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Items 1 to 100 of about 170
1. Benitez D, Tkatchouk E, Gonzalez AZ, Goddard WA 3rd, Toste FD: On the impact of steric and electronic properties of ligands on gold(I)-catalyzed cycloaddition reactions. Org Lett; 2009 Nov 5;11(21):4798-801
Hazardous Substances Data Bank. GOLD, ELEMENTAL .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Both steric and electronic properties of the AuL(+) catalyst affect the electronic structure of the intermediate gold-stabilized carbene and its subsequent reactivity.

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  • (PMID = 19780543.001).
  • [ISSN] 1523-7052
  • [Journal-full-title] Organic letters
  • [ISO-abbreviation] Org. Lett.
  • [Language] ENG
  • [Grant] United States / NIGMS NIH HHS / GM / GM073932-04S1; United States / NIGMS NIH HHS / GM / R01 GM073932; United States / NIGMS NIH HHS / GM / R01 GM073932-04S1
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Alkadienes; 0 / Organogold Compounds; 4AV0LZ8QKB / propadiene; 7440-57-5 / Gold
  • [Other-IDs] NLM/ NIHMS149287; NLM/ PMC2783583
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2. Eiter LC, Hall NW, Day CS, Saluta G, Kucera GL, Bierbach U: Gold(I) analogues of a platinum-acridine antitumor agent are only moderately cytotoxic but show potent activity against Mycobacterium tuberculosis. J Med Chem; 2009 Nov 12;52(21):6519-22
Hazardous Substances Data Bank. GOLD, ELEMENTAL .

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  • Cationic gold(I) complexes containing 1-[2-(acridin-9-ylamino)ethyl]-1,3-dimethylthiourea (1), [AuL(1)](n+) (where L is Cl(-), Br(-), SCN(-), PEt(3), PPh(3), or 1), derived from a class of analogous platinum(II) antitumor agents, have been synthesized.
  • Unlike platinum, gold does not form permanent adducts with DNA, and its complexes are 2 orders of magnitude less cytotoxic in non-small-cell lung cancer cells than the most active platinum-based agent.

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  • (PMID = 19803526.001).
  • [ISSN] 1520-4804
  • [Journal-full-title] Journal of medicinal chemistry
  • [ISO-abbreviation] J. Med. Chem.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA101880-06; United States / NCI NIH HHS / CA / R01 CA101880; United States / NCI NIH HHS / CA / CA101880; United States / NCI NIH HHS / CA / R01 CA101880-06
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 1-(2-(acridin-9-ylamino)ethyl)-1,3-dimethylthiourea; 0 / Acridines; 0 / Antineoplastic Agents; 0 / Antitubercular Agents; 0 / Chelating Agents; 0 / Coordination Complexes; 0 / DNA Adducts; 0 / DNA, Bacterial; 0 / Ligands; 0 / Organogold Compounds; 49DFR088MY / Platinum; 7440-57-5 / Gold; 8W8T17847W / Urea; GYV9AM2QAG / Thiourea
  • [Other-IDs] NLM/ NIHMS150910; NLM/ PMC3176588
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3. Davey ML, Tsuneda A, Currah RS: Pathogenesis of bryophyte hosts by the ascomycete Atradidymella muscivora. Am J Bot; 2009 Jul;96(7):1274-80
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  • Pycnidia of the Phoma anamorph (P. muscivora) and uniloculate pseudothecia were initiated as tightly packed masses of stromatic dematiaceous hyphae within a single host cell.
  • A new microniche among bryophilous fungi is described, whereby A. muscivora supplants the gemmae of Aul. palustre and exploits the normal nutrient-flow of the moss gametophyte.
  • Atradidymella muscivora produced both cellulases and soluble polyphenolic oxidases, allowing it to also function as a saprobe and degrade the cell walls of bryophytes.

