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1. Verma D, O'Brien S, Thomas D, Faderl S, Koller C, Pierce S, Kebriaei P, Garcia-Manero G, Cortes J, Kantarjian H, Ravandi F: Therapy-related acute myelogenous leukemia and myelodysplastic syndrome in patients with acute lymphoblastic leukemia treated with the hyperfractionated cyclophosphamide, vincristine, doxorubicin, and dexamethasone regimens. Cancer; 2009 Jan 1;115(1):101-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Therapy-related acute myelogenous leukemia and myelodysplastic syndrome in patients with acute lymphoblastic leukemia treated with the hyperfractionated cyclophosphamide, vincristine, doxorubicin, and dexamethasone regimens.
  • BACKGROUND: Secondary malignancies including myeloid neoplasms occur infrequently in acute lymphoblastic leukemia (ALL) and to the authors' knowledge have not been as well documented in adults as in children.
  • RESULTS: Sixteen patients (2.49%) developed secondary acute myelogenous leukemia (AML) (6 patients) or myelodysplastic syndrome (MDS) (10 patients).
  • At the time of ALL diagnosis, the median age was 53 years; cytogenetics were normal in 11 patients, pseudo-diploidy with del(2) in 1 patient, t(9;22) in 1 patient, and unavailable in 3 patients.
  • Frontline therapy included hyper-CVAD in 7 patients, hyper-CVAD with rituximab in 8 patients, and hyper-CVAD with imatinib in 1 patient.
  • Karyotype at time of AML/MDS diagnosis was -5, -7 in 9 patients, normal in 1 patient, complex in 1 patient, inv(11) in 1 patient, t(4;11) in 1 patient, del(20) in 1 patient, and unavailable in 2 patients.
  • Secondary AML/MDS developed at a median of 32 months after ALL diagnosis.
  • Cytarabine plus anthracycline-based treatment was given to 12 patients with AML and high-risk MDS.
  • Response to treatment was complete remission in 3 patients, partial remission in 6 patients, and no response in 6 patients; 1 patient was untreated.
  • CONCLUSIONS: Secondary AML and MDS occur infrequently in adult patients with de novo ALL treated with the hyper-CVAD regimens, and response to therapy is poor.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Myeloid, Acute / chemically induced. Myelodysplastic Syndromes / chemically induced. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Cyclophosphamide / administration & dosage. Dexamethasone / administration & dosage. Doxorubicin / administration & dosage. Drug Administration Schedule. Humans. Middle Aged. Vincristine / administration & dosage


2. Simon M, Blatter J, Granzow C: Antifolate pseudo-resistance due to elevated levels of thymidine and hypoxanthine in a commercial serum preparation. Anticancer Res; 2007 Mar-Apr;27(2):769-73
Hazardous Substances Data Bank. GUANINE .

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  • [Title] Antifolate pseudo-resistance due to elevated levels of thymidine and hypoxanthine in a commercial serum preparation.
  • FCS Gold fully protected the cells from antifolate drug cytotoxicity.
  • Dialysis of FCS Gold restored responsiveness to antifolate drugs.
  • FBS Gold, should not be used in studies on antifolate drug action.
  • [MeSH-minor] Cell Growth Processes. Cell Line, Tumor. Dialysis. Drug Screening Assays, Antitumor / methods. Humans. KB Cells. Leukemia, T-Cell / drug therapy. Leukemia, T-Cell / metabolism. Leukemia, T-Cell / pathology. Pemetrexed. Serum

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  • (PMID = 17465201.001).
  • [ISSN] 0250-7005
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Culture Media; 0 / Folic Acid Antagonists; 0 / Glutamates; 04Q9AIZ7NO / Pemetrexed; 2TN51YD919 / Hypoxanthine; 5Z93L87A1R / Guanine; VC2W18DGKR / Thymidine; YL5FZ2Y5U1 / Methotrexate
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3. Prebet T, Lhoumeau AC, Arnoulet C, Aulas A, Marchetto S, Audebert S, Puppo F, Chabannon C, Sainty D, Santoni MJ, Sebbagh M, Summerour V, Huon Y, Shin WS, Lee ST, Esterni B, Vey N, Borg JP: The cell polarity PTK7 receptor acts as a modulator of the chemotherapeutic response in acute myeloid leukemia and impairs clinical outcome. Blood; 2010 Sep 30;116(13):2315-23
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  • [Title] The cell polarity PTK7 receptor acts as a modulator of the chemotherapeutic response in acute myeloid leukemia and impairs clinical outcome.
  • The pseudo tyrosine kinase receptor 7 (PTK7) is an orphan tyrosine kinase receptor assigned to the planar cell polarity pathway.
  • It plays a major role during embryogenesis and epithelial tissue organization.
  • We demonstrated that PTK7 is expressed in acute myeloid leukemia (AML) and is mostly assigned to granulocytic lineage differentiation.
  • Patients with PTK7-positive AML are more resistant to anthracycline-based frontline therapy with a significantly reduced leukemia-free survival in a multivariate analysis model.
  • In vitro, expression of PTK7 in cultured leukemia cells promotes cell migration, cell survival, and resistance to anthracycline-induced apoptosis.
  • We conclude that PTK7 is a planar cell polarity component expressed in the myeloid progenitor compartment that conveys promigratory and antiapoptotic signals into the cell and that represents an independent prognosis factor of survival in patients treated with induction chemotherapy.
  • [MeSH-major] Cell Adhesion Molecules / metabolism. Leukemia, Myeloid, Acute / drug therapy. Leukemia, Myeloid, Acute / metabolism. Receptor Protein-Tyrosine Kinases / metabolism
  • [MeSH-minor] Anthracyclines / pharmacology. Antibiotics, Antineoplastic / pharmacology. Apoptosis. Base Sequence. Cell Line, Tumor. Cell Movement. Cell Polarity. Cytogenetic Analysis. DNA Primers / genetics. Drug Resistance, Neoplasm. HL-60 Cells. Humans. Immunophenotyping. In Vitro Techniques. Jurkat Cells. K562 Cells. Prognosis. Treatment Outcome. U937 Cells

