5^th World Hematologists Congress August 18-19, 2016 London, UK

Biography:

Shaoying Li has received her MD from Beijing Medical University (Current name: Peking University Health Science Center). She is an Assistant Professor in the Department of Hematopathology at the University of Texas MD Anderson Cancer Center. She is board certified in Anatomic Pathology, Clinical Pathology and Hematology. In addition to clinical responsibilities on lymphoma, leukemia and flow cytometry services, she has been actively participating in multiple research projects in lymphoma and leukemia, which has led to 50 research papers and multiple book chapters. She also serves as Member of Editorial Boards and ad hoc Reviewer for multiple journals. Her major research interests include molecular cytogenetic risk stratification of DLBCL with a focus on “double hit” lymphoma and clinicopathologic and molecular study of mantle cell lymphoma.

Abstract:

Double-hit lymphoma (DHL) has been defined by 2008 WHO as a B-cell lymphoma with MYC/8q24 rearrangement in combination with a translocation involving another gene such as BCL2 or BCL6. The most common form of DHL has translocations involving MYC and BCL2, also known as MYC/BCL2 DHL. In the past few years, numerous case series of MYC/BCL2 DHL have been reported in the literature. Most cases of MYC/BCL2 DHL morphologically resemble diffuse large B-cell lymphoma (DLBCL) or high grade B-cell lymphoma, not otherwise specified (previous name in 2008 WHO: B-cell lymphoma, unclassifiable with features intermediate between DLBCL and Burkitt lymphoma). These tumors have a germinal center B-cell immunophenotype but an aggressive clinical course characterized by a high proliferation rate, advanced-stage disease, extranodal involvement, high International Prognostic Index score and high serum lactate dehydrogenase levels. All tumors have a complex karyotype. Despite a variety of therapeutic approaches that have been used to date, patients with DHL have a poor prognosis. Here we will discuss the clinicopathologic, immunophenotypic, cytogenetic and prognostic features of MYC/BCL2 DHL and some remaining issues.

Biography:

John Batchelor is currently a Consultant in Emergency Medicine at Central Manchester Foundation Trust, UK. He is also Honorary Lecturer at Manchester Metropolitan University. He was graduated from Leeds University England in 1982. He is a Fellow of the Royal College of Surgeons of Ireland and Fellow of the Faculty of Emergency Medicine of England. He undertook his MD training at University College London, UK. He has written extensively on the subject of minor head injuries. He has presented a paper in Paris in 2012 on meta-analysis looking at the relationship between cerebral microbleeds and anitiplatelet agents. He has also recently published a meta-analysis on the effect on mortality of platelet transfusions in adults with spontaneous or traumatic antiplatelet associated intracranial hemorrhage. His current research interest lies in the area of risk factors for intracranial hemorrhage in both adults and pediatrics secondary to coagulopathy and thrombocytopenia.

Abstract:

With an ever increasing elderly population, falls in the elderly is a common condition presenting on a daily basis to Emergency departments. Many of these elderly fallers will have head injuries and will be taking antiplatelet agents, notably aspirin. The risk of traumatic intracranial hemorrhage is increased in patients taking antiplatelet agents although the risk is less than that of warfarin (odds ratio of 2.5 versus 1.5). The risk of mortality in patients’ taking aspirin with traumatic brain injury is slightly increased in patients on antiplatelet agents in contrast to warfarin where the mortality is doubled. On the basis of this level of evidence some clinicians advocate the use of a platelet transfusion in patients with traumatic brain hemorrhage who are on antiplatelet agents. The evidence for this will be reviewed. Desmopressin is an alternative agent which might have a potential role in this area. Finally the role of platelet function assays will be reviewed based upon the current research evidence in this area.

Biography:

C Cameron Yin has received her MD degree from Beijing Medical University and PhD from the University of Wisconsin-Madison. She is currently an Associate Professor in the Department of Hematopathology at the University of Texas MD Anderson Cancer Center. In addition to clinical responsibilities on the Leukemia, Lymphoma and Molecular Diagnostic services, she has been actively participating in multiple research projects in the molecular genetic abnormalities in leukemia and lymphoma, which has led to over 100 research papers and over 20 book chapters.