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  • (PMID = 21628276.001).
  • [ISSN] 0002-9122
  • [Journal-full-title] American journal of botany
  • [ISO-abbreviation] Am. J. Bot.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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4. Gujral S, Badrinath Y, Kumar A, Subramanian PG, Raje G, Jain H, Pais A, Amre Kadam PS, Banavali SD, Arora B, Kumar P, Hari Menon VG, Kurkure PA, Parikh PM, Mahadik S, Chogule AB, Shinde SC, Nair CN: Immunophenotypic profile of acute leukemia: critical analysis and insights gained at a tertiary care center in India. Cytometry B Clin Cytom; 2009 May;76(3):199-205
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  • [Title] Immunophenotypic profile of acute leukemia: critical analysis and insights gained at a tertiary care center in India.
  • BACKGROUND: To analyze the spectrum of various types and subtypes of acute leukemia.
  • METHODS: Two thousand five hundred and eleven consecutive new referral cases of acute leukemia (AL) were evaluated based on WHO classification.
  • RESULTS: It included 1,471 cases (58%) of acute lymphoblastic leukemia (ALL), 964 cases (38%) of acute myeloid leukemia (AML), 45 cases (1.8%) of chronic myelogenous leukemia in blast crisis (CMLBC), 37 cases (1.5%) of biphenotypic acute leukemia (BAL), 1 case of Triphenotypic AL, and 2 cases of acute undifferentiated leukemia (AUL).
  • Common subtypes of ALL were B-cell ALL (76%), which comprised of intermediate stage/CALLA positive (73%), early precursor/proBALL (3%).
  • T-cell ALL constituted 24% (351 cases) of ALL.
  • CONCLUSION: B-cell ALL was the commonest subtype in children and AML in adults.
  • A minimal primary panel of nine antibodies consisting of three myeloid markers (CD13, CD33, and CD117), B-cell lymphoid marker (CD19), T-cell marker (CD7), with CD45, CD10, CD34, and HLADR could assign lineage to 92% of AL.
  • [MeSH-major] Immunophenotyping. Leukemia / immunology. Leukemia / pathology
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Aged, 80 and over. Child. Child, Preschool. Cytogenetic Analysis. Female. Histocytochemistry. Humans. In Situ Hybridization. India. Infant. Infant, Newborn. Male. Middle Aged. Retrospective Studies. Reverse Transcriptase Polymerase Chain Reaction. Young Adult

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  • [Copyright] (c) 2008 Clinical Cytometry Society.
  • (PMID = 18803279.001).
  • [ISSN] 1552-4957
  • [Journal-full-title] Cytometry. Part B, Clinical cytometry
  • [ISO-abbreviation] Cytometry B Clin Cytom
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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5. Hashmi KU, Khan B, Ahmed P, Raza S, Hussain I, Mahmood A, Iqbal H, Malik HS, Anwar M: FLAG-IDA in the treatment of refractory/relapsed acute leukaemias: single centre study. J Pak Med Assoc; 2005 Jun;55(6):234-8
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  • [Title] FLAG-IDA in the treatment of refractory/relapsed acute leukaemias: single centre study.
  • OBJECTIVE: To evaluate the efficacy and toxicity profile of the combination of fludarabine, high dose cytarabine, idarubicin, and granulocyte colony stimulating factor in refractory relapsed cases of acute leukaemia, a study is being conducted at Armed Forces Bone Marrow Transplant Centre (AFBMTC) Rawalpindi since January 2003.
  • METHODS: Twelve Patients with refractory/relapsed (Ref/Rel) acute leukaemia (AL) were treated with fludarabine 30 mg/m2 and cytosine arabinoside (AraC) Arac 2 g/m2 for 5 days, idarubicin 10 mg/m2 for 3 days, and granulocyte colony stimulating factor G-CSF 5 micro g/kg from day 0 till neutrophil recovery (ANC > 1.0 x 10(9)/1).
  • RESULTS: Patients included were refractory acute lymphoblastic leukaemia (ALL) (n=2), relapsed ALL (n = 3), refractory acute myeloid leukaemia (AML) (n = 3), secondary AML (n=2) relapsed AML (n = 1) and acute undifferentiated leukaemia (AUL) (n = 1).
  • Out of 8 patients who achieved CR, 4 underwent allogeneic bone marrow transfusion (BMT), 1 is being evaluated for the same, 1 received idorubicin, AraC and etopuside (ICE) and high dose AraC, 1 did not receive further chemotherapy and 1 relapsed two months after remission.
  • CONCLUSION: In our experience, FLAG-IDA is well tolerated and effective regimen in relapsed/refractory acute leukaemias.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Leukemia, Myeloid / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Vidarabine / analogs & derivatives
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Antibiotics, Antineoplastic / therapeutic use. Antimetabolites, Antineoplastic / therapeutic use. Child. Cytarabine / therapeutic use. Female. Granulocyte Colony-Stimulating Factor / therapeutic use. Humans. Idarubicin / therapeutic use. Male. Middle Aged. Recurrence