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  • (PMID = 20558616.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anthracyclines; 0 / Antibiotics, Antineoplastic; 0 / Cell Adhesion Molecules; 0 / DNA Primers; EC 2.7.1.- / PTK7 protein, human; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases
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4. Venizelos I, Theodoridou S, Vakalopoulou S, Perifanis V, Vyzantiadis T, Garipidou V: Acute large bowel pseudo-obstruction due to multiple myeloma. Leuk Lymphoma; 2004 Sep;45(9):1943-5
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  • [Title] Acute large bowel pseudo-obstruction due to multiple myeloma.
  • We report 1 case of a 61-year-old woman who presented with clinical and radiographic features of an acute large bowel pseudo-obstruction.
  • An abdominal computerized tomography (CT) showed a large tumor of the rectum.
  • The patient received combined chemotherapy and radiotherapy which led to the disappearance of the tumor.
  • A review of the literature revealed that this is the first reported case of MM presented as acute large bowel pseudo-obstruction due to a rectal myeloma tumor.
  • [MeSH-major] Colonic Pseudo-Obstruction / etiology. Colonic Pseudo-Obstruction / pathology. Multiple Myeloma / complications

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  • [Copyright] Copyright 2004 Taylor and Francis Ltd
  • (PMID = 15223660.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Membrane Glycoproteins; 0 / Proteoglycans; 0 / Syndecans
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5. Chen S, Wu D, Sun A, Qiu H, Jin Z, Tang X, Miao M, Fu Z, Ma X, Han Y, Hu X: Itraconazole-enhanced vindesine neurotoxicity in adult acute lymphoblastic leukaemia. Am J Hematol; 2007 Oct;82(10):942
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  • [Title] Itraconazole-enhanced vindesine neurotoxicity in adult acute lymphoblastic leukaemia.
  • [MeSH-major] Antifungal Agents / adverse effects. Intestinal Pseudo-Obstruction / chemically induced. Itraconazole / adverse effects. Peripheral Nervous System Diseases / chemically induced. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Vindesine / adverse effects
  • [MeSH-minor] Adult. Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Combined Modality Therapy. Cyclophosphamide / administration & dosage. Dexamethasone / administration & dosage. Doxorubicin / administration & dosage. Drug Synergism. Fatal Outcome. Female. Hematopoietic Stem Cell Transplantation. Humans. Idarubicin / administration & dosage. Male. Prednisolone / administration & dosage. Vincristine / administration & dosage

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  • (PMID = 17617780.001).
  • [ISSN] 0361-8609
  • [Journal-full-title] American journal of hematology
  • [ISO-abbreviation] Am. J. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antifungal Agents; 304NUG5GF4 / Itraconazole; 5J49Q6B70F / Vincristine; 7S5I7G3JQL / Dexamethasone; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; 9PHQ9Y1OLM / Prednisolone; RSA8KO39WH / Vindesine; ZRP63D75JW / Idarubicin; CVAD protocol; DVP regimen
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6. Ghosh K, Mitra S, Hiwase D: Choroidal infiltrates simulating fundal changes of acute leukemia during hematological recovery following high-dose chemotherapy in acute myelomonocytic leukemia in remission. Am J Hematol; 2000 Jan;63(1):42-5
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  • [Title] Choroidal infiltrates simulating fundal changes of acute leukemia during hematological recovery following high-dose chemotherapy in acute myelomonocytic leukemia in remission.
  • A young female patient of 18 who was diagnosed to have acute myelomonocytic leukemia (AML M4) developed choroidal infiltrate and fundal changes suggestive of acute leukemia deposits while she was in remission and was recovering from chemotherapy induced myelosuppression.
  • The choroidal lesion resolved on its own in 2 week's time, when the peripheral and CSF monocytosis subsided.
  • Interestingly this patient had pseudo-Chediak Higashi inclusions in leukemic blasts with normal karyotype.
  • [MeSH-major] Choroid / pathology. Leukemia, Myelomonocytic, Acute / drug therapy. Leukemia, Myelomonocytic, Acute / pathology
  • [MeSH-minor] Adolescent. Antineoplastic Agents / adverse effects. Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Cerebrospinal Fluid / cytology. Cytarabine / administration & dosage. Cytoplasmic Granules / pathology. Daunorubicin / administration & dosage. Female. Humans. Leukocyte Count. Mitoxantrone / administration & dosage. Monocytes / pathology. Remission Induction

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  • (PMID = 10602168.001).
  • [ISSN] 0361-8609
  • [Journal-full-title] American journal of hematology
  • [ISO-abbreviation] Am. J. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] UNITED STATES
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 04079A1RDZ / Cytarabine; BZ114NVM5P / Mitoxantrone; ZS7284E0ZP / Daunorubicin
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7. Cohen Y, Rund D, Moualem E, Kalish Y, Polliack A: Carbamazepine-induced generalized "pseudoleukemia lymphoma"--like syndrome. Isr Med Assoc J; 2003 Jun;5(6):457
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  • [Title] Carbamazepine-induced generalized "pseudoleukemia lymphoma"--like syndrome.
  • [MeSH-major] Anticonvulsants / adverse effects. Carbamazepine / adverse effects. Drug Hypersensitivity / etiology. Leukopenia / chemically induced. Lymphatic Diseases / chemically induced. Thrombocytopenia / chemically induced
  • [MeSH-minor] Adult. Biopsy. Epilepsy, Tonic-Clonic / drug therapy. Female. Fever / chemically induced. Fever / diagnosis. Fever / metabolism. Humans. L-Lactate Dehydrogenase / blood. Splenomegaly / chemically induced. Splenomegaly / diagnosis. Splenomegaly / metabolism