Abstract:

It has been assumed that immunoglobulin (Ig) can only be produced by B-cells and plasma cells. Recently, we have reported that Ig can be expressed by other types of cells such as epithelial cancer cells. In this study, we studied Ig expression in acute myeloid leukemia (AML). We found that Ig was expressed at a high frequency and level in AML cell lines and primary myeloblasts, but not in monocytes or neutrophils from healthy controls by RT-PCR, immunohistochemistry and flow cytometry. We further assessed rearrangements of IgG VHDJH transcripts and found that AML-IgG had restricted (AML cell lines) or biased (primary myeloblasts) V usage. Moreover, its gene rearrangements showed evidence of somatic hypermutation. Anti-human IgG reduced cell viability and induced apoptosis in AML cell lines, whereas anti-human IgK increased cell migration and chemotaxis. Our findings suggest that AML-Ig may play a role in leukemogenesis and AML progression and it may serve as a useful molecular marker for monitoring minimal residual disease or designing target therapy. Study on the correlation between level of AML-Ig expression and morphologic and molecular genetics features as well as clinical outcome of AML patients is in progress.

Biography:

Simon Durrants has completed his undergraduate studies at the University of London and Postgraduate studies at Royal Postgraduate School of Medicine/Hammersmith Hospital. He is the Director of Clinical Hematology & Bone Marrow Transplantation, Royal Brisbane Hospital. He has published more than 100 papers in reputed journals and has been serving as an Editorial Board Member of repute.

Abstract:

Polycythemia vera (PV) is a myeloproliferative neoplasm characterized by erythrocytosis, burdensome symptoms and an increased risk of thrombosis. Hematocrit (Hct) control (i.e., <45%) is a key therapeutic goal and has been shown to decrease the risk of cardiovascular death and major thrombotic events. Hydroxyurea (HU) is currently the first-line therapy for cytoreduction in high-risk patients; however, substantial proportions (15%) become resistant to or intolerant of HU by stringent ELN criteria. Ruxolitinib, a potent Janus kinase JAK1/JAK2 inhibitor, was well tolerated and superior to best available therapy (BAT) in maintaining Hct control without phlebotomy, normalizing blood cell count, reducing spleen volume and improving symptoms in the phase 3 RESPONSE-1 trial. RESPONSE-2 is an open-label, phase 3b study comparing the efficacy and safety of Ruxolitinib with BAT in HU-resistant/intolerant patients with PV without splenomegaly. In PV patients with an inadequate response to or unacceptable side effects from HU both with and without splenomegaly, Ruxolitinib is well tolerated and superior to BAT in controlling Hct without phlebotomy, achieving CHR and improving PV-related symptoms. Most patients in RESPONSE-2 (70.5%) had been treated with only 1 prior line of therapy (HU). In RESPONSE-1 and RESPONSE-2, patients treated with Ruxolitinib had fewer thromboembolic events compared with BAT. Taken together, findings from RESPONSE-1 and RESPONSE-2 suggest that Ruxolitinib could be considered as a standard of care for second-line therapy in this post-HU patient population.

Biography:

Osaro Erhabor is currently a Professor of Hematology, Transfusion Medicine and Laboratory Total Quality Management. He is an Alumni of Rivers State University of Science and Technology, Nigeria, University of Greenwich in the United Kingdom and Francis Tuttle College of Technology in Oklahoma, USA. He is the author of 5 books and 5 book chapters. He has published more that 190 papers in the field of infectious diseases, hematology, blood transfusion science and total quality management. He is also a Member of the Editorial Board as well as an article Reviewer to several international scientific journals.