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  • (PMID = 16045091.001).
  • [ISSN] 0030-9982
  • [Journal-full-title] JPMA. The Journal of the Pakistan Medical Association
  • [ISO-abbreviation] J Pak Med Assoc
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Pakistan
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / Antimetabolites, Antineoplastic; 04079A1RDZ / Cytarabine; 143011-72-7 / Granulocyte Colony-Stimulating Factor; FA2DM6879K / Vidarabine; P2K93U8740 / fludarabine; ZRP63D75JW / Idarubicin
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6. Afkir S, Nguelefack TB, Aziz M, Zoheir J, Cuisinaud G, Bnouham M, Mekhfi H, Legssyer A, Lahlou S, Ziyyat A: Arbutus unedo prevents cardiovascular and morphological alterations in L-NAME-induced hypertensive rats Part I: cardiovascular and renal hemodynamic effects of Arbutus unedo in L-NAME-induced hypertensive rats. J Ethnopharmacol; 2008 Mar 5;116(2):288-95
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  • The aim of the present study was to investigate whether chronic treatment with Arbutus unedo leaf (AuL) or root (AuR) aqueous extracts can prevent these alterations.
  • Six groups of rats were used: control group received tap water; N(G)-nitro-l-arginine methyl-ester (L-NAME) group treated with L-NAME at 40 mg/kg/day; AuL and AuR groups received simultaneously L-NAME (40 mg/kg/day) and Au leaves or roots extract at the same concentration 250 mg/kg/day; l-arginine and enalapril groups received simultaneously L-NAME (40 mg/kg/day) and l-arginine at 50mg/kg/day or enalapril at 15 mg/kg/day.
  • The co-administration of AuL or AuR extracts with L-NAME reduces the development of increased SBP, ameliorates the vascular reactivity as well as the baroreflex sensitivity and normalizes the renal function.
  • AuR reduces the ventricular hypertrophy but AuL do not.

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  • (PMID = 18191352.001).
  • [ISSN] 0378-8741
  • [Journal-full-title] Journal of ethnopharmacology
  • [ISO-abbreviation] J Ethnopharmacol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Plant Extracts; V55S2QJN2X / NG-Nitroarginine Methyl Ester
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7. Garg JA, Blacque O, Fox T, Venkatesan K: Stable and tunable phosphorescent neutral cyclometalated Au(III) diaryl complexes. Inorg Chem; 2010 Dec 20;49(24):11463-72

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  • A series of novel luminescent cyclometalated Au(III) neutral complexes of the type cis-[(N(∧)C)AuL] [N(∧)C = 2-phenylpyridine (ppy), L = 1,1'-biphenyl (1)] and cis-[(N(∧)C)AuL(2)] [N(∧)C = 2-phenylpyridine (ppy), L = C(6)H(5) (2), C(6)F(5) (3), C(6)H(4)-CF(3)-p (4), 2-C(4)H(3)S (5)]; [N(∧)C = 2-(2-thienyl)pyridine (thpy), L = C(6)H(5) (6), C(6)F(5) (7)]; [N(∧)C = 2-(5-methyl-2-thienyl)pyridine (5 m-thpy), L = C(6)F(5) (8)] were successfully synthesized.

