ВИЗНАЧЕННЯ РОЛІ ДЕЛЕЦІЇ ГЕНУ ТР53
|
|
- Helen Gilbert
- 8 years ago
- Views:
Transcription
1 Keywords: сhronic lymphoproliferative neoplasms, B-cell chronic lymphocytic leukemia, multiple myeloma, diffuse large B-cell lymphoma, gene deletion TP 53, fluorescent in situ hybridization ВИЗНАЧЕННЯ РОЛІ ДЕЛЕЦІЇ ГЕНУ ТР53 В ДІАГНОСТИЦІ ТА ПРОГНОЗІ ПЕРЕБІГУ ХРОНІЧНИХ ЛІМФОПРОЛІФЕРАТИВНИХ НЕОПЛАЗІЙ ЗА ДОПОМОГОЮ МЕТОДУ ФЛУОРЕСЦЕНТНОЇ IN SITU ГІБРИДИЗАЦІЇ Ж. А. Мішаріна *, В. В. Сітько, А. І. Курченко *, С. М. Кравченко, Н. І. Костюкова, В. Г. Бебешко ДУ «Національний науковий центр радіаційної медицини НАМН України», Київ * Національний медичний університет імені О.О.Богомольця, Київ Резюме. Представлені результати молекулярно-цитогенетичних досліджень у 60 хворих на хронічні лімфопроліферативні неоплазії (ХЛПН). Клональні делеції гену ТР 53 були виявлені у 25% хворих на ХЛПН: у восьми із 20 хворих на хронічну B-клітинну лімфоцитарну лейкемію (В-ХЛЛ), у шести із 20 хворих на дифузну крупноклітинну В-лімфому (ДКВЛ) та одного із 20 хворих на множинну мієлому (ММ). Аномалії гена ТР53 достовірно частіше реєструвались у хворих на В-ХЛЛ з тяжким перебігом хвороби в порівнянні з групою хворих на ММ (40% та 5%), відповідно (p < 0,05). Ключові слова: хронічні лімфопроліферативні неоплазії, хронічна B-клітинна лімфоцитарна лейкемія, множинна мієлома, дифузна крупноклітинна В-лімфома, делеція гену ТР 53, флуоресцентна in situ гібридизація. ОПРЕДЕЛЕНИЕ РОЛИ ДЕЛЕЦИИ ГЕНА ТР 53 В ДИАГНОСТИКЕ И ПРОГНОЗЕ ТЕЧЕНИЯ ХРОНИЧЕСКИХ ЛИМФОПРОЛИФЕРАТИВНЫХ НЕОПЛАЗИЙ С ПОМОЩЬЮ МЕТОДА ФЛУОРЕСЦЕНТНОЙ IN SITU ГИБРИДИЗАЦИИ Ж. А. Мишарина *, В. В. Ситько, А. И. Курченко *, С. М. Кравченко, Н. И. Костюкова, В. Г. Бебешко ГУ "Национальный научный центр радиационной медицины НАМН Украины", Киев * Национальный медицинский университет имени А. А. Богомольца, Киев Резюме. Представлены результаты молекулярно-цитогенетических исследований у 60 больных хроническими лимфопролиферативными неоплазиями (ХЛПН). Клональные делеции гена ТР 53 были обнаружены в 25% больных ХЛПН: у восьми из 20 больных с хронической B-клеточной лимфоцитарной лейкемией (В- ХЛЛ), у шести из 20 больных с диффузной крупноклеточной В-лимфомой (ДКВЛ) и одного из 20 больных множественной миеломой (ММ). Аномалии гена ТР 53 достоверно чаще регистрировались у больных с тяжелым течением болезни В-ХЛЛ по сравнению с группой больных ММ (40% и 5%), соответственно (p < 0,05). Ключевые слова: хронические лимфопролиферативные неоплазии, хроническая B-клеточная лимфоцитарная лейкемия, множественная миелома, диффузная крупноклеточных В-лимфома, делеция гена ТР 53, флуоресцентная in situ гибридизация.
2 Recent achievements in the research of mechanisms of development and progression of chronic lymphoproliferative neoplasms (CLPN) and analysis of the effectiveness of treatment depending on the type of therapeutic interventions are a valid basis for a new strategy in the diagnosis, prognosis and treatment of these patients. The introduction into clinical practice of modern research methods, including cytogenetic and molecular cytogenetic, allows to determine the genomic reorganization that determine the development of the tumor, the degree of malignancy and metastatic potential level of sensitivity to anticancer drugs therapy. Unfortunately, cytogenetic studies of chronic lymph proliferative neoplasia are associated with certain difficulties. Thus, the substrate cells for this disease have very low spontaneous mitotic activity, and their response to used mitogens is very weak. Therefore, only in some CLPN patients we can get enough of metaphase in unstimulated cell culture for further study. Today, opportunities of cytogenetic diagnosis of CLPN much expanded with the application of new technologies of molecular cytogenetics, based on fluorescent in situ hybridization (FISH) of nucleic acids. FISH method was developed to determine the localization of specific DNA sequences directly in cytological preparations. This method is based on the ability to form stable chromosomal DNA hybrid molecules of DNA (RNA) tests that labeled fluorophore. The size of the DNA fragment under study can range from 60 to 1,500 kb [16]. For the diagnosis of chromosome abnormalities in patients with CLPN interphase fluorescence in situ hybridization (I-FISH) becomes most widely used technique, because it allows you to record the presence of abnormal clone in samples of tumor cells, determine amplification in it, translocations and deletions of certain genes, and evaluate the effectiveness of chemotherapy, performed to patients with / or without transplantation of stem cells (SC) of bone marrow and / or peripheral blood with B-cell chronic lymphocytic leukemia (B-CLL), multiple myeloma (MM), diffuse large B-cell lymphoma (DLBCL). Unlike standard methods of cytogenetic analysis when changes of karyotype are recorded only in 30-45% of patients with newly diagnosed CLPN, fluorescent in situ hybridization allows the identification of chromosomal aberrations in more than 80% of patients [8]. The aim was to determine the role of genomic disorders of chromosome 17 in the region 17p13.1, where suppressor gene of malignant transformation TP53 is localized in substrate cells of bone marrow and biopsy material of lymph nodes in patients with B-CLL, MM and DLBCL to provide prognostic assessments of the progress of CLPN sub-variants, and early detection of resistant to therapy cases and recurrence of CLPN
3 Subjects and methods. Molecular cytogenetic studies were performed in molecular genetic laboratory of diagnosis and prognosis of radiation induced oncohematological pathology of department of Hematology and Transplantology in SI "National Research Centre of Radiation Medicine of NAMS of Ukraine". Bone marrow cells, peripheral blood samples of substrate cells of biopsy material were analyzed and a statistical analysis of results of 60 patients with diagnosis CLPN, including 20 people with B-cell chronic lymphocytic leukemia (B-CLL), 20 with diffuse large B-cell lymphoma (DLBCL) and 20 with multiple myeloma (MM) was conducted. The age of patients at diagnosis ranged from 21 to 75 years and averaged in patients with B-CLL 60,30 ± 2,73, in patients with DLBCL 48,95 ± 3,31 and 58,45 ± 1.83 in patients with MM. The average age of patients with CLPN was 55,9 ± 1,66 years, 7 (11,67%) of patients were younger than 40 years. 