Abstract:

Hypertension is a global public health problem that adversely affects the health status of individuals, families and communities. L-arginine and nitric oxide levels of a total of 90 consecutively recruited hypertensive subjects and 50 age-matched non-hypertensive controls were studied. Plasma from subjects and control participants were analyzed for L-arginine and nitric oxide L-arginine and nitric oxide levels was significantly lower among the hypertensive subjects compared to those of the non-hypertensive controls (p=0.04 and 0.05) respectively. There was no statistically significant difference in the L-arginine and nitric oxide levels of the hypertensive subjects based on gender and age group (p=0.87 and 0.22) and (p=0.23 and 0.47) respectively. L-arginine level was significantly higher among married hypertensive subjects compared to single subjects (p=0.03). There was no statistically significant difference in the nitric oxide level of hypertensive subjects based on marital status (p=0.81). The difference in the L-arginine and nitric oxide level of hypertensive subjects based on ethnicity was not statistically significant (p=0.57 and 0.25) respectively. The mean nitric oxide level was significantly higher among hypertensive subjects with mildly raised blood pressure compared to those with high blood pressure (p=0.01). The findings in this study confirm that that the level of L-arginine and nitric oxide is lower among hypertensive subjects compared to non-hypertensive controls. It may be necessary to routine prescribe nitric oxide generating L-arginine supplement to hypertensive patient. It may be necessary to carry out public enlightenment of hypertensive patients in the area on the need to maintain a balanced diet containing sufficient level of L-arginine.

Biography:

Abstract:

The Polycythemia Vera Study Group (PVSG) and WHO classifications distinguished the Philadelphia (Ph1) chromosome positive chronic myeloid leukemia from the Ph1 negative myeloproliferative neoplasms (MPN) essential thrombocythemia (ET), polycythemia vera (PV) and primary myelofibrosis (MF) or primary megakaryocytic granulocytic myeloproliferation (PMGM). Half of PVSG/WHO defined ET patients show low serum erythropoietin levels and carry the JAK2 V617F mutation, indicating prodromal PV. The positive predictive value of a JAK2 V617F PCR test is 95% for the diagnosis of PV and about 50% for ET and MF. The WHO defined JAK2 V617F positive ET comprises three ET phenotypes at clinical and bone marrow level when the integrated WHO and European Clinical, Molecular and Pathological (ECMP) criteria are applied: Normocellular ET (WHO-ET), hypercellular ET due to increased erythropoiesis (prodromal PV) and hypercellular ET associated with megakaryocytic granulocytic myeloproliferation (EMGM). Four main molecular types of clonal MPN can be distinguished: JAK2 V617F positive ET and PV; JAK2 wild-type ET carrying the MPL 515; mutations in the calreticulin (CALR) gene in JAK2/MPL wild-type ET and MF and a small proportion of JAK2/MPL/CALR wild-type ET and MF patients. The JAK2 V617F mutation load is low in heterozygous normocellular WHO-ET. The JAK2 V617F mutation load in hetero/homozygous PV and EMGM is clearly related to MPN disease burden in terms of splenomegaly, constitutional symptoms and fibrosis. The JAK2 wild-type ET carrying the MPL 515 mutation is featured by clustered small and giant megakaryocytes with hyperlobulated stag-horn like nuclei, in a normocellular bone marrow (WHO-ET) and lacks features of PV. JAK2/MPL wild-type, CALR mutated hypercellular ET associated with PMGM is featured by dense clustered large immature dysmorphic megakaryocytes and bulky (cloud-like) hyperchromatic nuclei, which are never seen in WHO-ECMP defined JAK2 V617F mutated ET, EMGM and PV and neither in JAK2 wild-type ET carrying the MPL 515 mutation. Two thirds of JAK2/MPL wild-type ET and MF patients carry one of the CALR mutations as the cause of the third distinct MPN entity. WHO-ECMP criteria are recommended to diagnose, classify and stage the broad spectrum of MPN of various molecular etiologies.

Biography:

C Cameron Yin has received her MD from Beijing Medical University and her PhD from the University of Wisconsin-Madison. She is currently an Associate Professor in the Department of Hematopathology at the University of Texas MD Anderson Cancer Center. In addition to clinical responsibilities on the leukemia, lymphoma and molecular diagnostic services, she has been actively participating in multiple research projects in the molecular genetic abnormalities in leukemia and lymphoma, which has led to over 100 research papers and over 20 book chapters.

