PPT-Case 274 T lymphoblastic leukemia with t(5;14)(q35;q32) and lineage switch to acute myeloid

Author : ellena-manuel | Published Date : 2018-03-12

Rebecca L King Gerald Wertheim Michele E Paessler The Childrens Hospital of Philadelphia Perelman School of Medicine at the University of Pennsylvania Philadelphia

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Case 274 T lymphoblastic leukemia with t(5;14)(q35;q32) and lineage switch to acute myeloid: Transcript


Rebecca L King Gerald Wertheim Michele E Paessler The Childrens Hospital of Philadelphia Perelman School of Medicine at the University of Pennsylvania Philadelphia PA Clinical History 13 year old boy. Marisa Juntilla, MD, PhD. Stanford University Medical Center Stanford, California. Case 121: 58 year old man . Past medical history:. type II diabetes, coronary artery disease and severe diverticulitis, 1 month status-post colectomy, reported normal CBCs at his yearly primary care visits. . Hina. . Naushad. , M.D., Timothy C. Greiner M.D., . Radwa. El . Behery. M.D., Greg . Bociek. M.D., . Phuong L. Nguyen . M.D. . University of Nebraska Medical Center. Mayo Clinic. History. 24-year-old . Clinical History. A 6 year old female with past medical history of septo-optic dysplasia (congenital hypoplasia of the optic nerve, septum pellucidum absence, agenesis of the corpus callosum and pituitary hormone deficiencies) and growth hormone deficiency presented to the emergency department with limping and progressive left knee pain. MRI demonstrated findings suspicious for leukemia.. Clinical History. A 6 year old female with past medical history of septo-optic dysplasia (congenital hypoplasia of the optic nerve, septum pellucidum absence, agenesis of the corpus callosum and pituitary hormone deficiencies) and growth hormone deficiency presented to the emergency department with limping and progressive left knee pain. MRI demonstrated findings suspicious for leukemia.. Dr. . B.V.Vydehi. M.D. PROFESSOR OF PATHOLOGY. NARAYANA MEDICAL COLLEGE,NELLORE. Uncontrolled & abnormal proliferation of one of white blood cells & their precursors in the bone marrow and peripheral blood. 27. Learning Objectives—Level I. At the end of this unit of study, the student should be able to:. Define . acute lymphoblastic leukemia . (. ALL. ) and . lymphoblastic lymphoma . (. LBL. ) and differentiate them from acute myeloid leukemia (AML).. PROGNOSTIC FACTORS. Although the first published reports of leukemia occurred in 1845 by Bennett and Virchow, the lack of refined diagnostic methodology limited the distinction between myeloid and lymphoid acute leukemia, With the development of refined staining techniques, followed by microscopy and histochemical staining by the mid-20th century, this distinction was . Charles G. Eberhart M.D., Ph.D.. Johns . Hopkins University. Clinical History. The patient was a 43 year-old female with a past medical history significant for . monocytic. acute myeloid leukemia (AML) with FLT3 ITD mutation. . ental College (JIMDC); 201 3 ;2 ( 4 ): 58 - 63 58 Original Article Acute Myeloid Leukemia amongst Adults Naghmi Asif 1 and Khalid Hassan 2 1 Assistant Professor, Department of Pathology, Islamabad Me Medical Science Erythroleukemia with Complex Cytogenetic Abnormalities: A case report with review of literature Pooja K SureshPurnima S RaoUrmila N KhadilkarDepartment of Pathology, Kasturba Medical C Kelsey Shaffer. CHTN. Staff Meeting Presentation. What is it?. Acute Lymphoblastic Leukemia (ALL) is a blood cancer. White Blood Cells (WBC). Lymphocytes or Lymphoblast . Too many immature WBC. Crowd the bone marrow. Goals. Incidence. Etiology. Diagnosis. Types/Classification. Treatment. Primary Care Pearls. Incidence. 30% of all cancers in childhood. Peak incidence 2-5 years of age. males > females. Caucasian > African American. . A. ccumulation of abnormal blasts (. I. mmature precursors of WBC). . in bone marrow and blood leading to:. . 1- Bone marrow failure. . (. anemia ,neutropenia & thrombocytopenia). . 2- Organ infiltration . Jayllex Mills,. PharmD Candidate. AML Background. Hematologic malignancy affecting the blood and bone marrow. Result of proliferation of abnormal myeloid stem cell derivatives and interference of normal blood cell production.

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