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  • (PMID = 21073200.001).
  • [ISSN] 1520-510X
  • [Journal-full-title] Inorganic chemistry
  • [ISO-abbreviation] Inorg Chem
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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8. Kasumagic-Halilovic E, Prohic A, Karamehic J: Serum concentrations of interferon-gamma (IFN-g) in patients with alopecia areata: correlation with clinical type and duration of the disease. Med Arh; 2010;64(4):212-4
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  • A wide range of clinical presentations can occur-from a single patch of hair loss (alopecia unilocularis, AUl), multiple patches (alopecia multilocularis, AM) to complete loss of hair on the scalp (alopecia totalis, AT) or the entire body (alopecia universalis, AU).
  • The cause ofAA is unknown although most evidence supports the hypothesis that AA is a T-cell mediated autoimmune disease of the hair follicle and that cytokines play an important role.
  • Significantly elevated serum IFN-g were noticed in patients with AU type (11.81 +/- 1.11 pg/mL), expecialy those suffering from AT (12.30 +/- 0.93 pg/mL), compared with both patients with AUl (10.20 +/- 0.59 pg/mL) and patients with AM clinical type (10.21 +/- 0.78 pg/mL).
  • There was no significant difference in serum IFN-g concentration between patients with AUl and AM group, as well as between patients with AT and AU.

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  • (PMID = 21246917.001).
  • [Journal-full-title] Medicinski arhiv
  • [ISO-abbreviation] Med Arh
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Bosnia and Herzegovina
  • [Chemical-registry-number] 82115-62-6 / Interferon-gamma
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9. Chen S, Avakian H, Burkert VD, Eugenio P, Adams G, Amarian M, Ambrozewicz P, Anghinolfi M, Asryan G, Bagdasaryan H, Baillie N, Ball JP, Baltzell NA, Barrow S, Batourine V, Battaglieri M, Beard K, Bedlinskiy I, Bektasoglu M, Bellis M, Benmouna N, Berman BL, Biselli AS, Bonner BE, Bouchigny S, Boiarinov S, Bosted P, Bradford R, Branford D, Briscoe WJ, Brooks WK, Bültmann S, Butuceanu C, Calarco JR, Careccia SL, Carman DS, Carnahan B, Cazes A, Cole PL, Collins P, Coltharp P, Cords D, Corvisiero P, Crabb D, Crannell H, Crede V, Cummings JP, DeMasi R, DeVita R, De Sanctis E, Degtyarenko PV, Denizli H, Dennis L, Deur A, Dharmawardane KV, Dhuga KS, Djalali C, Dodge GE, Donnelly J, Doughty D, Dugger M, Dytman S, Dzyubak OP, Egiyan H, Egiyan KS, El Fassi L, Elouadrhiri L, Fatemi R, Fedotov G, Feldman G, Feuerbach RJ, Forest TA, Funsten H, Garçon M, Gavalian G, Gilfoyle GP, Giovanetti KL, Girod FX, Goetz JT, Golovatch E, Gonenc A, Gothe RW, Griffioen KA, Guidal M, Guillo M, Guler N, Guo L, Gyurjyan V, Hadjidakis C, Hafidi K, Hakobyan H, Hakobyan RS, Hardie J, Heddle D, Hersman FW, Hicks K, Hleiqawi I, Holtrop M, Huertas M, Hyde-Wright CE, Ilieva Y, Ireland DG, Ishkhanov BS, Isupov EL, Ito MM, Jenkins D, Jo HS, Joo K, Juengst HG, Keith C, Kellie JD, Khandaker M, Kim KY, Kim K, Kim W, Klein A, Klein FJ, Klusman M, Kossov M, Kramer LH, Kubarovsky V, Kuhn J, Kuhn SE, Kuleshov SV, Lachniet J, Laget JM, Langheinrich J, Lawrence D, Li J, Lima AC, Livingston K, Lu H, Lukashin K, MacCormick M, Markov N, McAleer S, McKinnon B, McNabb JW, Mecking BA, Mestayer MD, Meyer CA, Mibe T, Mikhailov K, Minehart R, Mirazita M, Miskimen R, Mokeev V, Morand L, Morrow SA, Moteabbed M, Mueller J, Mutchler GS, Nadel-Turonski P, Napolitano J, Nasseripour R, Natasha N, Niccolai S, Niculescu G, Niculescu I, Niczyporuk BB, Niroula MR, Niyazov RA, Nozar M, O'Rielly GV, Osipenko M, Ostrovidov AI, Park K, Pasyuk E, Paterson C, Philips SA, Pierce J, Pivnyuk N, Pocanic D, Pogorelko O, Polli E, Popa I, Pozdniakov S, Preedom BM, Price JW, Prok Y, Protopopescu D, Qin LM, Raue BA, Riccardi G, Ricco G, Ripani M, Ritchie BG, Ronchetti F, Rosner G, Rossi P, Rowntree D, Rubin PD, Sabatié F, Salgado C, Santoro JP, Sapunenko V, Schumacher RA, Serov VS, Sharabian YG, Shaw J, Shvedunov NV, Skabelin AV, Smith ES, Smith LC, Sober DI, Stavinsky A, Stepanyan SS, Stepanyan S, Stokes BE, Stoler P, Strakovsky II, Strauch S, Suleiman R, Taiuti M, Tedeschi DJ, Thoma U, Tkabladze A, Tkachenko S, Todor L, Tur C, Ungaro M, Vanderhaeghen M, Vineyard MF, Vlassov AV, Watts DP, Weinstein LB, Weygand DP, Williams M, Wolin E, Wood MH, Yegneswaran A, Yun J, Zana L, Zhang J, Zhao B, Zhao Z, CLAS Collaboration: Measurement of deeply virtual compton scattering with a polarized-proton target. Phys Rev Lett; 2006 Aug 18;97(7):072002
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  • The longitudinal target-spin asymmetry AUL for the exclusive electroproduction of high-energy photons was measured for the first time in ep-->e;'pgamma.