Abstract:

CD5-posiitve B-cell lymphomas are heterogenous group of neoplasms. Classification of this group of lymphomas has important clinical and prognostic significance. CD5-positive B-cell lymphomas consist primarily of chronic lymphocytic leukemia/small lymphocytic lymphoma (CLL/SLL) and mantle cell lymphoma (MCL). However, CD5 expression has been reported in a number of other B-cell lymphomas. We report the clinical, morphologic, immunophenotypic and molecular genetics features of several series of CD5-positive B-cell lymphomas that lack the prototypic characters of CLL/SLL or MCL, including follicular lymphoma, MALT lymphoma, nodal marginal zone lymphoma and lymphoplasmacytic lymphoma. Our results show that CD5 expression is often associated with an increased tendency of disseminated disease in MALT lymphoma and nodal marginal zone lymphoma, but these patients usually have an indolent clinical course and excellent overall survival with appropriate management. However, in follicular lymphoma, CD5 expression is associated with a higher International Prognostic Index, higher rate of transformation to diffuse large B-cell lymphoma and shorter progression-free survival. We summarize that CD5 expression not only produces diagnostic challenges in the classification of CD5-positive B-cell lymphomas but also bears prognostic significance.

Biography:

Ken Mills is the Chair of Experimental Hematology in the Centre for Cancer Research and Cell Biology (CCRCB) in Queen’s University Belfast. He coordinates the activities of the Blood Cancer Research Group with a focus on the molecular aspects of MDS and AML to identify novel therapies. He has published over 135 papers, several book chapters and he is an Editorial Board Member and Reviewer for high impact journals.

Abstract:

There is an urgent and unmet need for new effective and less toxic therapies for acute myeloid leukemia (AML) and myelodysplastic syndrome (MDS) patients. This is particularly important for the elderly patients who are often unfit for intensive therapies. The number of mutations that have now been reported as being associated with both AML and MDS mean the potential mutation combinations would mean a plethora of drugs may be required. The number of new therapies being developed through the drug pipeline of pre-clinical, phase 1, 2 and 4 before FDA approval is very low and can take up to 15-18 years and billions of dollars. However, there are a large range of approved therapies for all types of conditions such as diabetes, epilepsy, cardiac diseases, mental disorders etc., which are known to the safe and well tolerated in humans. The question is could any of these therapies be repurposed or repositioned to be a treatment for AML or MDS and if so how can the most effective be identified? We have employed alternative approaches to identify candidate drugs for repurposing and these approaches and the results will be discussed in context of AML and MDS.

Biography:

Rashmi Kanagal-Shamanna is an Assistant Professor in Hematopathology and Molecular Diagnostics Laboratory at The University of Texas at MD Anderson Cancer Center, USA. She is board certified by the American Board of Pathology in Anatomic and Clinical Pathology, Hematopathology and Molecular Genetic Pathology. She has received her MD from St. John’s Medical College, Bangalore, India. She has completed Residency in Anatomic and Clinical Pathology from Henry Ford Hospital, Detroit, Michigan. She has completed her Fellowships in Hematopathology, Advanced Hematopathology as well as Molecular Genetic Pathology at The University of Texas MD Anderson Cancer Center, USA. She is actively involved in bone marrow/lymph node pathology and clinical development and reporting of next generation sequencing-based assays for cancers. Her primary research interest includes application of novel molecular techniques to understand tumor pathogenesis and ultimately guide therapy. She has numerous highly cited peer-reviewed publications in her field and has given talks at many national meetings.

Abstract:

Isolated isochromosome 17q, i(17q), accounts for less than 1% of myeloid neoplasms that are commonly classified as myelodysplastic/myeloproliferative neoplasms, acute myeloid leukemia (AML), myelodysplastic syndrome (MDS) or myeloproliferative neoplasms (MPN). These cases have distinctive clinicopathologic features with an aggressive clinical course and poor prognosis. However, their molecular mutation profile has not been studied. Here, we present the mutation profile of myeloid neoplasms with isolated i(17q) that included AML, MDS/MPN, MDS and MPN. In addition to the i(17q) as a common finding, these neoplasms had frequent mutations in SRSF2 (55%), SETBP1 (59%), ASXL1 (55%) and NRAS (31%); TET2 and TP53 mutations were rare. Eight of 28 patients (29%) showed concurrent mutations in ASXL1, SRSF2, SETBP1 and RAS. There was a significant association between mutations in SETBP1 and RAS (p=0.003). The mutation pattern was independent of the morphologic diagnosis. Sequential mutational analysis of a subset of cases showing evolution from a diploid karyotype to i(17q) showed that SRSF2 and ASXL1 mutations precede the detection of i(17q) whereas SETBP1 mutations are associated with i(17q).

