Clinicopathological Correlations of E-Cadherin, Vimentin, and EGFR in Oral Squamous Cell Carcinoma | Chapter 14 | Medicine and Medical Research: New Perspectives Vol. 8

Aims: The present study aimed to determine the clinicopathological features in suspected oral squamous cell carcinoma patients.2-To study the expression of epithelial-mesenchymal transition markers (E-Cadherin and Vimentin) in oral squamous cell carcinoma. 3-To correlate the expression of E-Cadherin and Vimentin with the expression of EGFR.

Study Design: This is a Prospective Cross-Sectional Study.

Place and Duration of Study: Sample: Department of Pathology, JNMCH, AMU, Aligarh, between August 2020 to July 2022.

Methodology: The study was conducted on 252 samples out of which IHC of E-cadherin, Vimentin, and EGFR was applied on 75 representative samples. All the demographic details were noted and H and E were applied to all samples. All the cases were classified into well, moderate, and poorly differentiated OSCC. Later on, after applying IHC on representative samples correlation was done between the expression of three IHC markers results.

Results: Out of 252 cases a maximum number of cases i.e., 125 (49.60%) were moderately differentiated followed by 109 (43.25%) well-differentiated and the least number i.e.,18 (7.14%) were poorly differentiated oral squamous cell carcinoma. The mean age of patients in different grades of OSCC was 49 years with a significant p value of <0.01. males clearly outnumbered females. 83.33% (210 cases) were found in males while 16.67% (42 cases) were found in females. Buccal mucosa was found to be the most common site of involvement by OSCC with 45.24% (114) cases. The majority of cases had multiple risk factors involved. The most frequent association was with tobacco/betel quid, which was seen in 35.71% (90) cases.

As the tumour progressed towards poor differentiation, there was a decrease in the mean IHC score of E-cadherin from 10.37 to 2.13, which was found statistically significant (p<0.001) while the mean IHC score of Vimentin increased from 2.60 to 9.20 implying the inverse correlation of both and proving epithelial-mesenchymal transition.  with a decrease in differentiation from well to poor mean IHC score of EGFR increases from 1.90 to 10.60, which was found statistically significant (p<0.001). E-cadherin was found to be inversely proportional to EGFR with significant results (r = -0.829, p< 0.01). Vimentin was found to be directly proportional to EGFR with significant results (r = 0.760, p< 0.01).

Conclusion: With regard to the histologic grades of oral squamous cell carcinoma, loss of E-cadherin expression and overexpression of Vimentin and EGFR are prognostic indicators, indicating that the expression of these molecules changes as the tumour progresses to a reduced differentiation. Immunoreactivity of E-cadherin, Vimentin, and EGFR can be utilized to assess the prognosis, metastatic behaviour, survival, and management of patients.

 

Author (s) Details

Syeda Iqra Usman
Department of Pathology, AMU, Aligarh, India.

 

Veena Maheshwari
Department of Pathology, AMU, Aligarh, India.

 

Nishat Afroz
Department of Pathology, AMU, Aligarh, India.

 

Please see the book here:- https://doi.org/10.9734/bpi/mmrnp/v8/2018

The Role of Cadmium Induced EGFR/STAT5 Pathway Activation in Epithelial to Mesenchymal Transition | Chapter 4 | Current Innovations in Disease and Health Research Vol. 7

 Cadmium (Cd) is a poisonous and carcinogenic heavy metal about cigarette fume, air and drinking water, due to land and industrial endeavors, posing a health risk to the inexact population. Prolonged, depressed-dose Cd exposure by way of inhalation or ingestion induces alveolus and kidney cancers in two together humans and animal models. While exposure to extreme-dose Cd is cytotoxic and is equated with the occupational background, low-dose Cd uncovering is carcinogenic and mainly correlated with the inexact population. Even though Cd is classification as a group 1 “human carcinogen” by IARC, the means by which Cd-unprotected cells overcome calcium chelation and induce diseased transformation remains imprecise. This study examines the system by which cells unprotected to low doses of Cd live the loss of E-cadherin cell-cell grip and induce epithelial-to-mesenchymal change (EMT). Two epithelial cell lines, BEAS-2B and HEK293, were exposed to 0.4 µM and 1.6 µM of Cadmium chloride hemipentahydrate (CdCl2.2.5H2O) for 24 hours (h) and 9 weeks (wks). The preferred doses are environmentally relevant to levels of Cd found in bread and cigarettes. A dose-helpless decrease in E-cadherin and an increase in N-cadherin protein expression was observed in containers treated accompanying low-dose Cd. Moreover, Cd medicated cells exhibited a faster increase rate when compared accompanying control cells. This observation surpassed to the examination of the EGFR/STAT5 road activation, which has again been noticed to be activated in studies exhausted cancer cells. Our results accompanied a dose-weak and time-dependent increase in two together total EGFR and phosphorylated EGFR (p-EGFR) protein. Similar results were observed accompanying STAT5 and phosphorylated STAT5 (pSTAT5) protein in both short-term and complete exposures, nevertheless the 0.4 µM dose had the highest verbalization at 24 h. EGFR/STAT5 inducible genes were also upregulated in Cd-medicated cells in just 24 h. These dossier demonstrate that epithelial cells can overcome Cd-intervened toxicity by activating the EGFR/STAT5 road to induce cell continuation and proliferation, chief to EMT.

Author(s) Details:

Aikaterini Stavrou,
Department of Medicine, Division of Environmental Medicine, New York University Grossman School of Medicine, New York, NY 10010, USA.

Angelica Ortiz,
Department of Medicine, Division of Environmental Medicine, New York University Grossman School of Medicine, New York, NY 10010, USA.

Max Costa,
Department of Medicine, Division of Environmental Medicine, New York University Grossman School of Medicine, New York, NY 10010, USA.

