BackgroundThe aim of this pilot study was to identify proteins associated with advancement of colon cancer (CC).MethodsA quantitative proteomics approach was used to determine the global changes in the proteome of primary colon cancer from patients with non-cancer normal colon (NC), non-adenomatous colon polyp (NAP), non-metastatic tumor (CC NM) and metastatic tumor (CC M) tissues, to identify up- and down-regulated proteins. Total protein was extracted from each biopsy, trypsin-digested, iTRAQ-labeled and the resulting peptides separated using strong cation exchange (SCX) and reverse-phase (RP) chromatography on-line to electrospray ionization mass spectrometry (ESI-MS).ResultsDatabase searching of the MS/MS data resulted in the identification of 2777 proteins which were clustered into groups associated with disease progression. Proteins which were changed in all disease stages including benign, and hence indicative of the earliest molecular perturbations, were strongly associated with spliceosomal activity, cell cycle division, and stromal and cytoskeleton disruption reflecting increased proliferation and expansion into the surrounding healthy tissue. Those proteins changed in cancer stages but not in benign, were linked to inflammation/immune response, loss of cell adhesion, mitochondrial function and autophagy, demonstrating early evidence of cells within the nutrient-poor solid mass either undergoing cell death or adjusting for survival. Caveolin-1, which decreased and Matrix metalloproteinase-9, which increased through the three disease stages compared to normal tissue, was selected to validate the proteomics results, but significant patient-to-patient variation obfuscated interpretation so corroborated the contradictory observations made by others.ConclusionNevertheless, the study has provided significant insights into CC stage progression for further investigation.

The aim of the study is to identify cornulin (CRNN) protein expression associated with advancement of tongue squamous cell carcinoma (TSCC). A comparison of addictive (containing potential carcinogens) versus non-addiction causative agents was expected to allow detection of differences in CRNN expression associated with TSCC. Bespoke tissue microarrays (TMAs) were prepared and immunohistochemistry (IHC) performed to determine the changes in CRNN expression in epithelial cells of node-negative (pN-), node-positive (pN +) TSCC and non-cancer patients' oral tissues. TMAs were validated by performing IHC on whole diagnostic tissues. Chi-square test or Fisher's-exact tests were used to establish significant expression differences. Analogous analyses were performed for biomarkers previously associated with TSCC, namely collagen I alpha 2 (COL1A2) and decorin (DCN) to compare the significance of CRNN. Keratinisation and its level (low, extensive) were studied in relation to CRNN so that the extent of squamous differentiation could better be assessed. IHC immunoreactive score (IRS) clustered the patients based on weak/moderate (Low (IRS ≤ +3)) or strong (High (IRS ≥ +4)) expression groups. A low expression was observed in a larger number of patients in control proteins COL1A2 (77.3%), DCN (87.5%) and target protein CRNN (52.3%), respectively. Low CRNN expression was observed in TSCC where nodes were involved (pN+: mean 1.4 ± 2.1) (p = 0.248). Keratinisation (%) was low (0% ≤ 50%) in 42.2% and extensive (1% ≥ 50.0%) in 57.8% patients. In conclusion, our study suggested that Low CRNN expression was associated with grade and lymph node metastasis in TSCC. CRNN expression is independent of addiction, however potentially carcinogenic addictive substances might be aiding in the disease progression.

The educational needs must drive the development of the appropriate technology”. They should not be viewed as toys for enthusiasts. Nevertheless, the human element must never be dismissed. Scientific research will continue to offer exciting technologies and effective treatments. For the profession and the patients, it serves to benefit fully from modern science, new knowledge and technologies must be incorporated into the mainstream of dental education. The technologies of modern science have astonished and intrigued our imagination. Correct diagnosis is the key to a successful clinical practice. In this regard, adequately trained neural networks can be a boon to diagnosticians, especially in conditions having multifactorial etiology.

Background: Genetics could be one of the factors in determining oral health and disease in families and the interplay of genetics with environmental factors can affect the prevalence of oral diseases. Aim: To evaluate the genetic influence on dental caries and malocclusion. Objective: To assess the prevalence of dental caries and malocclusion in the family tree. Materials and Methods: A descriptive study was conducted among 26 families of Barwala, District Panchkula, Haryana, India. Clinical examination was conducted to assess dental caries [Decayed Filled Surface Index (DFS/dfs)] and malocclusion (Dental Aesthetic Index). Heritability within the study population was assessed within the pairs: grandparent–grandchildren pair and parent–children pair. Data were analyzed in IBM SPSS Statistics version-24. Results: Dental caries prevalence in grandfather–grandchildren pairs was 35.29% as compared to grandmother–grandchildren pair (36.36%), whereas father–children pair had 38% and mother–children pair had 42.59%. Statistically significant results were obtained for caries in grandmother–grandchildren pairs, father–children pair, and mother–children pair but not for grandfather–grandchildren. The prevalence of malocclusion in grandfather–grandchildren pairs was 70.58% as compared to grandmother–grandchildren pairs (13.63%), whereas the father–children pair had 52% and mother-children pair had 20.37%. Statistically, a significant result was obtained for a malocclusion among grandparent–grandchildren pair and parent–children pair. Conclusion: This study attempts at defining genetic implications in dental caries and malocclusion process. Caries prevalence was higher in mother–children pairs than in the father-children pair. The grandfather–grandchildren pairs had a higher prevalence of malocclusion than grandmother-grandchildren pairs. Thus, the study leads to improved understanding and prevention of the factors leading to them.

Aims: A sub-population of cells named cancer stem cells (CSCs) that initiate and promote tumour growth have been demonstrated to exist in several malignancies including colon carcinoma. The objective of our pilot study was to isolate CD133+ CSCs from patient colon tumours, culture spheres or organoids and observe their proliferation in primary cultures. Parallel cultures of non-cancer controls from colon normal lining and nonadenomatous polyps were set up.Methods: Magnetic activated cell sorting was used to isolate CD133 + CD26 + CD44 + cell populations followed by primary cell culturing under stem cell culture conditions. Number, cells/organoid and daughter generations of organoids were calculated using phase contrast microscope. Trypan blue exclusion method was used to test the viability of the cells.Results: Both colon tumour and colon non-adenomatous polyp formed floating organoids in suspension; however non-adenomatous polyp cultures did not show self-renewal properties for more than 1 passage. Normal colon singlecell suspension did not create organoids. Metastatic colon tumours rapidly produce cancer cell organoids in less than 24 hours in larger numbers compared to non-metastatic colon tumours (1-3 weeks). Metastatic colon tumour organoids have the ability for proliferation for upto five daughter generations in primary culture compared to three generations for those grown from non-metastatic tumours. Conclusions:This in vitro CSC organoid model will help study colon cancer biology, in particular providing a valuable source of primary cell-derived tissue for studying personalized molecular profiling using 'omics strategies to direct therapeutic intervention. Keywords: StatementThis study was performed on primary cultures of fresh sitespecific colon tissues to generate in vitro cancer cell organoid models. As opposed to current literature, we cultured non-cancer colon and compared proliferation patterns to that of tumor tissues and observed differences. This study established a model for in vitro colon tissue generation to study colorectal disease progression.