17^th World Congress on Biomarkers, Cancer Therapy & Clinical Research September 23-24, 2022 Vancouver, Canada

Biography:

Sopio Badzgaradze did her studies from 1992-1998 in institute of Critical Care Medicine at Tbilisi medical State University. In 2010 she completed her PhD at American University in Tbilisi. She did her training courses such as: The Basics of Homotoxicology in the Rheumatology and Gastroenterology, Symposium - "Modern Aspects of Bioregulation Medicine", Modern Clinical Medicine, Achievements and Latest Technologies, Scientific Practical Relations in Medicine - Reality and Perspectives, 34^th Euro Global Summit on Cancer Therapy and Radiation oncology, 37 th Conference of the International Clinical Hyperthermia Society and many other courses.

Abstract:

Topicality: Treatment of oncological patients and getting clinical remission is an unfortunate topic even for the 21st century; despite the correctly selected therapy, which gives minimal risks of complications because of the chemo sensitive tests, there are important problems connected with the quality of life of patients and naturally we ask questions to ourselves: How could we manage to increase the quality of life in oncological patients on the 3rd and 4th levels and decrease the number of the side effects that accompany Ch/therapy and R/therapy procedures.

Aim: The aim of the study was the patient with a 55-year diagnosis: NSCLC Thigh bone MTS, 3rd stage; R /therapy and 4 Courses CH /therapy; ECOG-2 . Clinical remission was not achieved; Symptoms of progression of the hip fracture were strengthened, and the institution was addressed with the aforementioned history.

Methods and Materials: For the patient was selected CH/courses with hyperthermia and target therapy, we use Docetaxel 80 mg / m2 and obpivo recommended to strengthen the course effectiveness, weaken toxicity and to improve the quality of life recommended for the treatment CH/therapy + target therapy with hyperthermia and hypoglycemia; For this procedure, a hyperthermic camera was installed, where the procedure is carried out at 43-48 degrees Celsius, and we have a sugar content of 25-30000 per one 40-45 mm / l in the bloodstream.

Results: Only 2 courses were conducted with the patient with a CH/therapy and target therapy with hyperthermia.

Conclusion: So, we managed to get maximal results through high-tech hyperthermic chemotherapy, patient’s clinical remission and this was without any side effects. Increasing the quality of life, We recommend giving a hyperthermic chemotherapy and target therapy in oncological patients at 3rd and 4th stage, which is a firm guarantee of increasing their quality of life.

Biography:

Dr. Anna Eiring is an Assistant Professor in the Department of Molecular and Translational Medicine at Texas Tech University Health Sciences Center in El Paso, Texas, a Title V Hispanic-serving institution. Her lab focuses on disease progression and drug resistance in myeloid leukemias driven by constitutively active tyrosine kinases, namely BCR-ABL1-driven chronic myeloid leukemia (CML) and FLT3-mutated acute myeloid leukemia (AML). She has published nearly 50 papers on cancer biology and immunology, and has further interests in understanding the biology underlying worse outcomes for minority cancer patients

Abstract:

Acute myeloid leukemia (AML) patients with mutations in the FMS-like tyrosine kinase 3 (FLT3) gene can be treated with tyrosine kinase inhibitors (TKIs) targeting FLT3. However, many patients develop resistance or experience adverse side effects (1,2). The ubiquitin-proteasome system (UPS) plays an important role in regulating protein homeostasis, cell cycle progression, and apoptosis, thereby representing a potential target for combination therapies. However, similar to FLT3 TKIs, proteasome inhibitors are prone to adverse side effects and drug resistance, highlighting the need for alternative therapeutic strategies. We recently reported an oncogenic role for two members of the 19S regulatory complex, 26S proteasome non-ATPase subunits 1 (PSMD1) and 3 (PSMD3), in disease progression and drug resistance of chronic myeloid leukemia (CML) and various solid tumors (3,4). We hypothesized that these genes may also play an oncogenic role in AML.

TCGA data revealed that high levels of PSMD3 but not PSMD1 expression correlated with worse overall survival (OS) in AML (p=0.0029, Figure 1A-B). However, when we zoomed in on patients with FLT3 mutations, AML patients with high levels of PSMD3 mRNA expression had a sharp reduction in OS (FLT3+ AML, p=0.0015, Figure 1C-D). PSMD3 knockdown impaired colony formation of the FLT3-mutant AML cells lines, MOLM-13 and MOLM-14, correlating with increased OS in xenograft models. In contrast with our data in CML, PSMD3 knockdown had little effect on apoptosis or nuclear factor-kappa B transcription. Rather, mass spectrometry-based proteomics analyses revealed a potential role for PSMD3 in regulating energy metabolism. Consistently, PSMD3 knockdown resulted in reduced oxygen consumption rates in MOLM‐14 cells. Altogether, PSMD3 may represent a novel molecular biomarker in FLT3+ AML and may be a novel target for combination therapies.

Biography:

Dr. Ananda M. Mondal is an assistant professor of computer science in the Knight Foundation School of Computing at Florida International University (FIU). He is the director of the Machine Learning and Data Analytics Group (MLDAG) at FIU. Dr. Mondal is also a faculty member of the Bioinformatics Research Group (BioRG) at FIU, headed by Professor Giri Narasimhan. Dr. Mondal’s research interests are Machine Learning, Deep Learning, Explainable Artificial Intelligence (XAI), and Bioinformatics. More specifically, Dr. Mondal’s group applies Machine Learning, Deep Learning, and XAI to develop tools for discovering cancer biomarkers using genomic, epigenomic, and transcriptomic data.

