Hematologists Global Summit July 13-14, 2018 Sydney, Australia

Biography:

Thipaporn Jaroonsirimaneekul has completed her M.Sc. (Clinical Pathology), B.Sc.(Med.Tech) from Mahidol and Khon Kaen university, respectively. She is a medical technician specialist in All blood transfusion science; HLA, genotyping, serology, etc. At present, her position is the head of blood components preparation in Blood Transfusion Centre, faculty of Medicine, Khon Kaen University, Thailand

Abstract:

Introduction: Quality assurance of white blood cells (WBC) depletion require in QC blood products. Inline filter and automate centrifuge (Reveos-system) produce the leuko-depleted blood product in routine, therefore we need the new method for WBC counting, to assure the blood products.

Objective: To count WBC in leukocyte depleted red blood cell (LD-PRC) from inline filter or Reveos blood bag and leukocyte depleted pooled platelet concentrates (LD-PC).

Method: At least 1% were sampling from total units of LD-PRC (N=20) and LD-PC (N=12) in routine unit for WBC enumeration within 6-8 hours after collection. The WBC in samples was stain by fluorescent dye, use LED excitation and CCD detection technologies makes the WBC analysis result.

Result: Residual WBC in LD-PRC and LD-PC are 0.26+0.21 and 0.23+0.12x10⁶ cells /unit (X+SD), respectively. The maximum WBC residual in both products are 0.47 and 0.35x10⁶ cells/unit. The waiting time for results interpretation was almost 8 minutes per test.

Conclusion: The leuko-depleted blood product in blood transfusion centre, faculty of medicine, Khon Kaen University are accepted by standard of American Associated of Blood Transfusions (AABB) and European Standard, by the new standard of automatic residual leukocyte counting (rWBC-ADAM). And the technique was easy to use and effective in routine.

Biography:

Malinee Meesaeng is currently working in the field of Hematology and she pursued Degree at the Khon Kaen University Thialand.

Abstract:

Introduction: Blood and blood components are irradiated prior transfusion to prevent the proliferation of certain types of T lymphocytes that can inhibit the immune response and cause graft-versus-host disease. This procedure is necessary for transfusion recipients at risk for GVHD, including fetuses receiving intrauterine transfusions, select immunocompetent or immunocompromised recipients, patients undergoing hematopoietic transplantation, individuals receiving platelets selected for HLA or platelet compatibility, and individuals receiving units from blood relation.

Method: The data for blood components which requested irradiated was collected in 2017. All data are divided into diagnosis and type of components.

Result: 1,751 requested irradiated blood components were: pediatric, thalassemia, newborn, stem cells transplant, intra-uterine and other; 1001, 236, 264, 106, 31 and 113, respectively. Total of units for irradiated are 2.377 units (LDB=1.039 u, LPRC=609 u, SDP=617 u, RDP=65 u, LPPC=47 u), none of PRC.

Conclusion: Blood transfusion centre, faculty of medicine, Khon Kaen University can afford the irradiated blood components for patients in Srinagarind Hospital and another hospital in nearby area.

Biography:

Nuanchan Mungkhunkhamchaw has completed her BSc (Transfusion Science) from Mahidol University, Thailand. She is the Supervisor in blood components preparation at Blood Transfusion Centre, Faculty of Medicine, Khon Kaen University, Thailand.

Abstract:

Introduction: The pooled component represents a source of concentrated FVIII:C, von Willebrand factor, fibrinogen, FXIII and fibronectin from primary cryoprecipitate components derived from units of fresh frozen plasma. Plasma should be selected from male donors or consideration should be given to screening female donors for HLA/HNA antibodies, as a TRALI risk reduction measure. For storage, cryoprecipitate pooled should be rapidly frozen to a core temperature of –25 ℃ or below within 2 hours of preparation.

Method: Cryoprecipitate was prepared by standard conventional method the male unit was selected for re-suspend cryoprecipitate 120-150 mL per pool. Five to six iso-blood group were pooled by connecting device within 5 minutes. The pooled cryoprecipitate were rapid frozen by -50 ℃ blast. The evaluated of pooled were determine for factor VIII and fibrinogen.

Result: Pooled cryoprecipitate from 5 units by A, B, O blood group were determination of factor VIII and fibrinogen found 109/282, 136/358 and 70/288, respectively. Six units pooled were found 113/342, 139/318 and 78.5/259, respectively. Pooled no group five units in plasma B and AB were found 143/400 and 114/400.

