]. Oral erythroplakia carries the greatest potential for malignant transformation of all the OPMDs with a malignant transformation rate ranging from 14 to 50% [18] and thus early diagnosis and treatment of oral erythroplakia is crucial.
Understanding the complex microenvironment in oral cancer: the contribution of the Faculty of Dentistry, University of Otago over the last 100 years
Published in Journal of the Royal Society of New Zealand, 2020
Alison Mary Rich, Haizal Mohd Hussaini, Benedict Seo, Rosnah Bt Zain
How Tregs modulate the immune system is not fully understood but one way might be through TLR. TLR were first recognised on the surface of inflammatory cells, especially macrophages where they alert the body to external pathogens, particularly bacteria, and set off an immune response, but it is now well known that they recognise endogenous damage as well. Danger signals arising from injured or altered cells are known as damage–associated molecular patterns (DAMPS) and these are recognised by certain TLRs. Perhaps cancer cells and/or potentially malignant cells release DAMPS? Our group assessed 50 cases each of inflamed irritative hyperplasia (IH), epithelial dysplasia (ED) and OSCC and found that more inflammatory cells expressed TLR2 in the stroma of OSCC than in hyperplastic tissue (Figure 4A,B). No hyperplastic samples showed TLR2+ keratinocytes but keratinocytes in 64% of cases of OSCC were TLR2+. Positive TLR2 expression in the TME suggests that immune surveillance is activated against the altered epithelial cells while TLR2 expression by malignant keratinocytes may correlate with apoptosis resistance and hence the survival of tumour cells (Ng et al. 2011). Double immunofluoresence studies showed that TLR2+FoxP3+ Tregs were present in the OSCC microenvironment (Figure 5) with apparent cell-to-cell contact between TLR2+ and FoxP3+ cells. The presence of FoxP3+TLR2+ cells may represent a dendritic cell-dependent pathway capable of inhibiting Treg suppressive activity, potentially beneficial to the anti-tumour response (Hussaini et al. 2017).