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  • (PMID = 12841027.001).
  • [ISSN] 1565-1088
  • [Journal-full-title] The Israel Medical Association journal : IMAJ
  • [ISO-abbreviation] Isr. Med. Assoc. J.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Israel
  • [Chemical-registry-number] 0 / Anticonvulsants; 33CM23913M / Carbamazepine; EC 1.1.1.27 / L-Lactate Dehydrogenase
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8. Chiang M, Fleming M: The pseudo-Pelger-Huët anomaly in pyoderma gangrenosum associated with myelodysplastic syndrome. Am J Dermatopathol; 2007 Jun;29(3):293-5
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  • [Title] The pseudo-Pelger-Huët anomaly in pyoderma gangrenosum associated with myelodysplastic syndrome.
  • We report a case of pyoderma gangrenosum in which most of the neutrophils exhibited the pseudo-Pelger-Huët (pPH) anomaly, a cytologic abnormality affecting the neutrophil nucleus.
  • These patients are also at risk for developing neutrophilic dermatosis as well as leukemia cutis, the main differential diagnosis.
  • [MeSH-minor] Administration, Oral. Administration, Topical. Aged, 80 and over. Fatal Outcome. Glucocorticoids / therapeutic use. Humans. Leg Ulcer / drug therapy. Leg Ulcer / etiology. Leg Ulcer / pathology. Male. Prednisone / therapeutic use


9. Park JA, Yun JH, Kang HJ, Shin HY, Ahn HS: Acute intestinal pseudo-obstruction after induction treatment of relapsed acute promyelocytic leukemia with arsenic trioxide. Pediatr Blood Cancer; 2008 Apr;50(4):872-4
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  • [Title] Acute intestinal pseudo-obstruction after induction treatment of relapsed acute promyelocytic leukemia with arsenic trioxide.
  • Arsenic trioxide (As(2)O(3)) is an effective agent for the treatment of relapsed acute promyelocytic leukemia (APL).
  • We report a patient with intestinal pseudo-obstruction, which occurred while treating relapsed APL with As(2)O(3).
  • A 6-year-old female with relapsed APL developed paralytic ileus, hyperleukocytosis, and a high fever while being treated with As(2)O(3).
  • This case history suggests that As(2)O(3) when used for reinduction therapy for APL may adversely affect the intestine and cause acute intestinal pseudo-obstruction.
  • [MeSH-major] Antineoplastic Agents / adverse effects. Arsenicals / adverse effects. Intestinal Pseudo-Obstruction / chemically induced. Intestinal Pseudo-Obstruction / pathology. Leukemia, Promyelocytic, Acute / drug therapy. Oxides / adverse effects
  • [MeSH-minor] Child. Digestive System Surgical Procedures. Female. Humans. Neoplasm Recurrence, Local / drug therapy

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  • [Copyright] (c) 2008 Wiley-Liss, Inc.
  • (PMID = 17635008.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Arsenicals; 0 / Oxides; S7V92P67HO / arsenic trioxide
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10. Young RP, Wu H: Intestinal pseudo-obstruction caused by diltiazem in a neutropenic patient. Ann Pharmacother; 2005 Oct;39(10):1749-51
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  • [Title] Intestinal pseudo-obstruction caused by diltiazem in a neutropenic patient.
  • OBJECTIVE: To describe a case of diltiazem-induced intestinal pseudo-obstruction in a neutropenic patient.
  • CASE SUMMARY: A 74-year-old male with newly diagnosed acute myelogenous leukemia developed atrial fibrillation on day 12 of induction chemotherapy.
  • Diltiazem 30 mg orally 4 times daily and amiodarone continuous infusion were started thereafter.
  • Amiodarone therapy was discontinued after one day due to an untoward adverse effect.
  • By day 14, the patient was receiving diltiazem 120 mg orally 4 times daily.
  • On day 15, he developed increasing abdominal distention with hyperactive bowel sounds.
  • On day 16, a radiographic examination showed multiple dilated loops of both the small and large bowel representing possible intestinal pseudo-obstruction; diltiazem was discontinued that day.
  • Starting on day 18, the patient showed recovery of intestinal pseudo-obstruction without intervention.
  • No further GI complications developed during his remaining hospital course.
  • DISCUSSION: Intestinal pseudo-obstruction is usually associated with underlying medical conditions such as trauma, infection, cardiac disease, and after surgery.
  • Medications rarely cause such a condition.
  • Detailed examination of the patient's record indicated neither infection nor other medications contributed to the development of intestinal pseudo-obstruction.
  • Use of the Naranjo probability scale indicated a probable relationship between pseudo-obstruction and diltiazem in this patient.
  • CONCLUSIONS: Although calcium-channel blockers rarely cause intestinal pseudo-obstruction, clinicians must be aware of this serious but reversible adverse effect.
  • [MeSH-major] Calcium Channel Blockers / adverse effects. Diltiazem / adverse effects. Intestinal Pseudo-Obstruction / chemically induced. Neutropenia / complications
  • [MeSH-minor] Aged. Atrial Fibrillation / complications. Atrial Fibrillation / drug therapy. Gastrointestinal Motility / drug effects. Humans. Male