34 (56,67%) analyzed samples of bone marrow cells were obtained from male patients and 26 (43,33%) female. Control group was formed from five healthy people aged 40 to 55 years (mean 48,00 ± 2,43). For each person in the control group nuclei and metaphase lymphocytes in peripheral blood and bone marrow were studied. Patients and subjects were informed about the purpose and objectives of the study and consent from them was obtained. Cytogenetic abnormalities research of gene TP 53 was performed on 24- hour unstimulated cultures of bone marrow cells that were received by sternal puncture. Cultivation of native bone marrow (0,5 ml) for 24 hours was carried out in 5 ml culture medium RPMI-1640 ("Sigma", USA) supplemented with 20% fetal calf serum ("Sigma", USA) and 20 ml colchicine ("Sigma", USA) for 2 hours before fixation. Cell suspension was incubated in a thermostat at 37,0 о C for 24 hours. Upon completion of the cultivation hypotonic treatment of cells was carried with heated to 38 о C and prepared ex tempore 0,075 M solution of potassium chloride for 20 min. at 37,0 о C (rate of 1 ml hypotonic solution to precipitate obtained from 1 ml of culture). To the cell suspension 8 ml of cooled holder (a mixture of methanol and glacial acetic acid in a ratio of 3: 1) was added. Samples left at + 4 о С 15 minutes. Replacement of clamp was performed three times. FISH studies in interphase nuclei and metaphase that were received during cytogenetic studies were conducted using commercial test LSI TP53/CEP 17 FISH Probe Kit (Abbott Molecular, USA) according to manufacturer's instructions. Analysis was performed on the software and hardware complex CytoVision (Applied Imaging, UK) based on microscope Olympus BX51, Japan. To visualize the signal samples Vysis TP53/CEP 17 FISH Probe Kit (17p13.1) filters used:
4 Chromosome Locus Probe Fluorochrome 17 17p13.1 Vysis LSI TP53 - Orange 17 17p11.1-q11.1 Vysis CEP 17 Alpha Satellite Green Figure 1 Scheme of the sample Vysis TP 53/CEP 17 (Abbot Molecular Catalog 2011 for Oncology, Automation and Genetics). CY3/FITC/DAPI (Fig. 1). In each case at least 200 interphase nuclei with clear signals were analyzed. Statistical analysis of the results of studies was performed using Statistica 6.0 and Microsoft Office Excel Significance of differences between groups that were analyzed was assessed using χ2 criterion and the Fisher criterion point recommended for the small group size. The difference was considered as statistically significant at p < 0,05. Determined parameters: mean, standard deviation, mean error and measurement error, minimum and maximum values, the maximum level of cells with abnormal set of signals [3; 16]. Cutoff level was calculated in the program Microsoft Office Excel 2007 by function BETAINV (A; B; C), where A level of probability; B number of false-positive nuclei +1; C total number of nuclei analyzed. Results and discussion. At present, the main clinical problem of treatment of B-CLL, MM and DLBCL is that substrate cells are resistant to modern, standard polychemotherapy that is given to patients, and recurrence of disease including molecular-genetic, which are associated with inactivation of the gene TP 53 due to deletions of chromosome 17 (17p13.1). To verify the results and determine the characteristics of the sample Vysis TP 53/CEP 17 FISH Probe Kit (17p13.1), which was used, hybridization of the interphase nuclei of peripheral blood lymphocytes and bone marrow of five healthy people were performed. In addition, in all cases metaphase were
5 studied 100 per sample. Total number of analyzed metaphase and interphase nuclei is Pattern of signals 1O (TP 53, Orange)х2G(CEP 17, Green) was considered for positive. It should be noted that this test allows you to record not only changes in the number of signals corresponding to gene TP 53, but also take into account the quantitative changes of chromosome 17 as a whole (mono or polisomy). In chronic lymphoproliferative neoplasms dignosticly and prognostically for disease course and response to therapy significant is only deletion of gene TP 53. Research of control group is associated with the need of imposing percentage of nuclei with false-positive signals, the main reason of which may be the imposition of locuses or their close spatial arrangement, resulting in normal nuclei pattern of signals (1O: 1G: 1F), (1O: 2G) or (2O: 1G) is observed. A similar pattern of signals can be observed in the abnormal nuclei, where as a result of deletion of the partner area translocation after hybridization is observed fewer on one signal. In addition, in some cases bodysized location of the site that is being analyzed, is the cause of the weak binding of sample in the nuclei one signal is observed or signals are completely absent. According the study of preparations of interphase nuclei of bone marrow cells and peripheral blood threshold level (cutoff level) of signals that corresponded to distribution 1O: 2G test for TP53/СEP 17, was 4,28% at mean values of 2,15%; and 3,93% (average 2,10%) for pattern 3O: 3G and. At the same time in all metaphase a double yellow signal and a double green signal (2Oх2G pattern signals)were determined that testified about balance of genetic structures regarding gene TP 53 in healthy individuals and confirmed false-positive character of detected in the interphase nuclei changes (Table. 1). Table 1 Characteristics of changes of chromosome 17 and gene TP 53 in patients with chronic lymphoproliferative neoplasms Groups Total amount of analyzed nuclei Chromosome 17 Gene ТP 53 (%) monsomy, (%) polysomy, (%) nonclonal deletion, (%) clonal deletion, (%) В-CLL (n = 20) 237,00 ± 11, * DLBCL (n = 20) 234,25 ± 11, ** ММ (n = 20) 270,00 ± 10, Control group (n = 5) 240,00 ± 13,58 0 2,10 2,15 0 * P < 0,01; ** P < 0,05 compared with the group of patients and the control group
6 An examination of the main group of persons in 23,33% (14/60) cases in patients with CLPN aneuploidy was recorded with a change in the set amount from one to three or more chromosomes 17, in 76,67% (46/60) distribution of signals 2Oх2G was observed that corresponds to normal. The least common chromosomal abnormalities (3,33%, two of 60 patients) was monosomy of chromosome 17, and the most common was gene TP 53 deletion, which was found in 45,00% (27 of 60 patients) of cases. Also in the samples polisomy of chromosome 17 was observed, which was identified in 20% (12 of 60 patients) of cases. Analysis of chromosome 17 aneuploidies showed statistically significant differences of detected aberrations (p < 0,05). In the bone marrow cells of 20 patients with B-CLL pattern signals 1O (TP 53) were identified in 13 individuals (65%). In eight (40%) patients TP 53 deletion that had clonal nature was registered. For each sample from 200 to 320 interphase nuclei were analyzed, total 4740 (an average of 237,00 ± 11,63), of which with a normal distribution of signals (2Ox2G) 4116 (an average of 205,80 ± 13,41), which is 86,84% (Fig. 2). A. B. Figure 2. Picture of hybridization of bone marrow cells of patients with CLPN. A. Normal distribution signals (2Ox2G). B. Pattern of signals (1Ox2G), which corresponds to TP 53 (17p13.1) gene deletions; Vysis TP53/CEP 17, 10x100. In substrate cells of patients with B-CLL number of cores with deletion of chromosome 17p13.1 varied in the range of with an average 26,70 ± 8,48. Accordingly, the percentage of abnormal cells on average was 11,45 ± 3,43. Thus, in five of 20 patients (25%) the number of cores with deletions not exceeded 8%, and although these changes were not clonal nature, but far exceeded the limits of error of the method, which was about 2,15% (p < 0,05). Another eight patients (40%) had clonal deletion of gene TP 53 that is associated with a poor prognosis for the disease [11, 6], and in three of them the number of abnormal nuclei exceeded 40% (40%, 47% and 47%, respectively)
