Day 1 :
- Accepted Presentations
Location: Prague, Czech Republic
Loyola University Chicago, USA
Dr. Dariusz Borys is an Professor of Pathology and Orthopaedic Surgery, head of Orthopaedic and Pediatric Pathology and Director of Digital Pathology at Loyola University Chicago. He received his Doctor of Medicine from the University of Wroclaw, Poland in 1994 and completed a residency program in anatomic pathology at County General Hospital in Wroclaw, Poland in 1995. He completed his postdoctoral research at the University of Arizona, Tucson, Arizona in 1998. He continued on with and completed residency training in both anatomic pathology and clinical pathology at University of Illinois at Chicago in 2001. He received a Pediatric Pathology Fellowship at New York University, New York, New York in 2005 and followed that with an Orthopedic Pathology Fellowship at NYU Hospital for Joint Diseases, New York, New York in 2006. After completing his fellowships, Dr. Borys become faculty member in the rank of assistant professor at University of California and then he finally moved to Loyola University Chicago in 2013. At LUMC he is appointed as a an Professor of Pathology and Orthopaedic Surgery and is serving as the head of orthopaedic and pediatric pathology and director of digital pathology. Currently Dr. Borys research focuses on the molecular markers in diagnostic, prognostic and targeted therapy in osteosarcoma.
Osteosarcoma (OS) is a malignant primary tumor of bone affecting adolescents and young adults. There are few if any molecular markers to predict its behavior and prognosis. In our study we investigated the relationship of expression of different molecular markers in osteosarcoma tumors before treatment to pathologic necrotic response after neoadjuvant chemotherapy. In summary, deletion of RB1 (72%), gain of RUNX2 (68%), deletion of TP53 (52%), deletion 18q23 (48%) by molecular studies and p16-negative by IHC (38%) were common findings. Most abnormalities, particularly RB1 and TP53 deletions and RUNX2 gain, did not correlate with chemotherapy response. IHC p16-negative status correlated strongly with failed chemotherapy response (15/40). Alterations of 18q correlated slightly with poor response (p=0.0796). Poor response cases included 3 cases with deletion of 18q23, 3 cases with LOH for 18q23, and 1 case with copy gain (trisomy 18). Comparison of 18q genomic abnormalities in cases with a favorable versus poor response suggested a smallest region of overlap for a negative factor at 18q23. In conclusion we identified complex genotypes in the OS samples with frequent occurrence of previously identified biomarkers such as deletion RB1, deletion TP53, deletion 18q23 and gain of RUNX2. Comparison of genomic findings to p16-negative status and chemotherapy response revealed p16-negative status to be the best overall indicator of a poor chemotherapy response, with the poorest responders being both p16 negative and altered for 18q23. Additional studies are warranted to validate these findings and further characterize the role of CDKN2A and other factors that influence response to therapy in osteosarcoma patients.
Queen Mary University of London
Dania Zuhier Ragheb completed MSc Experimental Oral Pathology from Queen Mary University of London, She is serving as a Lecturer at Faculty of Dentistry at Al-Quds university
Vimentin is a type 3 intermediate filament cytoskeletal protein. It is known to be over expressed in cells that undergo epithelial mesenchymal transition and metastasis. In this project, Neo-pLPC-wild type vimentin DNA and Neo-pLPC-empty-no insert- control DNA were retrovirally transduced into MCF7 cells which showed no gene expression of vimentin in a previous study .
Aim: To test whether transducing vimentin in cells with low/no endogenous levels will induce filament formation. Moreover, to screen the level of vimentin expression in 14 different cell lines. In addition, to test whether when transfecting AcGFP N-terminus tagged vimentin MCF7 cells with wild type vimentin DNA, the aggregates formed will rearrange into filaments or not.
Materials and Methods: Western blotting was done to observe the level of vimentin protein expression in MCF7 cells transduced with wild type vimentin. QPCR was done for different cell lines to investigate the levels of vimentin gene expression. Immunofluorescence was done to demonstrate vimentin expression in MCF7 transduced with vimentin. Transfection of ACGFP N-Terminus tagged vimentin transduced MCF7 cells with non-tagged vimentin DNA was done and proceeded with immunofluorescence.
Results: Immunofluorescence showed an increased expression of vimentin filament when using 5mg/ml of G418 drug compared to 1mg/ml for cell selection. Western blot showed expression of vimentin protein in Neo-pLPC-wild type vimentin MCF7 cells. QPCR showed high level of vimentin expression in Neo-pLPC-wild type vimentin transduced MCF7 cells. In addition, HT1080 expressed vimentin the highest and T47D the lowest. Immunofluorescence after transfection showed that most aggregates didn’t dissolve into filaments.
Conclusion: Vimentin was found to be highly expressed in progressive cancer cell lines. Low endogenous levels of Vimentin were detected in MCF7 cells. When transducing MCF7 cells with a wild type vimentin, all experiments showed that vimentin was expressed in these cells with 5 mg/ml being the G418 drug concentration for selection. Transfecting with a wild type vimentin has a little effect on the vimentin aggregates formed in N- terminus tagged vimentin MCF7 cells, as most aggregates didn’t dissolve into filaments.