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  • (PMID = 16144882.001).
  • [ISSN] 1060-0280
  • [Journal-full-title] The Annals of pharmacotherapy
  • [ISO-abbreviation] Ann Pharmacother
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Calcium Channel Blockers; EE92BBP03H / Diltiazem
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11. Diezi M, Nydegger A, Di Paolo ER, Kuchler H, Beck-Popovic M: Vincristine and intestinal pseudo-obstruction in children: report of 5 cases, literature review, and suggested management. J Pediatr Hematol Oncol; 2010 May;32(4):e126-30
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  • [Title] Vincristine and intestinal pseudo-obstruction in children: report of 5 cases, literature review, and suggested management.
  • SUMMARY: Intestinal pseudo-obstruction is a rare complication resulting from a variety of disorders.
  • Vincristine-related pseudo-obstruction has been reported in the literature, but its description in children and recommendations for management are lacking.
  • A review of the literature revealed 21 reported pediatric cases of vincristine-related pseudo-obstruction.
  • Most have, however, been attributed to a drug interaction with itraconazole, accidental vincristine overdose, or liver failure.
  • We present here 5 cases of pseudo-obstruction related to vincristine without any identifiable predisposing factors, and a suggested algorithm for management.
  • [MeSH-major] Antineoplastic Agents, Phytogenic / adverse effects. Hodgkin Disease / drug therapy. Intestinal Pseudo-Obstruction / chemically induced. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Vincristine / adverse effects. Wilms Tumor / drug therapy
  • [MeSH-minor] Adolescent. Algorithms. Child. Child, Preschool. Female. Humans. Kidney Neoplasms / drug therapy. Male. Survival Rate. Treatment Outcome

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  • (PMID = 20418785.001).
  • [ISSN] 1536-3678
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 5J49Q6B70F / Vincristine
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12. Pouw NM, Westerlaken EJ, Willemsen RA, Debets R: Gene transfer of human TCR in primary murine T cells is improved by pseudo-typing with amphotropic and ecotropic envelopes. J Gene Med; 2007 Jul;9(7):561-70

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Gene transfer of human TCR in primary murine T cells is improved by pseudo-typing with amphotropic and ecotropic envelopes.
  • BACKGROUND: T cell receptor (TCR) gene therapy represents an attractive anti-cancer treatment but requires further optimization of its efficacy and safety in clinically relevant models, such as those using a tumor antigen and TCR of human origin.
  • Currently, however, there is no consensus as to what protocol is most optimal for retroviral human TCR gene transfer into primary murine T cells, most notably with respect to virus pseudo-type.
  • To this end, murine leukemia virus (MLV) retroviruses were produced upon transfection of various packaging cells with genes encoding either green fluorescent protein (GFP) or TCRalphabeta specific for human melanoma antigen gp100(280-288) and the helper elements GAG/POL and ENV.
  • RESULTS: The pseudo-type of virus produced by packaging cells critically determines T cell transduction efficiencies.
  • In fact, MLV-A and MLV-E pseudo-typed viruses derived from a co-culture of Phoenix-A and 293T cells resulted in T cell transduction efficiencies that were two-fold higher than those based on retroviruses expressing either VSV-G, GALV, MLV-A or MLV-E envelopes.
  • CONCLUSIONS: We set up a quick and versatile method to genetically modify primary murine T cells based on transient production of TCR-positive retroviruses, and show that retroviral gene transfer of a human TCR into primary murine T cells is critically improved by viral pseudo-typing with both MLV-A and MLV-E envelopes.
  • [MeSH-major] Membrane Glycoproteins / metabolism. Receptors, Antigen, T-Cell / genetics. Receptors, Virus / metabolism. Sodium-Phosphate Cotransporter Proteins, Type III / metabolism. T-Lymphocytes / metabolism. T-Lymphocytes / virology. Transduction, Genetic / methods. Virus Assembly
  • [MeSH-minor] Animals. Antibodies, Monoclonal. Antigens, CD28 / immunology. Antigens, CD3 / immunology. Cell Count. Cell Proliferation / drug effects. Concanavalin A / pharmacology. Humans. Lymphocyte Activation / drug effects. Mice. Mice, Inbred C57BL. Retroviridae / genetics. Retroviridae / metabolism. Solubility / drug effects

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  • (PMID = 17471588.001).
  • [ISSN] 1099-498X
  • [Journal-full-title] The journal of gene medicine
  • [ISO-abbreviation] J Gene Med
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antigens, CD28; 0 / Antigens, CD3; 0 / Membrane Glycoproteins; 0 / Receptors, Antigen, T-Cell; 0 / Receptors, Virus; 0 / Sodium-Phosphate Cotransporter Proteins, Type III; 0 / ecotropic murine leukemia virus receptor; 11028-71-0 / Concanavalin A
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13. Breccia M, Girmenia C, Mecarocci S, Cartoni C, Carmosino I, Tafuri A, Alimena G: Ogilvie's syndrome in acute myeloid leukemia: pharmacological approach with neostigmine. Ann Hematol; 2001 Oct;80(10):614-6
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  • [Title] Ogilvie's syndrome in acute myeloid leukemia: pharmacological approach with neostigmine.
  • Acute colonic pseudo-obstruction, the so-called Ogilvie's syndrome, is a rare and life-threatening digestive complication usually observed in critically ill patients.
  • It is characterized by signs of large-bowel obstruction, without a mechanical cause, and has been reported in various settings, including acute leukemias as a complication of neutropenic enterocolitis after intensive chemotherapy.
  • We describe the case of a young woman who, during the neutropenic phase following autologous bone marrow transplantation for relapsed acute myeloid leukemia, developed neutropenic enterocolitis complicated by an acute pseudo-obstruction of descendent colon and sigma.
  • This process was associated with sepsis and resolved with conservative therapy of the underlying condition, using granulocyte colony-stimulating factor and intravenous neostigmine.
  • [MeSH-major] Cholinesterase Inhibitors / therapeutic use. Colonic Pseudo-Obstruction / drug therapy. Colonic Pseudo-Obstruction / etiology. Leukemia, Myeloid, Acute / complications. Neostigmine / therapeutic use
  • [MeSH-minor] Adult. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Bone Marrow Transplantation / adverse effects. Enterocolitis / complications. Female. Humans. Neutropenia / complications. Recurrence