7 The results of analysis of samples of bone marrow and lymph nodes of 20 patients with DLBCL using FISH-method showed that the normal pattern of signals (2Ox2G) was registered in 3945 (an average of 197,25 ± 18,96) cells, which is 84,20%. In 498 nuclei (10,63% of the total number of analyzed cells) an abnormal distribution of signals (1Ox2G) was determined. The number of cells with deletion of chromosome 17p13.1 varied in the range of with an average of 24,90 ± 9,67. Accordingly, the percentage of abnormal cells on average was 12,30 ± 4,84. Thus, in six of 20 patients (30%) a yellow hybridization signal was determined, indicating the presence of deletions of chromosome 17p13.1, including two patients with the number of abnormal nuclei was 10%; in other cases 30%, 35% and 36%, indicating their clonal nature. One patient with DLBCL marked with especially high level 90% nuclei 1Ox2G, which may indicate a lack of good response to treatment and require further review of cytostatic therapy [13]. Analysis of bone marrow cells of patients with MM showed that the normal pattern of signals (2Ox2G) was registered in 5326 (an average of 266,30 ± 10,30) cells, which is 98,63%. In 44 nuclei (0,81% of the total number of analyzed cells) an abnormal distribution of signals (1Ox2G) was determined. Average signals (1Ox2G), which are characteristic of gene TP 53 deletions, were determined in double with MM. In one patient the deletion 17p13 was recorded in 10% plasma cells, indicating its clonal nature. In another patient the number of abnormal nuclei (10 of 200) did not exceed 5%. Also in one of the patient s monosomy in 10 of 200 analyzed nuclei (5%) and polisomy 30 of 300 cells (10%) were registered. According to literature data gene TP 53 deletion may be an independent prognostic factor in MM. Patients with deletion17p13 have shorter progression-free remission period and overall survival, even after high-dose chemotherapy with autologous SC transplantation than patients without deletions of the gene [10]. Therefore, in this work we have studied the substrate cells of bone marrow and biopsy material of lymph nodes in patients with B-CLL, MM and DLBCL for the deletion of the gene TP 53. A characteristic feature of these hematologic diseases is significant heterogeneity and individual variability of chromosomal abnormalities in tumor cells. Although each malignancy in this group the most frequently recurring changes in the genotype were identified, identification by methods of classical cytogenetics is significantly limited due to the low proliferative activity in vitro of B-cells. In addition, some submicroscopic adjustments, such as deletions of 11q, 13q and 17p, are almost impossible to determine on the chromosomal level. Therefore, in this study we used a more accurate method of analysis that allows you to record anomalies at the molecular level, namely interphase FISH. The results of our research and a number of similar data from other authors are presented in Table
8 Table 2 Results of studies of gene TP 53 deletions in bone marrow cells and biopsy material of lymph nodes in patients with B-CLL, MM and DLBCL Literature Country Diagnosis Tested patients Gene ТP 53 deletion, n 1 Stevens-Kroef et al. [6] Netherlands B-CLL Teimori H. et al. [15] Iran B-CLL Zenz T. et al. [18] Germany B-CLL Own data Ukraine B-CLL Akay O.M. et al. [1] Turkey DLBCL Sun G.-X. et al. [2] China DLBCL Simonitsch-Klupp I. et al. [13] Austria DLBCL Own data Ukraine DLBCL Chang H. et al. [10] Canada ММ Tǜrkmen S. et al. [14] Germany ММ Gole L. et al. [9] Singapore ММ Own data Ukraine ММ 20 1 According to the molecular-cytogenetic analysis pattern signals 1O (TP 53)x2G(CEP17), which corresponds to deletion TP 53, was found in 45,00% of patients with CLPN: 13 of 20 patients with B-CLL, 12 of 20 patients DLBCL and two of 20 patients with MM. Clonal deletion TP 53 was found in 25% of patients with CLPN: eight of 20 patients with B-CLL, six of 20 patients with DLBCL and one of 20 patients with MM. The average percentage of deletion of the gene TP 53 for patients with CLPN was respectively 40%, 30% and 5%, which corresponds to the data of other researchers. Clonal abnormalities of gene TP 53 were significantly more frequent in patients with B-CLL compared with a group of patients with MM (40% and 5%), respectively (p < 0,05). The table data demonstrates full compliance of own research results with research of other authors, especially in cases where the number of studied patients is almost identical. At the same time, in the group of patients with B- CLL, which was 328 persons significantly lower percentage of patients with available deletion of chromosome 17p13 (4,9%) was registered compared with our data (40%) [18]. Conversely, when examining 105 patients with MM deletion of the gene TP 53 was found in 10 persons (9,5%) [10], in our studies deletion of chromosome 17p13 determined only in one of 20 patients. Obviously, that it's not enough data about the presence of submicroscopic chromosome rearrangements of 17p, where malignant transformation suppressor gene TP 53 is localized, and therefore it is necessary to continue these studies