Biography:

Abstract:

Biography:

Jackleen Raafat Awadallah has received her PhD in Biochemistry, Faculty of Pharmacy, Suez Canal University, Egypt in 2014. She has completed her Master’s degree in Biochemistry at Faculty of Pharmacy, Cairo University, Egypt in 2010. Currently, she is working as a Researcher at the Medical Biochemistry Department, Medical Research Division and she is also a Member of the General Secretary Group of the Supreme Council of the Medical Division, National Research Center of Egypt.

Abstract:

Acute lymphocytic leukemia (ALL) is a malignant disorder common among children. Apoptosis is a morphological process that leads to controlled cellular self-destruction and defective apoptotic pathways are greatly involved in tumor formation, progression and metastasis. Apoptosis is the primary mechanism through which most chemotherapeutic agents induce tumor cell death. The purpose of this study was to monitor the expression of pro and anti-apoptotic proteins CD95 and Bcl-2 as well as copper and zinc levels in the peripheral blood of children with acute lymphocytic leukemia prior to and six months after starting chemotherapy. The study was performed on twenty five children attending the outpatient clinic of the National Cancer Institute, Cairo University. Ten normal children were included in the study and considered as control group. Results showed that Total Leukocyte Count (TLC) and bone marrow blast count were significantly higher in ALL children than controls while after treatment TLC was normalized whereas bone marrow blast count was significantly decreased, hemoglobin and platelet count were significantly decreased when compared to controls while significantly increased after treatment. CD95 was significantly decreased before treatment relative to controls while it was significantly increased after treatment whereas Bcl-2 concentration showed significant increase before treatment compared to controls while it was significantly decreased after treatment. Serum Cu level showed significant increase in ALL cases at presentation compared to controls while it was not significantly changed after treatment. Serum Zn level was significantly decreased before treatment compared to controls while it was normalized after treatment. Cu/Zn was significantly higher in newly diagnosed ALL children than controls while it showed significant decrease after treatment. Negative significant correlation was found between CD95 and Bcl-2 on one hand and between serum Cu and Zn levels on the other hand. It could be concluded that CD95 and Bcl-2 might be useful diagnostic markers not only in the diagnosis but also in the follow up of ALL cases.

Biography:

Mousa Mohammad Thalath Alhaosawi has completed his MD from Saudi Commission for Health Specialties in Orthopedic Surgery (Pediatric and Hip Surgeon). He is the Director of Almadinah General Hospital of Almadinah city in Saudi Arabia. He has published more than 9 papers in reputed journals

Abstract:

Introduction & Objectives: The hallmark of hemophilia is hemarthrosis. All efforts must be made to early diagnose joint bleeding as soon as it occurs and treat it not later than within 2 hours of onset by infusing the appropriate clotting factor. This will prevent the accumulation of blood in the joint as well as inflammation and a potential hemophilic arthropathy. Recurrent bleeding prevents the joint from regaining its range of motion, muscle strength and normal appearance. These changes become permanent, leading eventually to osteoarthritis. A bleeds joint requires urgent and comprehensive management, especially in young patients, if permanent damage is to be prevented.

Methods: The author conducted a comprehensive review and synthesis of the relevant literature. The author reviewed all compiled reports from computerized searches. Searches were limited to English language sources and human subjects. Literature citations were generally restricted to published manuscripts appearing in journals listed in Index Medicus and reflected literature published up to July, 2013.

Results: The aim of this study was to introduce the new criteria (joint at risk) for early identification of “bleeds joint” for early diagnosis and effective management to prevent the joint to become chronic synovitis “target joint”.

Conclusion: The new concept of identifying “target joint” in this study is aiming to prevent the joint of hemophilic patient to progress to stage of chronic synovitis “target joint” by early identification of bleeds joint.