Future work: To perform experiments using C tagged vimentin transduced cells to study its role in filament assembly. Invasion and migration assays should also take place on these transduced cells, as if a certain part of vimentin, the head or tail, is proved to play a role in migration and invasion, this could be linked clinically to metastasis. Therefore, this part could be targeted and blocked to stop metastasis and so the tumour could be confined in its place while including in mind other factors causing metastasis. As a result, the tumour could be treated more easily and effectively. This could be used as a potential future cancer treatment.
Mekelle UniversityAyder Referral Hospital, Mekelle, Ethiopia
Back ground; Lymphadenopathy is an abnormal increase in size and /or altered consistency of lymph nodes. Tuberculosisis the commonest cause of lymphadenopathy in developing countries like Ethiopia Fine-needle aspiration cytology (FNAC) is one of the diagnostic methods in pathology and used as a tool to obtain cells for the morphological diagnosis of numerous lesions.
Objective- This study was undertaken to evaluate the clinicocytologic characteristics of peripheral lymphadenopathies
Methodology- All 1500 cases were retrieved from the Ayder comprehensive teaching hospital record retrospectively from the patients who had presented with superficial lymphadenopathy from January 2017 to June 2018
Result-A total of 1500 lymph nodes were aspirated. Male and female accounts 53.1% and 46.9%, respectivelly.Cervical lymphadenopathy was the most frequent(52%).Most of tuberculosis cases have similar cytologic and clinical diagnosis (87%) but from Secondary tumors only 35% have similar clinical diagnosis and only 5% of Hodgkin’s lymphoma cases are correctly diagnosed clinically. The age group of 21-30 years was the most affected age group while age group above 70 with less frequency. Tuberculosis lymphadenitis was the highest (38.5%), reactive (27.1%), malignancy accounts for (15.8%) ,granulomatous lymphadenitis (8.3%) and non-diagnostics accounts about(5.6%).From total cases only 9 repeats of aspiration were done. Most patients with TB are at 21-30 and 31-40 years. Reactive lymphadenitis cases are mostly identified below age of 10 years. Malignancy accounts around 15.8% of the cases commonly with in age group of 60-70 years and males are dominant except in secondary tumors. Most cases with age above 70 are malignant (54%).Most patient with age less than 10years have benign diagnosis.
Discussion –Most of Hodgkin’s lymphoma patients are not correctly diagnosed clinically ,this is most likely because of single or smaller numbers of lymph node and young age of presentation, which limits the clinicians to think malignant lesions.
Conclusion: This study highlighted the various cytomorphological patterns of lymphadenopathy and revealed a huge burden of tuberculous lymphadenitis in this region and 87% cases are correctly diagnosed clinically
This study also shows the importance of repeats of aspiration because it results specific cytologic diagnosis in 89% of cases.
Key words- Fine-needle aspiration, Lymphadenopathy, Benign, Atypical, Malignant,
Dr. Mitrasadat Rezaei worked as Assistant professor of pathology at Flowcytometry department, High Institute for research and education in blood transfusion medicine, Tehran, Islamic Republic of Iran from 2011-2014. Currently she is working as Assistant professor of pathology at pathology department, National Research Institute of Tuberculosis and lung disease, Shahid Beheshti University of Medical Science,Tehran,Iran, from 2014 and she is the Director of Molecular pathology Laboratory , Masih Daneshvari Hospital from 2014 and she is the Head of cental lab in school of medicine, Shahid beheshti University of Medical Science, Tehran, Iran from 2016.
Shroque Zaher has completed her pathology training at both the London and East of England deaneries, and has been awarded her CCT. She gained her FRCPath from the Royal college of pathologists, United Kingdom in 2015. Her main interests are lung and haematopathology, as well as medical education.
This case represents a rare entity – primary pulmonary myxoid sarcoma, of which to the best of our knowledge , only 10 other cases have been reported in the literature.They are defined by distinctive histomorphological features and characterised by a recurrent fusion gene. All tumours involved pulmonary parenchyma with a predilection for the endobronchial component. They appear to have a a predilection for females, with 7 of the 10 reported cases, occurring in women. Microscopically, they are lobulated tumours comprising cords of polygonal, spindle, stellate cells within myxoid stroma, morphologically reminiscent of extra skeletal myxoid chondrosarcoma. Tumours were immunoreactive for only vimentin and weakly focal for EMA, although our specific case was negative for these markers. In 7 of the 10 tumours , a specific EWSR1-CREB1 fusion gene was demonstrated by reverse transcription -polymerase chain reaction. This gene fusion has been described previously in 2 histologically and behaviorally different sarcomas: clear cell sarcoma – like tumours of the gastrointestinal tract and angiomatoid fibrous histiocytomas, however this is a novel finding in tumours with the morphology described and occurring in the pulmonary region