9 Conclusion Thus during the molecular cytogenetic analysis of bone marrow cells, lymph nodes and peripheral blood of patients with CLPN, deletion TP 53 was found in 45% of patients: 13 of 20 patients with B-CLL, 12 of 20 patients with DLBCL and two of 20 patients with MM. Clonal deletion TP 53 were found in 25% of patients with CLPN. The average percentage of deletion of the gene TP 53 for patients with CLPN was respectively 40%, 30% and 5%, which corresponds to the data of other researchers. Clonal abnormalities of gene TP 53 were significantly more frequent in patients with B-CLL compared with a group of patients with MM (40% and 5%), respectively (p < 0,05). In most patients with B-CLL, MM and DLBCL (55%) changes in the genetic structure of CLPN substrate cells are not registered. It should be noted that the definition of differential prognostic markers of the disease, including chromosomal rearrangements is important not only for the choice of therapy, but also allows timely engage those measures to predict or minimize treatment failure and the development of complications associated with general toxicity of anticancer drugs, because by such a toxicity and effectiveness of standard chemotherapy is limited. Therefore, these data should be considered when oncohematologists assign first-line therapy, which should be as intense as possible for optimal outcomes. References 1. BCL2, BCL6, IGH, TP53, and MYC protein expression and gene rearrangements as prognostic markers in diffuse large B-cell lymphoma: a study of 44 Turkish patients / O. M. Akay, B. D. Aras, S. Isiksoy [et al.] // Cancer Genetics P [Correlation of BCL-6, MYC and p53 gene abnormalities with immunological subtypes and prognosis of diffuse large B-cell lymphoma] / Sun Guan-Xing [et al.] // Zhonghua Yi Xue Yi Chuan Xue Za Zhi V. 29, 5. P Glantz S. Biomedical Statistics. [Translated from English] / S. Glantz. М.: Practice, p. 4. Hanson K. P. Эpydemyolohyya and biology nehodzhkynskyh lymphoma / K. P. Hanson, E. N. Ymyanytov // Practical Oncology V. 5, 3. P Kazantseva T. V. Guidance for practical training for interns 2nd year "Differential diagnosis with Hodgkin's disease (including. Part. Diseases accompanied by prolonged high fever), differentiated treatment. " / MES Chernivtsi, Identification of prognostic relevant chromosomal abnormalities in chronic lymphocytic leukemia using microarray-based genomic profiling / M. J. Stevens-Kroef, E. Van den Berg, D. Olde Weghuis // Molecular Cytogenetics P Matutes E. Morphological and immunophenotypic features of chronic lymphocytic leukemia / E. Matutes, A. Pollack // Rev. Clin. Exp. Hematol
10 8. Molecular cytogenetic aberrations in patients with Multiple Myeloma studied by interphase fluorescence in situ hybridization / L.-J. Chen, J.-Y. Li [et al.] // Exp. Oncol V. 29, 2. P Modified cig-fish protocol for multiple myeloma in routine cytogenetic laboratory practice / L. Gole, A. Lin, C. Chua // Cancer Genetics P p53 gene deletion detected by fluorescence in situ hybridization is an adverse prognostic factor for patients with multiple myeloma following autologous stem cell transplantation / H. Chang, C. Qi, Qi-L Yi. [et al.] // Blood P Patients with chronic lymphocytic leukaemia and clonal deletion of both 17p13.1 and 11q22.3 have a very poor prognosis / P. T. Greipp, S. A. Smoley, D. S. Viswanatha [et al.] // British Journal of Haematology V. 163, 3. P Schnaiter A. 17p Deletion in Chronic Lymphocytic Leukemia. Risk Stratification and Therapeutic Approach / A. Schnaiter, S. Stilgenbauer // Hematology/oncology clinics of North America P Simonitsch-Klupp I. Diffuse large B-cell lymphomas with plasmablastic/ plasmacytoid features are associated with TP53 deletions and poor clinical outcome / I. Simonitsch-Klupp // Leukemia P Tǜrkmen S. High Prevalence of Immunoglobulin Light Chain Gene Aberrations as Revealed by FISH in Multiple Myeloma and MGUS / S. Tǜrkmen, A. Binder // GENES, CHROMOSOMES & CANCER P Teimori H. FISH Analysis for del6q21 and del17p13 in B-cell Chronic Lymphocytic Leukemia in Iranians / H. Teimori, S. Ashoori // Iranian Red Crescent Medical Journal V. 15, 2. P Wolff D. Guidance for fluorescence in situ hybridization testing in hematologic disorders / D. Wolff, A. Bagg, L. Cooley [et. al.] // Journal of Molecular Diagnostics V. 9, 2. P Xuesong H. Identification of Predictive Pathways for Non-Hodgkin Lymphoma Prognosis / H. Xuesong, L. Yang // Cancer Informatics P Zenz T. TP53 Mutation and Survival in Chronic Lymphocytic Leukemia / T. Zenz, B. Eichhorst // Journal of Clinical oncology V. 28, 29. P
Malignant Lymphomas and Plasma Cell Myeloma
Malignant Lymphomas and Plasma Cell Myeloma Dr. Bruce F. Burns Dept. of Pathology and Lab Medicine Overview definitions - lymphoma lymphoproliferative disorder plasma cell myeloma pathogenesis - translocations
More informationInteresting Case Review. Renuka Agrawal, MD Dept. of Pathology City of Hope National Medical Center Duarte, CA
Interesting Case Review Renuka Agrawal, MD Dept. of Pathology City of Hope National Medical Center Duarte, CA History 63 y/o male with h/o CLL for 10 years Presents with worsening renal function and hypercalcemia
More informationCancer. 9p21.3 deletion. t(12;21) t(15;17)
CANCER FISH PROBES INDIVIDUAL AND PANEL S Acute Lymphoblastic Leukemia (ALL) ALL FISH Panel (includes all probes below) 8010 LSI MYB/CEP6 LSI p16 (CDKN2A) LSI BCR/ABL with ASS LSI ETV6 (TEL)/AML1 (RUNX1)
More informationFastTest. You ve read the book... ... now test yourself
FastTest You ve read the book...... now test yourself To ensure you have learned the key points that will improve your patient care, read the authors questions below. Please refer back to relevant sections
More informationCHROMOSOMES Dr. Fern Tsien, Dept. of Genetics, LSUHSC, NO, LA
CHROMOSOMES Dr. Fern Tsien, Dept. of Genetics, LSUHSC, NO, LA Cytogenetics is the study of chromosomes and their structure, inheritance, and abnormalities. Chromosome abnormalities occur in approximately:
More informationAn overview of CLL care and treatment. Dr Dean Smith Haematology Consultant City Hospital Nottingham
An overview of CLL care and treatment Dr Dean Smith Haematology Consultant City Hospital Nottingham What is CLL? CLL (Chronic Lymphocytic Leukaemia) is a type of cancer in which the bone marrow makes too
More informationMarch 19, 2014. Dear Dr. Duvall, Dr. Hambrick, and Ms. Smith,
Dr. Daniel Duvall, Medical Officer Center for Medicare, Hospital and Ambulatory Policy Group Centers for Medicare and Medicaid Services 7500 Security Boulevard Baltimore, Maryland 21244 Dr. Edith Hambrick,
More informationPROGNOSIS IN ACUTE LYMPHOBLASTIC LEUKEMIA PROGNOSIS IN ACUTE MYELOID LEUKEMIA
PROGNOSIS IN ACUTE LYMPHOBLASTIC LEUKEMIA UNFAVORABLE Advanced age High leukocyte count at diagnosis Presence of myeloid antigens Late achievement of CR Chromosomal abnormalities: t(9:22)(q34:q11) t(4;11)(q21;q23)
More informationMULTIPLE MYELOMA. Dr Malkit S Riyat. MBChB, FRCPath(UK) Consultant Haematologist
MULTIPLE MYELOMA Dr Malkit S Riyat MBChB, FRCPath(UK) Consultant Haematologist Multiple myeloma is an incurable malignancy that arises from postgerminal centre, somatically hypermutated B cells.
More informationLYMPHOMA. BACHIR ALOBEID, M.D. HEMATOPATHOLOGY DIVISION PATHOLOGY DEPARTMENT Columbia University/ College of Physicians & Surgeons
LYMPHOMA BACHIR ALOBEID, M.D. HEMATOPATHOLOGY DIVISION PATHOLOGY DEPARTMENT Columbia University/ College of Physicians & Surgeons Normal development of lymphocytes Lymphocyte proliferation and differentiation:
More informationLauren Berger: Why is it so important for patients to get an accurate diagnosis of their blood cancer subtype?