Please see the link here: https://stm.bookpi.org/CIDHR-V7/article/view/12042

Methyl Donors Inhibit Panc-1 Cell Proliferation by Decreasing NFkB and Erk Signaling Levels and Raising E-Cadherin Expression | Chapter 11 | Current Practice in Medical Science Vol. 8

The physiology of cancer patients, particularly those with pancreatic cancer, may be improved by dietary methyl donors, which may also be utilised as intervention treatment. In this study, an aggressive pancreatic adenocarcinoma cell line (Panc-1) was treated with methyl-donors (L-methionine, choline chloride, folic acid, and vitamin B12), which significantly increased the levels of p21WAF1/Cip1 cyclin dependent kinase inhibitor and the SubG1 fractions while significantly decreasing the levels of phospho-Erk1/2 and the proliferation rate. Diet is one of the lifestyle-related factors in the genesis of pancreatic cancer, an aggressive malignancy with a high chance of metastasizing. Methyl-donors are dietary micronutrients that function as bioactive food ingredients by delivering methyl groups as cofactors and substrates for critical metabolic pathways. Pathological disorders have recently been related to methyl-donors' unbalanced nutritional status. Although Bak, Puma, and Caspase-9 levels were likewise raised by methyl donor treatments, cleaved Caspase-3 levels were not. The production of the transcription factor NFkB and the pro-inflammatory cytokine IL-17a was also markedly decreased by the therapy. After methyl-donor treatments, SDF-1a and VEGF levels were found to be much lower, which may indicate a reduced risk of metastatic dissemination. As was anticipated, E-cadherin expression increased following the methyl-donor therapy and was negatively correlated with these changes. It is determined that methyl-donors may have the ability to lessen Panc-1 cells' aggressive and proliferative character. This implies a potential function for dietary methyl-donors in enhancing

 

Author (s) Details

Eva Kiss

Department of Internal Medicine and Oncology, Oncology Profile, Semmelweis University, Budapest, 1083 Budapest Koranyi S u 2/a, Hungary.

 

Gertrud Forika

Department of Pathology and Experimental Cancer Research, Semmelweis University, Budapest, 1085 Ulloi u 26, Hungary.0

Istvan Takacs

Department of Internal Medicine and Oncology, Semmelweis University, Budapest, 1083 Budapest Koranyi S u 2/a, Hungary.

Tibor Krenacs

Department of Pathology and Experimental Cancer Research, Semmelweis University, Budapest, 1085 Ulloi u 26, Hungary.

Zsuzsanna Nemeth

Department of Internal Medicine and Oncology, Semmelweis University, Budapest, 1083 Budapest Koranyi S u 2/a, Hungary.

 

Please see the link here:-  https://stm.bookpi.org/CPMS-V8/article/view/7800

Study on Diagnostic and Prognostic Significance of E-Cadherin and Vimentin in Oral Cancer Metastasis | Chapter 10 | Current Practice in Medical Science Vol. 2

Background: To determine how the expression of E-cadherin and vimentin affects epithelial-to-mesenchymal transition in precancerous and cancerous lesions of the oral cavity and oropharynx, as well as to predict invasiveness based on the distinct pattern of expression of these two proteins.

Materials and methods: Haematoxylin and eosin sections, as well as immunohistochemistry expression of E-cadherin and vimentin, were used to investigate biopsies and samples from the oral cavity and oropharynx for any premalignant lesions and invasive epithelial squamous lesions where necessary. Patients' follow-up and therapy-related changes were also examined during the trial.

Results: In our study, there were 64 premalignant cases and 23 malignant cases, with 65 (71.0%) men and 22 (29.0%) females. The majority of malignant cases—15, or 64.2%—occurred in the fifth and sixth decades of life, while the majority of premalignant lesions—36, or 56.4%—occurred in the fourth and fifth. Leukoplakia accounted for 14 cases (21.9%) of the 64 premalignant oral lesions, of which 3 instances also exhibited mild to severe dysplasia. Premalignant lesions had significant 4+/3+ E-cadherin expression in the majority of cases, but vimentin expression was weaker or negative in both dysplasias and carcinoma-in-situ (p=0.013). Six out of ten (60%) instances of well-differentiated cancer had a 4+ degree of E-cadherin staining, compared to zero out of ten (0%), and just one, case, respectively, of poorly differentiated carcinoma. Vimentin was expressed to a higher degree in 6/10 (60%) instances of well-differentiated oral squamous cell carcinoma than it was in 6/10 (60%) cases of poorly-differentiated carcinoma. One (1.6%) of the positive lymph node metastasis cases had high E-cadherin staining, whereas four (66.6%) had no E-cadherin staining at all. In our investigation, the differences in the immunoreactivities between CIS and microinvasive or invasive carcinomas were statistically significant (p 0.001). When invasive carcinomas were compared to dysplasias and carcinoma-in-situ, E-cadherin expression was dramatically decreased, and the difference in immunoreactivity was statistically significant (p value 0.05). It was statistically significant (p value 0.05) that vimentin expression increased as the tumour developed from dysplasias to carcinoma-in-situ to invasive carcinomas.

Conclusions: The evaluation of tumour behaviour, prognosis, survival, and patient therapy can be aided by the use of immunohistochemistry E-cadherin and vimentin stains. Future research on tumour microinvasion for early detection and patient survival can use these substances as biomarkers.

Author(s) Details:

Anjum Ara,

Department of General Pathology, Faculty of Dentistry, Jamia Millia Islamia, New Delhi, India.

Kafil Akhtar,

Department of Pathology Jawaharlal Nehru Medical College, Faculty of Medicine, Aligarh Muslim University, Aligarh, India.

Please see the link here: https://stm.bookpi.org/CPMS-V2/article/view/7349