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  • (PMID = 17026221.001).
  • [ISSN] 0031-9007
  • [Journal-full-title] Physical review letters
  • [ISO-abbreviation] Phys. Rev. Lett.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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10. Sun XL, Fang MY, Jiang F, Jing Y: [Immunologic classification used in typing of 68 cases of acute leukemias]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2006 Feb;14(1):39-41
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  • [Title] [Immunologic classification used in typing of 68 cases of acute leukemias].
  • To evaluate the significance of immunologic classification for typing of acute leukemia (AL).
  • In conclusion, immunologic classification can improve the accuracy in acute leukemia diagnosis.
  • The diagnosis of some special AL, such as acute unidentified leukemia (AUL), AML-M(0) and so on, must rely on immunologic classification.

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  • (PMID = 16584588.001).
  • [ISSN] 1009-2137
  • [Journal-full-title] Zhongguo shi yan xue ye xue za zhi
  • [ISO-abbreviation] Zhongguo Shi Yan Xue Ye Xue Za Zhi
  • [Language] CHI
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, CD14; 0 / Antigens, CD34; 0 / Antigens, CD7; 0 / Antigens, Differentiation, Myelomonocytic; 0 / CD33 protein, human; 0 / Sialic Acid Binding Ig-like Lectin 3; EC 3.4.11.2 / Antigens, CD13
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11. Awaleh MO, Baril-Robert F, Reber C, Badia A, Brosse F: Gold(I)-dithioether supramolecular polymers: synthesis, characterization, and luminescence. Inorg Chem; 2008 Apr 21;47(8):2964-74
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  • In complexes 1 {[AuL(1-Me)Cl], where L(1-Me) is bis(methylthio)methane} and 2 {[Au2L(2-Ph)Cl2], where L(2-Ph) is 1,2-bis(phenylthio)ethane}, adjacent units are connected via aurophilic interactions.
  • The third polymorph, 4c, is a molecular complex, as it does not have metal-metal interactions.
  • Complexes 1, 2, and 6 {[AuL(3-Me)Cl], where L(3-Me) is 1,3-bis(methylthio)propane} exhibited solid-state luminescence at 5 K with vibronic progressions and band maxima at approximately 570 nm.