Hello, I m Lauren Berger and I m the Senior Director of Patient Services Programs at The Leukemia & Lymphoma Society. I m pleased to welcome Dr. Rebecca Elstrom. Dr. Elstrom is an Assistant Professor in
More informationWaldenström Macroglobulinemia: The Burning Questions. IWMF Ed Forum May 18 2014 Morie Gertz MD, MACP
Waldenström Macroglobulinemia: The Burning Questions IWMF Ed Forum May 18 2014 Morie Gertz MD, MACP Are my kids going to get this? Familial seen in approximately 5 10% of all CLL patients and can be associated
More informationThe following chapter is called "Preimplantation Genetic Diagnosis (PGD)".
Slide 1 Welcome to chapter 9. The following chapter is called "Preimplantation Genetic Diagnosis (PGD)". The author is Dr. Maria Lalioti. Slide 2 The learning objectives of this chapter are: To learn the
More informationCytogenetics for the Rest of Us: A Primer
Cytogenetics for the Rest of Us: A Primer James J. Stark, MD, FACP Medical Director Cancer Program Maryview Medical Center Diane Maia, M.D. Pathologist, Bon Secours Hampton Roads Case #1 78 y.o. lady seen
More informationWhy discuss CLL? Common: 40% of US leukaemia. approx 100 pa in SJH / MWHB 3 inpatients in SJH at any time
Why discuss CLL? Common: 40% of US leukaemia approx 100 pa in SJH / MWHB 3 inpatients in SJH at any time Median age of dx is 65 (30s. Incurable, survival 2-202 20 years Require ongoing supportive care
More informationWhat is Cancer? Cancer is a genetic disease: Cancer typically involves a change in gene expression/function:
Cancer is a genetic disease: Inherited cancer Sporadic cancer What is Cancer? Cancer typically involves a change in gene expression/function: Qualitative change Quantitative change Any cancer causing genetic
More information6/20/2014. PART I: Plasma Cell Myeloma. Plasma Cells
MULTIPLE MYELOMA: THE TESTING, VALIDATION AND IMPLEMENTATION OF CELL SEPARATION TECHNOLOGY FOR IMPROVED PATIENT CARE Elizabeth Harper CG(ASCP), Binh Vo CG(ASCP), Joey Pena CG(ASCP), Denise Lovshe CG(ASCP),
More informationCorporate Medical Policy
Corporate Medical Policy Microarray-Based Gene Expression Profile Testing for Multiple File Name: Origination: Last CAP Review: Next CAP Review: Last Review: microarray-based_gene_expression_profile_testing_for_multiple_myeloma
More informationtreatments) worked by killing cancerous cells using chemo or radiotherapy. While these techniques can
Shristi Pandey Genomics and Medicine Winter 2011 Prof. Doug Brutlag Chronic Myeloid Leukemia: A look into how genomics is changing the way we treat Cancer. Until the late 1990s, nearly all treatment methods
More informationLymphoplasmacytic Lymphoma. Hematology fellows conference 4/12/2013 Christina Fitzmaurice, MD, MPH
Lymphoplasmacytic Lymphoma versus IGM Multiple Myeloma Hematology fellows conference 4/12/2013 Christina Fitzmaurice, MD, MPH Hematology consult patient 48 yo woman presents to ER with nonspecific complaints:
More informationMultiple Myeloma Patient s Booklet
1E Kent Ridge Road NUHS Tower Block, Level 7 Singapore 119228 Email : ncis@nuhs.edu.sg Website : www.ncis.com.sg LIKE US ON FACEBOOK www.facebook.com/ nationaluniversitycancerinstitutesingapore Multiple
More informationAggressive lymphomas. Michael Crump Princess Margaret Hospital
Aggressive lymphomas Michael Crump Princess Margaret Hospital What are the aggressive lymphomas? Diffuse large B cell Mediastinal large B cell Anaplastic large cell Burkitt lymphoma (transformed lymphoma:
More informationIntroduction. About 10,500 new cases of acute myelogenous leukemia are diagnosed each
Introduction 1.1 Introduction: About 10,500 new cases of acute myelogenous leukemia are diagnosed each year in the United States (Hope et al., 2003). Acute myelogenous leukemia has several names, including
More informationCML. cure. A Patient s Guide. Molecular Biology Diagnosis Stem Cell Transplant Monitoring New Drugs Questions to Ask and More
A Patient s Guide to CML Molecular Biology Diagnosis Stem Cell Transplant Monitoring New Drugs Questions to Ask and More cure C a n c e r U p d at e s, R e s e a r c h & E d u c at i o n Based on science,
More informationEstimated New Cases of Leukemia, Lymphoma, Myeloma 2014
ABOUT BLOOD CANCERS Leukemia, Hodgkin lymphoma (HL), non-hodgkin lymphoma (NHL), myeloma, myelodysplastic syndromes (MDS) and myeloproliferative neoplasms (MPNs) are types of cancer that can affect the
More informationMEDICAL COVERAGE POLICY
Important note Even though this policy may indicate that a particular service or supply is considered covered, this conclusion is not necessarily based upon the terms of your particular benefit plan. Each
More informationUNDERSTANDING MULTIPLE MYELOMA AND LABORATORY VALUES Benjamin Parsons, DO bmparson@gundersenhealth.org Gundersen Health System Center for Cancer and
UNDERSTANDING MULTIPLE MYELOMA AND LABORATORY VALUES Benjamin Parsons, DO bmparson@gundersenhealth.org Gundersen Health System Center for Cancer and Blood Disorders La Crosse, WI UNDERSTANDING MULTIPLE
More informationStem Cell Transplantation
Harmony Behavioral Health, Inc. Harmony Behavioral Health of Florida, Inc. Harmony Health Plan of Illinois, Inc. HealthEase of Florida, Inc. Ohana Health Plan, a plan offered by WellCare Health Insurance
More informationChromosome 6 Abnormalities Associated with Prolymphocytic Acceleration in Chronic Lymphocytic Leukemia* f
ANNALS OF CLINICAL AND LABORATORY SCIENCE, Vol. 28, No. 1 Copyright 1998, Institute for Clinical Science, Inc. Chromosome 6 Abnormalities Associated with Prolymphocytic Acceleration in Chronic Lymphocytic
More informationGenomic Analysis of Mature B-cell Malignancies
Genomic Analysis of Mature B-cell Malignancies Update and Lessons Learned Omar Abdel-Wahab, MD Memorial Sloan Kettering Cancer Center Human Oncology and Pathogenesis Program and Leukemia Service Disclaimer:
More information亞 東 紀 念 醫 院 Follicular Lymphoma 臨 床 指 引
前 言 : 惡 性 淋 巴 瘤 ( 或 簡 稱 淋 巴 癌 ) 乃 由 體 內 淋 巴 系 統 包 括 淋 巴 細 胞 淋 巴 管 淋 巴 腺 及 一 些 淋 巴 器 官 或 組 織 如 脾 臟 胸 腺 及 扁 桃 腺 等 所 長 出 的 惡 性 腫 瘤 依 腫 瘤 病 理 組 織 型 態 的 不 同 可 分 為 何 杰 金 氏 淋 巴 瘤 (Hodgkin s disease) 與 非 何 杰 金
More informationAcute myeloid leukemia (AML)
Acute myeloid leukemia (AML) Adult acute myeloid leukemia (AML) is a type of cancer in which the bone marrow makes abnormal myeloblasts (a type of white blood cell), red blood cells, or platelets. Adult
More informationINSERM/ A. Bernheim. Overcoming clinical relapse in multiple myeloma by understanding and targeting the molecular causes of drug resistance
A. Bernheim Overcoming clinical relapse in multiple myeloma by understanding and targeting the molecular causes of drug resistance OVER-MyR is funded by the European Commission within its FP7 specific
More informationALCHEMIST (Adjuvant Lung Cancer Enrichment Marker Identification and Sequencing Trials)
ALCHEMIST (Adjuvant Lung Cancer Enrichment Marker Identification and Sequencing Trials) 3 Integrated Trials Testing Targeted Therapy in Early Stage Lung Cancer Part of NCI s Precision Medicine Effort in
More informationSECOND PRIMARY BREAST CANCERS FOLLOWING HAEMATOLOGIC MALIGNANCIES A CASE SERIES STUDY FARAH TANVEER PGY 3 DR.MEIR WETZLER DR.