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  • (PMID = 11732875.001).
  • [ISSN] 0939-5555
  • [Journal-full-title] Annals of hematology
  • [ISO-abbreviation] Ann. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Cholinesterase Inhibitors; 3982TWQ96G / Neostigmine
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14. Patton T, Zirwas M, Nieland-Fisher N, Jukic D: Inflammation of seborrheic keratoses caused by cytarabine: a pseudo sign of Leser-Trelat. J Drugs Dermatol; 2004 Sep-Oct;3(5):565-6
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  • [Title] Inflammation of seborrheic keratoses caused by cytarabine: a pseudo sign of Leser-Trelat.
  • Cytarabine, used for the treatment of acute myelogenous leukemia, can cause a rare reaction of inflammation of existing seborrheic keratoses.
  • We report a case of cytarabine induced inflammation of seborrheic keratoses mimicking a vesicular eruption in 53-year-old man with acute myelogenous leukemia.
  • [MeSH-minor] Humans. Leukemia, Myeloid, Acute / drug therapy. Male. Middle Aged

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  • (PMID = 15552612.001).
  • [ISSN] 1545-9616
  • [Journal-full-title] Journal of drugs in dermatology : JDD
  • [ISO-abbreviation] J Drugs Dermatol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 04079A1RDZ / Cytarabine
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15. He G, Wu D, Sun A, Xue Y, Jin Z, Qiu H, Tang X, Miao M, Fu Z, Ma X, Wang X, Chen Z, Ruan C: B-Lymphoid and myeloid lineages biphenotypic acute leukemia with t(8;21)(q22;q22). Int J Hematol; 2008 Mar;87(2):132-6
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  • [Title] B-Lymphoid and myeloid lineages biphenotypic acute leukemia with t(8;21)(q22;q22).
  • By analyzing the characteristics of morphology, immune phenotype, chromosome karyotype and clinical manifestations of six cases of B-lymphoid and myeloid lineages biphenotypic acute leukemia (BAL) with t(8;21)(q22;q22), a new subgroup of BAL was reported.
  • Bone marrow eosinophilia (more than 5%) and pseudo-Chediak abnormalities were not found.
  • Chemotherapy for myeloid and lymphoid leukemia simultaneously produced good response in the patients.
  • BAL with t(8; 21)(q22;.
  • q22) might be a new subgroup of BAL, and it was suggested that the leukemia clone with t(8;21)(q22;q22) might have originated from an early phase of hematopoiesis, and AML1/ETO fusion gene might be related to differentiation of B lymphocyte.
  • [MeSH-major] Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / pathology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology. Translocation, Genetic

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  • (PMID = 18288568.001).
  • [ISSN] 0925-5710
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, CD79; 0 / Antigens, Differentiation, Myelomonocytic; 0 / CD33 protein, human; 0 / CD79A protein, human; 0 / Sialic Acid Binding Ig-like Lectin 3
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16. Laille E, Ward R, Nasser A, Stoltz M, Cogle C, Gore S, Skikne BS, Garcia-Manero G: The pharmacokinetics of azacitidine following subcutaneous treatment in patients with myelodysplastic syndromes (MDS) or acute myelogenous leukemia (AML). J Clin Oncol; 2009 May 20;27(15_suppl):7087

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  • [Title] The pharmacokinetics of azacitidine following subcutaneous treatment in patients with myelodysplastic syndromes (MDS) or acute myelogenous leukemia (AML).
  • : 7087 Background: 5-azacitidine (AZA), through its effects on DNA metabolism, gene expression, and cell differentiation, has proven beneficial in treatment of MDS and AML and AZA therapy significantly increases survival in higher-risk MDS and AML compared to conventional care.
  • METHODS: Adult patients with MDS or AML and ECOG status 0-2 were treated with 7 consecutive daily SC doses of 75 mg/m<sup>2</sup> AZA during their first treatment cycle.
  • PK parameters of AZA were derived from drug concentrations in plasma and urine collected after the first and last dose (day 7) of AZA.
  • The AZA concs declined in a pseudo bi-phasic manner with an elimination half-life of 1.25 hours.
  • Vd/F was 4-5 fold greater than total body water suggesting extensive AZA tissue distribution.

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  • (PMID = 27961481.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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17. Işık P, Çetin I, Tavil B, Azik F, Kara A, Yarali N, Tunc B: All-transretinoic acid (ATRA) treatment-related pancarditis and severe pulmonary edema in a child with acute promyelocytic leukemia. J Pediatr Hematol Oncol; 2010 Nov;32(8):e346-8
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  • [Title] All-transretinoic acid (ATRA) treatment-related pancarditis and severe pulmonary edema in a child with acute promyelocytic leukemia.
  • Use of all-transretinoic acid (ATRA) with other chemotherapeutic agents in the treatment of acute promyelocytic leukemia (APL) has been shown to cause the differentiation of abnormally granulated specific blast cells into mature granulocytes by acting on the t(15;.
  • The complete remission rate is increased and survival time is prolonged in APL patients who receive chemotherapy plus ATRA, whereas ATRA syndrome and other ATRA-related adverse effects including pseudo tumor cerebri, headache, severe bone pain, mucosal and skin dryness, hypercholesterolemia, and cheilitis may be observed especially during induction phase of the treatment.
  • In this paper, we report a 9-year-old girl with APL who developed pancarditis while receiving the APL-93 treatment protocol.
  • In our patient, endocarditis and myocarditis were initially determined after ATRA treatment during the induction part of the protocol.
  • When ATRA was readministered in the maintenance part of the treatment protocol, she developed pancarditis and severe pulmonary edema.
  • As her symptoms decreased dramatically with the discontinuation of ATRA and the initiation of steroid treatment, the clinical picture strongly suggested the ATRA treatment as the causative factor.
  • To the best of our knowledge, this clinical picture of pancarditis secondary to ATRA treatment has not been reported earlier in the English literature.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / adverse effects. Leukemia, Promyelocytic, Acute / drug therapy. Myocarditis / chemically induced. Pulmonary Edema / chemically induced. Tretinoin / adverse effects

