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Year : 2022 | Volume
: 65
| Issue : 6 | Page : 1 |
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Best paper abstracts |
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Date of Web Publication | 28-Nov-2022 |
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How to cite this article: . Best paper abstracts. Indian J Pathol Microbiol 2022;65, Suppl S2:1 |
Abstract 1 | |  |
Aortopathy – A surgical pathology analysis
U Sujith, Pradeep Vaideeswar
Seth GS Medical College, Parel, Mumbai, Maharashtra, India
Background: Aortopathy is non-Inflammatory, non-atherosclerotic disease of aorta, which is produced by significant changes in the media. This often leads to thoracic aortic aneurysms and/or dissections in young individuals. Aims: This study aimed to analyze the clinical and pathological features in aortic resections performed for aortopathy. Materials and Methods: Over the span of 14 years (2008-2021), all surgically resected specimens of aorta showing aortopathy in all age groups were studied. Particular attention was paid to the changes in the media to assess extent, grade and severity of aortopathy. Results: During the 14-year study period, 68 surgically resected specimens of aorta showed features of aortopathy. There were 46 males and 22 females, who had chief complaints of dyspnea, chest pain and palpitation. Ascending aortic aneurysms, aortic dissections and aneurysms with dissections were observed in 33, 19 and 16 cases, respectively. Bicuspid aortic valve (22 cases), Marfan syndrome (12 cses) and hypertension (11 patients) were commonly identified. There was one case each of LoeysDietz syndrome and aortopathy possibly related to blunt chest trauma. In a significant number of patients (21 cases), the cause remained elusive. Moderate to severe aortopathy was observed in 47 cases. Conclusion: This study helps in standardizing the histological parameters of aortopathy. In large number of cases, where the cause is uncertain, it calls for the need of molecular and genetic studies.
Keywords: Aorta, aortic dissection, aortopathy, bicuspid aortic valve, hypertension, Marfan syndrome, mucoid extracellular matrix accumulation, thoracic aortic aneurysm, transforming tissue factor
Abstract 2 | |  |
Expression of PD-L1 correlates with tumor immune microenvironment (TIME) in colorectal carcinoma (CRC)
Mohammed Shahin, Susama Patra, Suvendu Purkait, Madhabananda Kar, Saroj Kumar Das Majumdar, Tushar Subhadarshan Mishra
AIIMS, Bhubaneswar, Odisha, India
Introduction/Background: Colorectal carcinoma (CRC) is a malignancy of diverse clinical, histopathological and molecular features. Tumor immune microenvironment, the interplay between various cells and molecules in a has significant role in deciding the tumor behaviour and overall prognosis. PD-L1 or programmed death ligand-1, has been crucially implicated in the regulation of the immune microenvironment of the tumor. There is limited data regarding the PD-L1 and the profile of immune cell in CRC, especially in Indian population. Objectives: To assess the expression of PD-L1 in the tumor cells of colorectal carcinoma and its association with the TIME, MSI status and various clinicopathological parameters in CRC. Methods: A hospital-based, observational, cross-sectional study. PD-L1 expression was assessed at protein level by Immunohistochemistry and mRNA level by qRT-PCR. Immune cell marker concentration (CD4, CD8, CD20, FOXP3 and CD163) interpreted using ImageJ (Fiji) software. Results: Of the 78 cases, 19% were PD-L1 positive, more in right-sided CRCs than in left sided ones. A significant association of PD-L1 expression with the concentration of CD8+ T-cells, CD20+ B-cells and CD163+ macrophages. No statistical significance was seen between PDL1 expression with other immune cells, clinical profile, pathological subtype, grade or stage, and survival. Conclusions: The present study showed a relatively lower frequency of PD-L1 in CRC from an Eastern Indian cohort. Further, PD-L1 This could mean that the PD-L1 blocking antibodies can modulate the host immune response against tumor progression, which is in accordance with the established trials with PD-L1 inhibitors like pembrolizumab.
Keywords: Colorectal carcinoma, ImageJ, PD-L1, tumor immune microenvironment
Abstract 3 | |  |
Does molecular subtypes in gastric cancer influence clinicopathological outcome?
Jesty Tom, Geethanjali Gude, Kim Vaiphei
Post Graduate Institute of Medical Education and Research, Chandigarh, India
Introduction: Classification systems for gastric cancer (GC) were based on comprehensive molecular analysis of that provided insights into developing personalised therapy. Aim of the Study: To establish a less cumbersome and clinically relevant assay for different histological tumor types describing associated clinico-pathological parameters in 100 hundred GCs. Materials and Methods: The cases were assessed for mismatch repair protein deficiency (MMRd), P53 aberrancy and E-cadherin aberrancy by immunohistochemistry (IHC). Her2/neu amplification by IHC and fluorescence in-situ hybridisation. Results: Fifty-seven cases were of Laurén intestinal subtype and 43 cases had diffuse morphology. Age range is 25-90yrs (Mean - 53.3 yrs), male female ratio is 3.3:1. Diffuse GC is more common in younger female patients (P - 0.041). Eight cases showed MMRd, are of intestinal subtype and more commonly seen in Gastric cancer with lymphoid stroma. MMRd is associated with older age, distal location and better outcome and survival (P 0.042). P53 aberrancy is identified in 51% of cases. MMRd and P53 showed inverse relation. P53 positive gastric cancer show a higher pT and lymph node involvement (P- 0.028). Her2 neu overexpression is identified in 15% of the cases of GC. All Her2 positive cases were of intestinal morphology which also include 2 cases of cribriform carcinoma and 1 hepatoid adenocarcinoma. Thirty cases were microsatellite stable, P53 and E-cadherin wild type. Conclusion: We have demonstrated that gastric carcinoma can be classified into clinically relevant subgroups by using a convenient screening tool.
Keywords: E-cadherin aberrancy, gastric cancer, mismatch repair protein deficiency, P53 aberrancy

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 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/0377-4929.362054

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