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  • (PMID = 18366159.001).
  • [ISSN] 0020-1669
  • [Journal-full-title] Inorganic chemistry
  • [ISO-abbreviation] Inorg Chem
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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12. Crespo O, Gimeno MC, Laguna A, Larraz C, Villacampa MD: Highly luminescent gold(I)-silver(I) and gold(I)-copper(I) chalcogenide clusters. Chemistry; 2007;13(1):235-46
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  • The reactions of [AuClL] with Ag(2)O, where L represents the heterofunctional ligands PPh(2)py and PPh(2)CH(2)CH(2)py, give the trigoldoxonium complexes [O(AuL)(3)]BF(4).
  • Treatment of these compounds with thio- or selenourea affords the triply bridging sulfide or selenide derivatives [E(AuL)(3)]BF(4) (E=S, Se).

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  • (PMID = 17009375.001).
  • [ISSN] 0947-6539
  • [Journal-full-title] Chemistry (Weinheim an der Bergstrasse, Germany)
  • [ISO-abbreviation] Chemistry
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
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13. Rao SR, Hassett M, Schwartz JH, Maloney B, Jacobson JO: Admissions for chemotherapy-related serious adverse effects (CR-SAEs) and rates of mortality among community cancer center patients. J Clin Oncol; 2009 May 20;27(15_suppl):6571

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  • METHODS: We conducted a prospective cohort study of adult cancer patients (excluding acute leukemia and stem cell transplant patients) admitted to a community hospital January 2003-December 2006.
  • The average time from chemotherapy to admission was shorter for fatal vs. non-fatal admissions (3.6 vs. 7.7 days; p<.01).
  • CONCLUSIONS: Fatalities during admissions for CR-SAE's in a community cancer center are relatively uncommon and are not associated with age or type of SAE/cancer.

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  • (PMID = 27963798.001).
  • [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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14. Aul K: Calling to say good-bye. Nursing; 2006 May;36(5):64hh8

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  • [Title] Calling to say good-bye.

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  • (PMID = 29019846.001).
  • [ISSN] 1538-8689
  • [Journal-full-title] Nursing
  • [ISO-abbreviation] Nursing
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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15. Dass A, Stevenson A, Dubay GR, Tracy JB, Murray RW: Nanoparticle MALDI-TOF mass spectrometry without fragmentation: Au25(SCH2CH2Ph)18 and mixed monolayer Au25(SCH2CH2Ph)(18-x)(L)(x). J Am Chem Soc; 2008 May 7;130(18):5940-6
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  • At increased laser pulse intensity, the first fragmentation step(s) for the Au25(SCH 2CH2Ph)18 nanoparticle results in losses of AuL units and, in particular, loss of Au4(SCH2CH2Ph)4.

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  • (PMID = 18393500.001).
  • [ISSN] 1520-5126
  • [Journal-full-title] Journal of the American Chemical Society
  • [ISO-abbreviation] J. Am. Chem. Soc.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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16. Rodríguez-Rodríguez CE, Marco-Urrea E, Caminal G: Degradation of naproxen and carbamazepine in spiked sludge by slurry and solid-phase Trametes versicolor systems. Bioresour Technol; 2010 Apr;101(7):2259-66
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  • Detectable laccase activity levels were found in the 10 and 25%-cultures (up to 1308 and 2588 AUL(-1), respectively) while it was negligible in the 38%-culture.

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  • [Copyright] Copyright 2009 Elsevier Ltd. All rights reserved.
  • (PMID = 20031398.001).
  • [ISSN] 1873-2976
  • [Journal-full-title] Bioresource technology
  • [ISO-abbreviation] Bioresour. Technol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Sewage; 33CM23913M / Carbamazepine; 57Y76R9ATQ / Naproxen; EC 1.10.3.2 / Laccase; IY9XDZ35W2 / Glucose
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17. Tan S, Wang G, Peng M, Zhang X, Shen G, Jiang J, Chen F: Detection of myeloperoxidase activity in primary leukemic cells by an enhanced chemiluminescent assay for differentiation between acute lymphoblastic and non-lymphoblastic leukemia. Clin Chim Acta; 2009 May;403(1-2):216-8
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  • [Title] Detection of myeloperoxidase activity in primary leukemic cells by an enhanced chemiluminescent assay for differentiation between acute lymphoblastic and non-lymphoblastic leukemia.
  • BACKGROUND: Myeloperoxidase (MPO) plays a crucial role in the differentiation of acute lymphoblastic leukemia (ALL) and acute non-lymphoblastic leukemia (ANLL).
  • In this report, we proposed the application of the enhanced chemiluminescent (ECL) technique to the determination of MPO activity in blasts of acute leukemia (AL).
  • METHODS: Bone-marrow samples were obtained from 23 patients with AL (ALL, 5 cases; ANLL, 13 cases; AUL, 1 cases; mixed-lineage AL, 4 cases).
  • In addition, this technique was able to demonstrate MPO activity in 4 mixed-lineage AL cases which did not stain for MPO in cytochemistry preparations.
  • [MeSH-major] Leukemia, Myeloid, Acute / enzymology. Leukemia, Myeloid, Acute / pathology. Luminescent Measurements / methods. Peroxidase / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / enzymology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology
  • [MeSH-minor] Adolescent. Adult. Aged. Child. Diagnosis, Differential. Female. HL-60 Cells. Humans. Infant. Male. Middle Aged