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  • (PMID = 20881874.001).
  • [ISSN] 1536-3678
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 5688UTC01R / Tretinoin
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18. Magro CM, De Moraes E, Burns F: Sweet's syndrome in the setting of CD34-positive acute myelogenous leukemia treated with granulocyte colony stimulating factor: evidence for a clonal neutrophilic dermatosis. J Cutan Pathol; 2001 Feb;28(2):90-6
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  • [Title] Sweet's syndrome in the setting of CD34-positive acute myelogenous leukemia treated with granulocyte colony stimulating factor: evidence for a clonal neutrophilic dermatosis.
  • BACKGROUND: Sweet's syndrome in the setting of hematologic dyscrasias can be categorized into paraneoplastic-associated SS, drug-induced SS, and SS with leukemia cutis.
  • METHODS: The authors present a patient with CD34+ acute myelogenous leukemia (AAML) who developed SS in the setting granulocyte colony stimulating factor (GCSF) therapy.
  • Routine light microscopy and molecular studies were carried on the patient's skin biopsy specimen and post-treatment marrow.
  • The neutrophils demonstrated dysplastic features including hypolobation compatible with a Pseudo Pelger-Huet anomaly.
  • X inactivation studies showed clonality both within her post-treatment marrow and skin biopsy specimen.
  • CONCLUSIONS: Sweet's syndrome developing in CD34+ AML patients following GCSF therapy likely reflects therapy induced differentiation of sequestered leukemic cells, hence indicative of a clonal neutrophilic dermatosis.
  • [MeSH-major] Granulocyte Colony-Stimulating Factor / therapeutic use. Leukemia, Myeloid / complications. Leukemia, Myeloid / drug therapy. Sweet Syndrome / etiology

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  • (PMID = 11168757.001).
  • [ISSN] 0303-6987
  • [Journal-full-title] Journal of cutaneous pathology
  • [ISO-abbreviation] J. Cutan. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Antigens, CD34; 143011-72-7 / Granulocyte Colony-Stimulating Factor; 9007-49-2 / DNA
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19. Yamamoto K, Yakushijin K, Nishikawa S, Minagawa K, Katayama Y, Shimoyama M, Matsui T: Imatinib resistance in a novel translocation der(17)t(1;17)(q25;p13) with loss of TP53 but without BCR/ABL kinase domain mutation in chronic myelogenous leukemia. Cancer Genet Cytogenet; 2008 May;183(1):77-81
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  • [Title] Imatinib resistance in a novel translocation der(17)t(1;17)(q25;p13) with loss of TP53 but without BCR/ABL kinase domain mutation in chronic myelogenous leukemia.
  • We describe here two novel translocations, t(7;14)(p22;q13) and der(17)t(1;17)(q25;p13), in a 41-year-old man with an accelerated phase (AP) of chronic myelogenous leukemia (CML).
  • Morphologically, dysplastic changes including pseudo-Pelger-Huët anomaly appeared in the bone marrow cells.
  • [MeSH-major] Chromosomes, Human, Pair 1. Chromosomes, Human, Pair 17. Genes, p53. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Piperazines / therapeutic use. Protein-Tyrosine Kinases / genetics. Pyrimidines / therapeutic use. Translocation, Genetic
  • [MeSH-minor] Adult. Benzamides. Disease Progression. Drug Resistance, Neoplasm / genetics. Fusion Proteins, bcr-abl. Gene Deletion. Genes, abl. Humans. Imatinib Mesylate. Male. Mutation. Protein Structure, Tertiary / genetics

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  • (PMID = 18474303.001).
  • [ISSN] 1873-4456
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / Fusion Proteins, bcr-abl
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20. Liu CZ, Persad R, Inghirami G, Sen F, Amorosi E, Goldenberg A, Ibrahim S: Transient atypical monocytosis mimic acute myelomonocytic leukemia in post-chemotherapy patients receiving G-CSF: report of two cases. Clin Lab Haematol; 2004 Oct;26(5):359-62
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Transient atypical monocytosis mimic acute myelomonocytic leukemia in post-chemotherapy patients receiving G-CSF: report of two cases.
  • Granulocyte colony-stimulating factor (G-CSF) is now widely used in patients with malignant disorders receiving intensive chemotherapy to increase leukocyte count and to upregulate phagocyte function during neutropenia.
  • We report two cases of pseudoleukemia secondary to G-CSF administration.
  • Both patients initially presented with myelodysplastic syndrome with chromosome 7 abnormalities that evolved into acute myeloid leukemia.
  • Case one had deletion 7q while case two initially had monosomy 7 and subsequently developed a balanced translocation between the short (p) arm of chromosome 1 and long (q) arm of chromosome 15.
  • Following the induction chemotherapy and G-CSF administration, both of these patients developed pseudoleukemia.
  • Patient 1 had white blood cell (WBC) count of 26 x 10(9)/l with 72% monocytes, while patient two had WBC of 14.1 x 10(9)/l with 30% monocytes.
  • In both patients the monocytosis resolved after the discontinuation of G-CSF therapy.
  • In those cases with pseudoleukemia discontinuation of the drug with no supplemental chemotherapy is probably enough to control the atypical monocytosis.
  • [MeSH-major] Granulocyte Colony-Stimulating Factor / therapeutic use. Leukemia, Myelomonocytic, Acute / diagnosis. Leukocytosis / chemically induced. Monocytes / drug effects
  • [MeSH-minor] Aged. Antineoplastic Agents / therapeutic use. Chromosome Aberrations. Cytogenetics. Diagnosis, Differential. Female. Humans. Leukemia, Myeloid / drug therapy. Leukemia, Myeloid / etiology. Leukemia, Myeloid / genetics. Leukocyte Count. Male. Myelodysplastic Syndromes / pathology