Abstract:

Statement of the Problem: The subtype of breast cancer dictates the choice of treatments. Researchers have reported that the genes responsible for breast cancer initiation and development are regulated by cis-regulatory elements such as long non-coding RNAs (lncRNAs). However, there have not been any studies to discover the biomarker lncRNAs specific to five breast cancer subtypes, including Basal, HER2, Luminal A, Luminal B, and Normal-like. This study aims to identify subtype-specific lncRNA biomarkers with clinical outcomes that might help develop appropriate cancer therapy.

 

Data and Methodology: The expression profiles of lncRNAs for breast cancer patients from The Cancer Genome Atlas (TCGA) were analyzed to discover the biomarkers. We proposed a simultaneous feature selection and classification approach for a multiclass problem combining recursive feature elimination (RFE) and l1-norm multiclass Support Vector Machine (L1MSVM), thus calling it RL1MSVM. The newly proposed model performs better than two state-of-the-art models, L1MSVM and Random Forest (RF), in selecting subtype-specific lncRNA biomarkers.

 

Results: A total of 196 lncRNAs, the optimum number of features based on RL1MSVM, were selected using all three methods for comparison. Finally, a stable set of 91 key lncRNAs was obtained using the union of the intersections of the two sets selected by two of the three approaches. Of 91 lncRNAs, 53 were previously identified, and the remaining 38 are novel. Significance: The novel and known key lncRNAs can augment breast cancer subtype-specific targeted therapy.

Biography:

Brandon Lucke-Wold was born and raised in Colorado Springs, CO. He graduated magna cum laude with a BS in Neuroscience and distinction in honors from Baylor University. He completed his MD/PhD, Master’s in Clinical and Translational Research, and the Global Health Track at West Virginia University School of Medicine. His research focus was on traumatic brain injury, neurosurgical simulation, and stroke. At West Virginia University, he also served as a health coach for the Diabetes Prevention and Management program in Morgantown and Charleston, WV, which significantly improved health outcomes for participants. In addition to his research and public health projects, he is a co-founder of the biotechnology company Wright-Wold Scientific, the pharmaceutical company CTE cure, and was a science advocate on Capitol Hill through the Washington Fellow’s program. 

 

He has also served as president of the WVU chapters for the American Association of Pharmaceutical Scientists, Neurosurgery Interest group, and Erlenmeyer Initiative Entrepreneur group. In addition, he has served as vice president for the graduate student neuroscience interest group, Nu Rho Psi Honor Society, and medical students for global health. He was an active member of the Gold Humanism Honor Society and Alpha Omega Alpha Honor Society. He is currently a member of the UF House Staff Council and Positive Culture Committee. He is married to Noelle Lucke-Wold and has two children.  As a family, they enjoy running with their dogs, rock climbing, and traveling.  In his spare time, Brandon frequently runs half marathons and 10ks together with his wife. Brandon also enjoys reading and discussing philosophy and playing chess. He is currently a Pgy4 neurosurgery resident at University of Florida and plans to pursue endovascular training.

Abstract:

Background: Cerebral vasospasm (CV) can contribute significant morbidity for subarachnoid hemorrhage (SAH) patients. A key unknown is how CV induction is triggered following SAH. 

Methods: c57/bl6 wild type and c57/bl6 IL-6 female knockout (KO) mice were utilized with groups: saline injected, SAH, SAH + IL-6 blockade, SAH IL-6 KO, SAH IL-6 KO + IL-6 administration. For SAH, 50mm blood was collected from tail puncture and administered into basal cisterns. IL-6 blockade was given at various time points. Various markers of neuroinflammation were measured with western blot and immunohistochemistry. Cerebral blood flow was also measured. Vasospasm was measured via cardiac injection of india-ink/gelatin. Turning test and Garcia’s modified SAH score were utilized. P<0.05 was considered significant. 

Results: IL-6 expression peaked 3 days following SAH (p<0.05). Human IL-6 was increased in aneurysmal blood (p<0.05). Receptor upregulation was periventricular and perivascular. A significant increase in BBB markers endothelin 1 and occludin were noted following SAH but reduced with IL-6 blockade (p<0.01). CV occurred 5 days post SAH but was absent in IL-6 KO mice and mitigated with IL-6 blockade (p<0.05). IL-6 blockade, and IL-6 KO mitigated effects of SAH on cerebral blood flow (p<0.05). SAH mice had impaired performance on turn test and poor Modified Garcia Scores compared to saline and IL-6 blockade. A distinct microglia phenotype was noted day 5 in the SAH group (overlap coefficients r=0.96 and r=0.94) for Arg1 and iNOS, which was altered by IL-6 blockade. Day 7, a significant increase in toll-like receptor 4 and Stat3 were noted. This was mitigated by IL-6 blockade and IL-6 KO, which also reduced Caspase 3 (p<0.05). Ventricular dilation and increased tunel positivity were noted day 9 but resolved by IL-6 blockade (p<0.05). 

Conclusion: correlation between IL-6 and CV has been well documented. We show that a mechanistic connection exists via the inflammatory response, and IL-6 blockade provides benefit in reducing CV and its consequences.