SECOND PRIMARY BREAST CANCERS FOLLOWING HAEMATOLOGIC MALIGNANCIES A CASE SERIES STUDY FARAH TANVEER PGY 3 DR.MEIR WETZLER DR. TRACEY O CONNOR RESEARCH QUESTON Patients with previously diagnosed hematologic
More informationAbstract. Keywords: multiple myeloma, fluorescence in-situ hybridization, FISH, DLEU1
Malaysian J Pathol 2015; 37(2) : 95 100 ORIGINAL ARTICLE Detection of chromosome 13 (13q14) deletion among Sudanese patients with multiple myeloma using a molecular genetics fluorescent in situ hybridization
More informationCorporate Medical Policy
Corporate Medical Policy Hematopoietic Stem-Cell Transplantation for CLL and SLL File Name: Origination: Last CAP Review: Next CAP Review: Last Review: hematopoietic_stem-cell_transplantation_for_cll_and_sll
More informationchronic leukemia lymphoma myeloma differentiated 14 September 1999 Pre- Transformed Ig Surface Surface Secreted Myeloma Major malignant counterpart
Disease Usual phenotype acute leukemia precursor chronic leukemia lymphoma myeloma differentiated Pre- B-cell B-cell Transformed B-cell Plasma cell Ig Surface Surface Secreted Major malignant counterpart
More informationShaji Kumar, M.D. Multiple Myeloma: Multiple myeloma (MM) is the second most common hematological
An update on the management of multiple myeloma and amyloidosis Shaji Kumar, M.D. Multiple Myeloma: Multiple myeloma (MM) is the second most common hematological malignancy in this country affecting nearly
More informationTargeted Therapy What the Surgeon Needs to Know
Targeted Therapy What the Surgeon Needs to Know AATS Focus in Thoracic Surgery 2014 David R. Jones, M.D. Professor & Chief, Thoracic Surgery Memorial Sloan Kettering Cancer Center I have no disclosures
More informationAbout B Cell Lymphomas Groupmeeting Klipp/Spang, December 09 2002 Dennis Kostka Max-Planck-Institute for Molecular Genetics Computational Molecular Biology Berlin 1 Overview Short History of Lymphoma Classification
More informationHaematopoietic Chimerism Analysis after Allogeneic Stem Cell Transplantation
Haematopoietic Chimerism Analysis after Allogeneic Stem Cell Transplantation Dr Ros Ganderton, Ms Kate Parratt, Dr Debbie Richardson, Dr Kim Orchard and Dr Liz Hodges Departments of Molecular Pathology
More informationSubtypes of AML follow branches of myeloid development, making the FAB classificaoon relaovely simple to understand.
1 2 3 4 The FAB assigns a cut off of 30% blasts to define AML and relies predominantly on morphology and cytochemical stains (MPO, Sudan Black, and NSE which will be discussed later). Subtypes of AML follow
More informationAdult Medical-Surgical Nursing H A E M A T O L O G Y M O D U L E : L E U K A E M I A 2
Adult Medical-Surgical Nursing H A E M A T O L O G Y M O D U L E : L E U K A E M I A 2 Leukaemia: Description A group of malignant disorders affecting: White blood cells (lymphocytes or leucocytes) Bone
More informationA 32 year old woman comes to your clinic with neck masses for the last several weeks. Masses are discrete, non matted, firm and rubbery on
A 32 year old woman comes to your clinic with neck masses for the last several weeks. Masses are discrete, non matted, firm and rubbery on examination. She also has fever, weight loss, and sweats. What
More informationChronic Lymphocytic Leukemia. Case Study. AAIM Triennial October 2012 Susan Sokoloski, M.D.
Chronic Lymphocytic Leukemia AAIM Triennial October 2012 Susan Sokoloski, M.D. Case Study 57 year old male, trial application for $1,000,000 Universal Life coverage Cover letter from sales agent indicates
More informationHodgkin Lymphoma Disease Specific Biology and Treatment Options. John Kuruvilla
Hodgkin Lymphoma Disease Specific Biology and Treatment Options John Kuruvilla My Disclaimer This is where I work Objectives Pathobiology what makes HL different Diagnosis Staging Treatment Philosophy
More informationCAP Accreditation Checklists 2015 Edition
CAP Accreditation Checklists 2015 Edition The College of American Pathologists (CAP) accreditation checklists contain the CAP accreditation program requirements, developed on more than 50 years of insight
More informationInteresting Case Series. Periorbital Richter Syndrome
Interesting Case Series Periorbital Richter Syndrome MarkGorman,MRCS,MSc, a Julia Ruston, MRCS, b and Sarath Vennam, BMBS a a Division of Plastic Surgery, Royal Devon and Exeter Hospital, Exeter, Devon,
More informationUpdate in Hematology Oncology Targeted Therapies. Mark Holguin
Update in Hematology Oncology Targeted Therapies Mark Holguin 25 years ago Why I chose oncology People How to help people with possibly the most difficult thing they may have to deal with Science Turning
More informationUMHS-PUHSC JOINT INSTITUTE
Imaging Biomarkers for Staging and Assessing Response to Therapy in Multiple Myeloma Qian Dong, MD. Radiology University of Michigan Wei Guo, MD. Orthopedic Oncology Peking University Second Hospital Team
More informationEnhance Sensitivity of FISH Analysis with Highly Purified Multiple Myeloma Cells Using RoboSep, the Fully Automated Cell Separator
Enhance Sensitivity of FISH Analysis with Highly Purified Multiple Myeloma Cells Using RoboSep, the Fully Automated Cell Separator Benoit Guilbault, PhD Field Applications Scientist t STEMCELL Technologies,
More informationCytogenetic Profile of Variant Philadelphia Translocations in Chronic Myeloid Leukemia
International Journal of Scientific and Research Publications, Volume 4, Issue 12, December 2014 1 Cytogenetic Profile of Variant Philadelphia Translocations in Chronic Myeloid Leukemia Chin Yuet Meng,
More informationA Focus on Multiple Myeloma
A Focus on Multiple Myeloma Guest Expert: Madhav Dhodapkar, MD Professor of Hematology, Yale Cancer Center www.wnpr.org www.yalecancercenter.org Welcome to Yale Cancer Center Answers with Dr. Ed and Dr.