Biography:

Ayesha Junaid is a graduate of King Edward Medical University, Pakistan and is a Fellow of Clinical Hematology (2002) from CPSP Pakistan. She has received training in Cytogenetics & FISH technique from UCLA, USA in year 2008. She has qualified the evaluation examination of Medical Council of Canada in year 2012. She is a Consultant Hematologist and In-Charge Blood Transfusion Services & Hematology Department at a tertiary care hospital Islamabad. She also works as a Transplant Consultant mainly involved in hematological malignancies. She is a Teacher in medical school since 17 years and is presently working as a Professor of Pathology in Shifa College of Medicine, Pakistan. She is an elected syndicate Member of Shifa Tameer-e-Millat University, Pakistan. She is Patron In-Charge of student organization for blood donation. She is also a Program Director, Hematology Fellowship in Shifa International Hospitals, Islamabad and Chairperson, Hospital Transfusion Committee. She works as a National Hemovigilance Coordinator appointed by Ministry of Health, Pakistan.

Abstract:

Thalassemia & hemophilia are two inherited blood disorders in which children are born with lifelong cellular or component dependency as curative treatment is either not available or not affordable. In Pakistan the estimated burden of the children suffering from inherited blood disorders is above six million. Thalassemia major & hemophilia claim more than 90% of this disease load. Considering factors affecting prevalence of these disorders like cultural, socioeconomic, education and awareness level, an increase is expected in near future. These disorders show up since early childhood and affect quality of life not only of the patients but of the families having these special children. Role of hematologists providing care to these under privileged patients becomes crucial, demanding and lifelong. Here not only skill and knowledge but a lot of passion is required to make a difference in effective management of these lifelong disorders. In Pakistan, Jamila Sultana Thalassemia Foundation and Pakistan Hemophilia Welfare Societies are two model organizations, among many who save lives and improve productivity of these young patients. JS foundation is working since year 2004 with a registered load of 611 thalassemic children, providing complete physical & psychological support free of cost. Their oldest patient maintained conservatively is 38 year old. Pakistan Hemophilia Society, with 510 registered hemophiliac children is delivering as a centre of excellence with free factor replacement and rehabilitation facilities. Though the journey of management of hereditary blood disorders in underserved country is tough but there is light at the end of the tunnel.

Biography:

Michael Retsky has received his PhD in Physics from University of Chicago in 1974 and made a career change into cancer research 30 years ago. He was on Judah Folkman’s staff for 12 years. He is a long term survivor of Stage IIIc colon cancer and noted for opting not to use maximum tolerated chemotherapy was the first person to use what is now called metronomic chemotherapy. He is the Founder and on the Board of Directors of Colon Cancer Alliance. He has published more than 70 papers in physics and cancer and currently editing a book on the cancer project for Nature/Springer.

Abstract:

My colleagues and I have been studying a bimodal relapse pattern for breast cancer patients treated with mastectomy. Most relapses occur in the 3 years post surgery and after a lull in the 4^th year, a broad period of late relapses extends from 5 to 15 and more years. Similar patterns have been seen in over 21 databases from US, Europe and Asia. We suspect that the host response to surgical wounding produces systemic inflammation that lasts for a week or so (identified by IL-6 in serum). Breast cancer patients can have circulating tumor cells and cancer cells that are dormant perhaps in marrow. Among the many possible results of systemic inflammation, capillaries become permeable and platelets degranulate that have previously sequestered angiogenesis controlling factors. According to our findings, the combination of these situations results in the wave of relapses in the initial 3 years after surgery. The surgery that triggers these events can be primary tumor removal, breast reconstruction or perhaps other such interventions. Based on a retrospective study, perioperative NSAID Ketorolac may reduce relapses by 5-fold in the 9-18 month period after surgery. There is one small randomized trial underway in Belgium and we are anxiously promoting other trials in locations where triple-negative breast cancer (that lack markers for targeted therapy) is common. This population will respond best to this perioperative NSAID therapy that incidentally is inexpensive, non-toxic and administered once just prior to surgery and perhaps over the 4 postoperative days.