Conclusion: Pooled cryoprecipitate seem useful for routine. The yield of Factor VIII are acceptable in A, B and AB. Blood group O is recommend for better mix with other group and should be resuspend in plasma B or A.

Biography:

Shaoguang Li has obtained his PhD degree from Tulane University, USA and completed his postdoctoral studies at Harvard Medical School. He is currently a Professor at University of Massachusetts Medical School, USA. He has published some seminal work related to leukemia stem cells in highly competitive journals such as Nature Genetics, JCI, PNAS, Blood, Leukemia, etc.

Abstract:

Cancer stem cells in many hematologic malignancies and some solid tumors are associated with cancer initiation and insensitivity to chemotherapy and need to be eradicated for achieving a cure. A successful cancer therapy relies on targeting critical signaling genes that play a key role in the maintenance of cancer stem cell survive and proliferation. Thus, it will be important to fully understand the molecular mechanisms by which cancer stem cells survival and proliferate. Toward this goal, a physiological cancer stem cell disease model is required for identifying and testing genes/pathways that play an essential role in functional regulation of cancer stem cells and can be targeted for eradicating these stem cells. Human chronic myeloid leukemia (CML) induced by the BCR-ABL oncogene is derived from a stem cell, serving as a good disease model for studying the molecular biology of cancer stem cells. In CML, BCR-ABL tyrosine kinase inhibitors including imatinib mesylate (Gleevec) are highly effective in controlling chronic phase CML, but they fail to eradicate leukemia-initiating cells or leukemia stem cells (LSCs) in CML mice and patients. Clinically, a complete and sustained molecular remission (undetectable levels of BCR-ABL transcripts) is difficult to attain even after a complete cytogenetic remission achieved through imatinib treatment. It has become clear that BCR-ABL kinase inhibitors can effectively kill highly proliferating leukemia cells but are incapable of eradicating LSCs for cure. An anti-LSC strategy needs to be developed. Our laboratory has been focusing on understanding the biology of LSCs in CML to identify key genes that regulate survival and proliferation of LSCs, helping us to develop new therapeutic strategies by targeting LSCs.

Biography:

Yu-Chen Enya Chen is pursuing her PhD degree at University of Queensland. She has published a review paper as first author in BBA Cancer Review 2017 (Chen et al.). Her PhD project so far has presented an interesting study towards the understanding of the antibody resistant of patients with progressive chronic lymphocytic leukemia disease.

Abstract:

Antibody therapies for treating chronic lymphocytic leukemia (CLL) remain a challenge for many CLL patients who are insensitive to antibody treatment. A high percentage of CLL patients that are resistant to the current combination therapy of chemotherapeutics and immune-therapeutics have always been a clinical challenge. Understanding the mechanisms driving disease progression and treatment resistance is key to improving patient outcomes. Many studies including our own laboratories have shown that resistance to therapeutic antibodies against CLL is due to the survival signals from the monocyte derived macrophages (MDMs) and also an acquired resistance of monocyte derived macrophages to participate in FcγR-dependent anti-tumor responses. However, the FcγR-dependent signaling pathway in macrophages has not been well studied. Our recently published data suggested that SYK and BTK are involved downstream of FcγR-dependent signaling pathway. In this study we investigate the involvement of PI3K isoforms as they have been known to be an important pathway regulator for cellular function in various immune cells such as T cells, B cells and NK cells as well as in cancerous cells. To examine the expression and involvement PI3K isoforms in contributing to FcγR-dependent ADCC by MDMs, we used different inhibitors to specifically target each PI3K isoform at a time to investigate the effect on ADCC responses by MDMs. Examination of PI3K expression showed that PI3Kα, β and δ are expressed in MDM whereas PI3Kγ is below the limit of detection. We also reported that the PI3Kδ-selective inhibitor, idelalisib and the pan PI3K inhibitor BKM120 (Buparlisib) were able to inhibit ADCC in response to the CD20-targeting therapeutic antibody, obinutuzumab. Similarly, both buparlisib and idelalisib were able to inhibit AKT phosphorylation at concentrations that also inhibited ADCC. This is the first report to show that PI3Kd is involved in FcgR signaling in MDMs from CLL patients or in MDMs from any tumor type. Based on these findings we conclude that PI3Kd is a critical effector molecule for anti-tumor responses to therapeutic antibodies in CLL.