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  • (PMID = 15485468.001).
  • [ISSN] 0141-9854
  • [Journal-full-title] Clinical and laboratory haematology
  • [ISO-abbreviation] Clin Lab Haematol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 143011-72-7 / Granulocyte Colony-Stimulating Factor
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21. Hagino T, Kaito K, Asai O, Dobashi N, Yano S, Takei Y, Sugiyama K, Saito T, Okawa Y, Aiba K, Usui N: [Pseudoleukocytosis and pseudothrombocytosis caused by fragmentation of leukemic cells in tumor lysis syndrome]. Rinsho Ketsueki; 2007 Dec;48(12):1559-62

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  • Tumor lysis syndrome (TLS) is a severe complication of chemotherapy brought about by the rapid destruction of tumor cells.
  • We present a 22-year-old woman with acute lymphoblastic leukemia (ALL) complicated with TLS, in whom elevation of leukocytes and platelet count was observed due to fragmented leukocytes.
  • The day after initiating chemotherapy, a rapid increase in intracellular enzymes was found and a diagnosis of TLS was made.
  • The automated hematology analyzer counted these fragments as leukocytes or platelets, with resulting pseudo-leukocytosis and pseudo-thrombocytosis.
  • [MeSH-minor] Adult. Female. Humans. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology

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  • (PMID = 18203517.001).
  • [ISSN] 0485-1439
  • [Journal-full-title] [Rinshō ketsueki] The Japanese journal of clinical hematology
  • [ISO-abbreviation] Rinsho Ketsueki
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
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22. Kvasnicka HM, Thiele J, Schmitt-Graeff A, Schaefer HE: [Prognostic factors and survival in chronic myeloproliferative disorders]. Pathologe; 2000 Jan;21(1):63-72
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  • Patients with chronic myeloid leukemia (CML) showed an average life expectancy of 5 years, with significantly longer survival times under interferon treatment.
  • Furthermore, Pseudo-Gaucher cells indicated a favorable outcome in the cohort of patients receiving chemotherapy.
  • [MeSH-major] Bone Marrow / pathology. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / pathology. Myeloproliferative Disorders / mortality. Myeloproliferative Disorders / pathology
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Chronic Disease. Female. Follow-Up Studies. Humans. Male. Middle Aged. Retrospective Studies. Survival Analysis. Time Factors

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  • (PMID = 10663670.001).
  • [ISSN] 0172-8113
  • [Journal-full-title] Der Pathologe
  • [ISO-abbreviation] Pathologe
  • [Language] ger
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] GERMANY
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23. Thiele J, Kvasnicka HM, Schmitt-Graeff A, Schaefer HE: [Histologic and hematological findings in CML. A comparative immunohistochemical-morphometric and clinical study on bone marrow biopsies from 604 patients derived from two institutes of pathology (Cologne/Freiburg)]. Pathologe; 2000 Jan;21(1):39-54
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  • An immunohistochemical and morphometric study was performed on bone marrow biopsies in 604 patients with chronic myelogenous leukemia (CML) to compare morphological and clinical features and to evaluate effects of interferon (IFN) and chemotherapy.
  • The (alpha-D-galactosyl residue-expressing) Pseudo-Gaucher cells were detectable in 30% of pretreatment specimens.
  • The dynamics of myelofibrosis and changes of major cell lineages during treatment were readily demonstrable by calculating corresponding indices.
  • These included the ratios between quantitative differences of corresponding variables at repeated examinations and time.
  • This change was opposed to a numerical reduction in the myelofibrotic subtype which occurred in 17 patients (36%), but predominantly in those under HU therapy.
  • [MeSH-major] Bone Marrow / pathology. Hematopoietic Stem Cells / pathology. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / blood. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / pathology

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  • (PMID = 10663668.001).
  • [ISSN] 0172-8113
  • [Journal-full-title] Der Pathologe
  • [ISO-abbreviation] Pathologe
  • [Language] ger
  • [Publication-type] Comparative Study; English Abstract; Journal Article
  • [Publication-country] GERMANY
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24. Yoshida H, Endo H, Tanaka S, Ishikawa A, Kondo H, Nakamura T: Recurrent paralytic ileus associated with strongyloidiasis in a patient with systemic lupus erythematosus. Mod Rheumatol; 2006;16(1):44-7
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  • She was also a carrier of human T-cell leukemia virus type I.
  • Recurrent episodes of paralytic ileus due to strongyloidiasis occurred during treatment of her SLE with corticosteroids.
  • This case shows that symptomatic strongyloidiasis can be induced in immunocompromised hosts by immunosuppressive therapy.
  • It is important to rule out strongyloidiasis prior to starting immunosuppressive therapy in patients from endemic areas.


25. Li-Wan-Po A, Farndon P, Craddock C, Griffiths M: Integrating pharmacogenetics and therapeutic drug monitoring: optimal dosing of imatinib as a case-example. Eur J Clin Pharmacol; 2010 Apr;66(4):369-74
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  • [Title] Integrating pharmacogenetics and therapeutic drug monitoring: optimal dosing of imatinib as a case-example.
  • PURPOSE: To illustrate the interface of pharmacogenetics and therapeutic drug monitoring and to estimate target blood level for imatinib in the treatment of chronic myelogenous leukemia METHODS: A literature review to provide the evidence and necessary data to support the case for the interface, and quantitative analysis of the data to estimate the target blood level for imatinib using receiver operating curve (ROC; signal detection theory) analysis.
  • RESULTS AND DISCUSSION: One study estimated the optimum target level of imatinib in chronic myelogenous leukaemia as 1002 ng/mL (1.70 microM) through ROC analysis.
  • CONCLUSION: A single-dose regimen for all pharmacogenetically eligible patients is not the optimum strategy for prescribing imatinib to patients with chronic myelogenous leukaemia.
  • We suggest that therapeutic drug monitoring aimed at ensuring a trough target level of 1 microM would reduce the incidence of pseudo-resistance and hence personalize treatment and optimise response to imatinib.
  • [MeSH-major] Drug Monitoring. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Mutation. Piperazines / blood. Pyrimidines / blood
  • [MeSH-minor] Benzamides. Humans. Imatinib Mesylate. Pharmacogenetics. Treatment Outcome