More informationWhat is a Stem Cell Transplantation?
What is a Stem Cell Transplantation? Guest Expert: Stuart, MD Associate Professor, Medical Oncology www.wnpr.org www.yalecancercenter.org Welcome to Yale Cancer Center Answers with Drs. Ed and Ken. I am
More informationCurrent Multiple Myeloma Treatment Adapted From the NCCN Guidelines
Current Multiple Myeloma Treatment Adapted From the NCCN Guidelines Diagnosis Survival 3-5 yrs Survival
More informationFDA approves Rituxan/MabThera for first-line maintenance use in follicular lymphoma
Media Release Basel, 31 January 2011 FDA approves Rituxan/MabThera for first-line maintenance use in follicular lymphoma Approval provides option that improves the length of time people with incurable
More informationRobert Bristow MD PhD FRCPC
Robert Bristow MD PhD FRCPC Clinician-Scientist and Professor, Radiation Oncology and Medical Biophysics, University of Toronto and Ontario Cancer Institute/ (UHN) Head, PMH-CFCRI Prostate Cancer Research
More informationChronic lymphocytic EBMT Slideleukemia. University of Heidelberg, Germany March 22, 2010. The European Group for Blood and Marrow Transplantation
Chronic lymphocytic EBMT Slideleukemia template Peter Barcelona Dreger Chairman, CLL 7 February subcommittee 2008 University of Heidelberg, Germany March 22, 2010 The European Group for Blood and Marrow
More informationEffects of Herceptin on circulating tumor cells in HER2 positive early breast cancer
Effects of Herceptin on circulating tumor cells in HER2 positive early breast cancer J.-L. Zhang, Q. Yao, J.-H. Chen,Y. Wang, H. Wang, Q. Fan, R. Ling, J. Yi and L. Wang Xijing Hospital Vascular Endocrine
More informationCANCER GENETICS, INC.
UNITED STATES SECURITIES AND EXCHANGE COMMISSION WASHINGTON, D.C. 20549 FORM 10-K (Mark One) x ANNUAL REPORT PURSUANT TO SECTION 13 OR 15(d) OF THE SECURITIES EXCHANGE ACT OF 1934 For the fiscal year ended
More informationfor Leucocyte Immunophenotyping Leukaemia Diagnosis Interpretation All Participants Date Issued: 08-September-2014 Closing Date: 26-September-2014
for Leucocyte Immunophenotyping Leukaemia Interpretation All Participants Participant: 4xxxx Trial No: 141502 Date Issued: 08-September-2014 Closing Date: 26-September-2014 Trial Comments This was an electronic
More informationOutline of thesis and future perspectives.
Outline of thesis and future perspectives. This thesis is divided into two different sections. The B- section involves reviews and studies on B- cell non- Hodgkin lymphoma [NHL] and radioimmunotherapy
More informationCLL: Disease Course, Treatment, Diagnosis, and Biomarkers
CLL: Disease Course, Treatment, Diagnosis, and Biomarkers Amy E. Hanlon Newell, Ph.D. Manager, Scientific Affairs Abbott Molecular Overview: Today s Take-away Understanding of: Cell phenotype and clinical
More informationMultiple Myeloma. This reference summary will help you understand multiple myeloma and its treatment options.
Multiple Myeloma Introduction Multiple myeloma is a type of cancer that affects white blood cells. Each year, thousands of people find out that they have multiple myeloma. This reference summary will help
More informationCT-guided Biopsy of Focal Lesions in Patients with Multiple Myeloma May Reveal New and More Aggressive Cytogenetic Abnormalities
AJNR Am J Neuroradiol 22:781 785, April 2001 CT-guided Biopsy of Focal Lesions in Patients with Multiple Myeloma May Reveal New and More Aggressive Cytogenetic Abnormalities Ramesh Avva, Rudy L. Vanhemert,
More informationOncology Best Practice Documentation
Oncology Best Practice Documentation Click on the desired Diagnoses link or press Enter to view all information. Diagnoses: Solid Tumors Lymphomas Leukemias Myelodysplastic Syndrome Pathology Findings
More informationSpecial report. Chronic Lymphocytic Leukemia (CLL) Genomic Biology 3020 April 20, 2006
Special report Chronic Lymphocytic Leukemia (CLL) Genomic Biology 3020 April 20, 2006 Gene And Protein The gene that causes the mutation is CCND1 and the protein NP_444284 The mutation deals with the cell
More informationLCFA/IASLC LORI MONROE SCHOLARSHIP IN TRANSLATIONAL LUNG CANCER RESEARCH
LCFA/IASLC LORI MONROE SCHOLARSHIP IN TRANSLATIONAL LUNG CANCER RESEARCH FUNDING OPPORTUNITY DESCRIPTION 2016 REQUEST FOR APPLICATION (RFA) Lung Cancer Foundation of America (LCFA) and the International
More informationPROTOCOLS FOR TREATMENT OF MALIGNANT LYMPHOMA
2012 1 31,, PROTOCOLS FOR TREATMENT OF MALIGNANT LYMPHOMA Version 1.0 2012 DIVISION OF HAEMATOLOGY / ONCOLOGY DEPARTMENT OF MEDICINE KAOHSING VETERAN GENERAL HOSPTIAL General Guide Diagnosis 1.Adequate
More informationSommaire projets sélectionnés mesure 29: Soutien à la recherche translationnelle
Sommaire projets sélectionnés mesure 29: Soutien à la recherche translationnelle TITLE PROJET NOM HOPITAL Assessment of tumor angiogenesis using PET/CT with 18 F-Galacto- RGD. (PNC_29_001) Division of
More informationAcute Myeloid Leukemia
Acute Myeloid Leukemia Introduction Leukemia is cancer of the white blood cells. The increased number of these cells leads to overcrowding of healthy blood cells. As a result, the healthy cells are not
More informationB-cell Chronic Lymphocytic Leukemia/Small Lymphocytic Lymphoma
2008 WHO Classification of Lymphoid Neoplasms: Small B-Cell Neoplasms Chronic lymphocytic leukemia/small lymphocytic lymphoma B-cell prolymphocytic leukemia Splenic marginal zone B-cell lymphoma Hairy
More informationEmerging New Prognostic Scoring Systems in Myelodysplastic Syndromes 2012
Emerging New Prognostic Scoring Systems in Myelodysplastic Syndromes 2012 Arjan A. van de Loosdrecht, MD, PhD Department of Hematology VU University Medical Center VU-Institute of Cancer and Immunology
More informationHER2 Testing in Breast Cancer
HER2 Testing in Breast Cancer GAIL H. VANCE, M.D. AGT MEETING JUNE 13, 2014 LOUISVILLE, KENTUCKY No Conflict of Interest to Report Human Epidermal Growth Factor Receptor 2-HER2 Human epidermal growth factor
More informationMonoclonal Gammopathy of Undetermined Significance (MGUS) Facts
Monoclonal Gammopathy of Undetermined Significance (MGUS) Facts Normal plasma cells (a type of white blood cell) produce antibodies (also known as immunoglobulins) which help fight infection. Each type
More informationFluorescence in situ hybridisation (FISH)
Fluorescence in situ hybridisation (FISH) rarechromo.org Fluorescence in situ hybridization (FISH) Chromosomes Chromosomes are structures that contain the genetic information (DNA) that tells the body
More informationHER2 Status: What is the Difference Between Breast and Gastric Cancer?