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  • (PMID = 20111860.001).
  • [ISSN] 1432-1041
  • [Journal-full-title] European journal of clinical pharmacology
  • [ISO-abbreviation] Eur. J. Clin. Pharmacol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate
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26. Allsup DJ, Cawley JC: Diagnosis, biology and treatment of hairy-cell leukaemia. Clin Exp Med; 2004 Dec;4(3):132-8
SciCrunch. KEGG: Data: Disease Annotation .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Diagnosis, biology and treatment of hairy-cell leukaemia.
  • Hairy-cell leukaemia (HCL) is usually readily diagnosed by seeing typical hairy cells (HCs) in the blood film.
  • This HC activation is responsible for many of the pathological features of the disease, including its distinctive bone marrow fibrosis, splenic red pulp invasion, and pseudo-sinus formation.
  • Chlorodeoxyadenasine is the treatment of first choice.
  • Deoxycoformycin and rituximab are useful for the treatment of relapsed/refractory disease.
  • [MeSH-major] Leukemia, Hairy Cell / diagnosis. Leukemia, Hairy Cell / drug therapy

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  • (PMID = 15599661.001).
  • [ISSN] 1591-8890
  • [Journal-full-title] Clinical and experimental medicine
  • [ISO-abbreviation] Clin. Exp. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Italy
  • [Number-of-references] 28
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27. Saban SD, Nepomuceno RR, Gritton LD, Nemerow GR, Stewart PL: CryoEM structure at 9A resolution of an adenovirus vector targeted to hematopoietic cells. J Mol Biol; 2005 Jun 10;349(3):526-37
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • We report a sub-nanometer resolution cryo-electron microscopy (cryoEM) structural analysis of an adenoviral vector, Ad35F, comprised of an adenovirus type 5 (Ad5) capsid pseudo-typed with an Ad35 fiber.
  • This structural study increases our knowledge of Ad capsid assembly, antibody neutralization mechanisms, and may aid further improvements in gene delivery to important human cell types.
  • [MeSH-minor] Cryoelectron Microscopy. Gene Transfer Techniques. Hematopoietic Stem Cells / metabolism. Leukemia / drug therapy. Protein Structure, Tertiary. Viral Proteins / chemistry

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  • (PMID = 15890367.001).
  • [ISSN] 0022-2836
  • [Journal-full-title] Journal of molecular biology
  • [ISO-abbreviation] J. Mol. Biol.
  • [Language] eng
  • [Grant] United States / NIGMS NIH HHS / GM / T32-GM008320; United States / NIAID NIH HHS / AI / R01-AI42929; United States / NEI NIH HHS / EY / R01-EY11431; United States / NHLBI NIH HHS / HL / R01-HL54352
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Viral Proteins
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28. Jessop M, Choo K, Little M: Acute colonic pseudo-obstruction in paediatric oncology patients. J Paediatr Child Health; 2010 Nov;46(11):698-9
Hazardous Substances Data Bank. NEOSTIGMINE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Acute colonic pseudo-obstruction in paediatric oncology patients.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Colonic Pseudo-Obstruction / etiology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / complications
  • [MeSH-minor] Child. Constipation / complications. Constipation / drug therapy. Constipation / etiology. Female. Humans. Male. Neostigmine / therapeutic use. Parasympathomimetics / therapeutic use

  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
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  • (PMID = 21077980.001).
  • [ISSN] 1440-1754
  • [Journal-full-title] Journal of paediatrics and child health
  • [ISO-abbreviation] J Paediatr Child Health
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] Australia
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Parasympathomimetics; 3982TWQ96G / Neostigmine
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29. Marie I, Joly P, Levesque H, Heron F, Courville P, Cailleux N, Courtois H: Pseudo-dermatomyositis as a complication of hydroxyurea therapy. Clin Exp Rheumatol; 2000 Jul-Aug;18(4):536-7
Hazardous Substances Data Bank. HYDROXYUREA .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Pseudo-dermatomyositis as a complication of hydroxyurea therapy.
  • [MeSH-major] Antineoplastic Agents / adverse effects. Dermatomyositis / chemically induced. Hydroxyurea / adverse effects. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy

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  • (PMID = 10949738.001).
  • [ISSN] 0392-856X
  • [Journal-full-title] Clinical and experimental rheumatology
  • [ISO-abbreviation] Clin. Exp. Rheumatol.
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Antineoplastic Agents; X6Q56QN5QC / Hydroxyurea
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30. Yamamoto Y, Morii T, Kimura H: Paralytic ileus occurring during treatment with all-trans retinoic acid for acute promyelocytic leukemia. Int J Hematol; 2004 Feb;79(2):198-9
Hazardous Substances Data Bank. ALL-TRANS-RETINOIC ACID .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Paralytic ileus occurring during treatment with all-trans retinoic acid for acute promyelocytic leukemia.
  • [MeSH-major] Antineoplastic Agents / adverse effects. Intestinal Pseudo-Obstruction / chemically induced. Leukemia, Promyelocytic, Acute / drug therapy. Tretinoin / adverse effects

  • Genetic Alliance. consumer health - Acute Promyelocytic Leukemia.
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  • (PMID = 15005352.001).
  • [ISSN] 0925-5710
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Letter
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  • [Chemical-registry-number] 0 / Antineoplastic Agents; 5688UTC01R / Tretinoin
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