Ask the Experts HER2 Status: What is the Difference Between Breast and Gastric Cancer? Bharat Jasani MBChB, PhD, FRCPath Marco Novelli MBChB, PhD, FRCPath Josef Rüschoff, MD Robert Y. Osamura, MD, FIAC
More informationLymphoma Diagnosis and Classification
Lymphoma Diagnosis and Classification By Atef Shrit, MD, Pathology B- and T/NK-cell lymphomas are clonal neoplasms of immature and mature B-lymphocytes, T-lymphocytes or natural killer cells at various
More informationA Career in Pediatric Hematology-Oncology? Think About It...
A Career in Pediatric Hematology-Oncology? Think About It... What does a pediatric hematologist-oncologist do? What kind of training is necessary? Is there a future need for specialists in this area? T
More informationMultiple Myeloma Workshop- Tandem 2014
Multiple Myeloma Workshop- Tandem 2014 1) Review of Plasma Cell Disorders Asymptomatic (smoldering) myeloma M-protein in serum at myeloma levels (>3g/dL); and/or 10% or more clonal plasma cells in bone
More informationLeukemias and Lymphomas: A primer
Leukemias and Lymphomas: A primer Normal blood contains circulating white blood cells, red blood cells and platelets 700 red cells (oxygen) 1 white cell Neutrophils (60%) bacterial infection Lymphocytes
More informationMALIGNANT LYMPHOMAS. Dr. Olga Vujovic (Updated August 2010)
MALIGNANT LYMPHOMAS Dr. Olga Vujovic (Updated August 2010) Malignant lymphomas consist of Hodgkin and non-hodgkin lymphomas. The current management of these diseases involves a multi-disciplinary approach.
More informationMolekylært målrettet medicinsk kræftbehandling for klinikere principper og metoder
Molekylært målrettet medicinsk kræftbehandling for klinikere principper og metoder Professor Claus Lindbjerg Andersen Department of Molecular Medicine (MOMA) Aarhus University hospital Outline The central
More informationWhat is New in Oncology. Michael J Messino, MD Cancer Care of WNC An affiliate of Mission hospitals
What is New in Oncology Michael J Messino, MD Cancer Care of WNC An affiliate of Mission hospitals Personalized Medicine Personalized Genomics Genomic Medicine Precision Medicine Definition Application
More informationUses of Flow Cytometry
Uses of Flow Cytometry 1. Multicolour analysis... 2 2. Cell Cycle and Proliferation... 3 a. Analysis of Cellular DNA Content... 4 b. Cell Proliferation Assays... 5 3. Immunology... 6 4. Apoptosis... 7
More informationMantle Cell Lymphoma Understanding Your Treatment Options
New Developments in Mantle Cell Lymphoma John P. Leonard, M.D. Richard T. Silver Distinguished Professor of Hematology and Medical Oncology Associate Dean for Clinical Research Vice Chairman, Department
More informationSupplementary appendix
Supplementary appendix This appendix formed part of the original submission and has been peer reviewed. We post it as supplied by the authors. Supplement to: Farooqui MZH, Valdez J, Martyr S, et al. Ibrutinib
More informationNarrator: Transplants using stem cells from the blood, bone marrow or umbilical cord blood
[Track 2: What Is a Transplant?] Narrator: Transplants using stem cells from the blood, bone marrow or umbilical cord blood can be an effective treatment for people with blood cancers such as leukemia,
More informationguides BIOLOGY OF AGING STEM CELLS An introduction to aging science brought to you by the American Federation for Aging Research
infoaging guides BIOLOGY OF AGING STEM CELLS An introduction to aging science brought to you by the American Federation for Aging Research WHAT ARE STEM CELLS? Stem cells are cells that, in cell cultures
More informationCutaneous Lymphoma FAST FACTS
Cutaneous Lymphoma FAST FACTS What is Cutaneous Lymphoma? Cutaneous lymphomas are types of non-hodgkin s lymphomas (NHL) that originate in the lymphocytes (white blood cells). Unlike most other types of
More informationMature Lymphoproliferative disorders (2): Mature B-cell Neoplasms. Dr. Douaa Mohammed Sayed
Mature Lymphoproliferative disorders (2): Mature B-cell Neoplasms Dr. Douaa Mohammed Sayed Small lymphocytic lymphoma/b-cell chronic lymphocytic leukemia BMB: nodular, interstitial, diffuse or a combination
More informationCorporate Medical Policy
Corporate Medical Policy File Name: Origination: Last CAP Review: Next CAP Review: Last Review: hematopoietic_stem-cell_transplantation_for_epithelial_ovarian_cancer 2/2001 11/2015 11/2016 11/2015 Description
More informationWhen B Cells Go Bad: Infection, Inflammation and Chronic B Cell Stimulation
When B Cells Go Bad: Infection, Inflammation and Chronic B Cell Stimulation Karen S. Anderson MD PhD Associate Professor, Biodesign Institute Arizona State University Mayo Clinic Arizona Conflicts of Interest
More informationAbstract. Bone marrow-level oxygen tension enables enhanced and sustained growth of 3 new pediatric acute lymphoblastic leukemia cell lines
Abstract Bone marrow-level oxygen tension enables enhanced and sustained growth of 3 new pediatric acute lymphoblastic leukemia cell lines Michael A. Sheard, Min Kang, Daniel Cabral, Joanne Lee, Lilia
More informationNon-Hodgkin s Lymphoma
Non-Hodgkin s Lymphoma Luis Fayad, MD Assistant Professor Clinical Medical Director Lymphoma/Myeloma Department Non-Hodgkin s Lymphoma Non-Hodgkin s lymphomas (NHL) are a heterogeneous group of malignant
More informationPulling the Plug on Cancer Cell Communication. Stephen M. Ansell, MD, PhD Mayo Clinic
Pulling the Plug on Cancer Cell Communication Stephen M. Ansell, MD, PhD Mayo Clinic Why do Waldenstrom s cells need to communicate? Waldenstrom s cells need activating signals to stay alive. WM cells
More informationBone Marrow/Stem Cell Transplant
Blue Distinction Centers for Transplants Program Selection Criteria for 2010 Mid-Point Designations To qualify as a Blue Distinction Center for Transplants (), each facility must satisfy s quality based
More informationLEUKEMIA LYMPHOMA MYELOMA Advances in Clinical Trials
LEUKEMIA LYMPHOMA MYELOMA Advances in Clinical Trials OUR FOCUS ABOUT emerging treatments Presentation for: Judith E. Karp, MD Advancements for Acute Myelogenous Leukemia Supported by an unrestricted educational
More informationHodgkin and Non-Hodgkin Lymphoma Pre-HCT Data
(Form 2018) This section of the CIBMTR Forms Instruction Manual is intended to be a resource for completing the Hodgkin and Non-Hodgkin Lymphoma Pre-HCT Data Form. E-mail comments regarding the content
More information