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  • (PMID = 19298796.001).
  • [ISSN] 1873-3492
  • [Journal-full-title] Clinica chimica acta; international journal of clinical chemistry
  • [ISO-abbreviation] Clin. Chim. Acta
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] EC 1.11.1.7 / Peroxidase
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18. Fields-Zinna CA, Sampson JS, Crowe MC, Tracy JB, Parker JF, deNey AM, Muddiman DC, Murray RW: Tandem mass spectrometry of thiolate-protected Au nanoparticles Na(x)Au25(SC2H4Ph)(18-y)(S(C2H4O)5CH3)(y). J Am Chem Soc; 2009 Sep 30;131(38):13844-51
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  • Prominent among the fragments is [Na(2)AuL(2)](1+), one precursor of which is identified as another nanoparticle fragment in the higher m/z region.
  • The detailed dissociation/rearrangement mechanisms of these species are not established, but they are observed in other mass spectrometry experiments, including those under non-CID conditions, namely, electrospray ionization mass spectrometry (ESI-MS) with both time-of-flight (TOF) and FT-ICR analyzers.

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  • (PMID = 19736992.001).
  • [ISSN] 1520-5126
  • [Journal-full-title] Journal of the American Chemical Society
  • [ISO-abbreviation] J. Am. Chem. Soc.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Sulfhydryl Compounds; 7440-57-5 / Gold
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19. Salmon JM, Slater NJ, Hall MA, McCormack MP, Nutt SL, Jane SM, Curtis DJ: Aberrant mast-cell differentiation in mice lacking the stem-cell leukemia gene. Blood; 2007 Nov 15;110(10):3573-81
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  • [Title] Aberrant mast-cell differentiation in mice lacking the stem-cell leukemia gene.
  • The stem cell leukemia (SCL) gene encodes a basic helix-loop-helix transcription factor expressed in erythroid, megakaryocyte, and mast-cell lineages.
  • SCL(-/Delta) mice had markedly increased numbers of mast-cell progenitors (MCPs) within the peritoneal fluid, bone marrow, and spleen.
  • Fractionation of bone marrow myeloid progenitors demonstrated that these MCPs were present in the megakaryocyte-erythroid-restricted cell fraction.
  • In contrast, unilineage MCPs from control mice were present in the cell fraction with granulocyte-macrophage potential.
  • The aberrant mast-cell differentiation of SCL(-/Delta) megakaryocyte-erythroid progenitors was associated with increased expression of GATA-2.
  • Despite increased numbers of MCPs in SCL(-/Delta) mice, numbers of mature tissue mast cells were not increased unless SCL(-/Delta) mice were treated with IL-3 and stem-cell factor.
  • In part, this may be due to a requirement for SCL in normal mast-cell maturation: SCL(-/Delta) mast cells had reduced expression of the high-affinity IgE receptor and mast cell proteases, MCP-5 and MCP-6.
  • Together, these studies suggest that loss of SCL leads to aberrant mast-cell differentiation of megakaryocyte-erythroid progenitors.
  • [MeSH-major] Basic Helix-Loop-Helix Transcription Factors / genetics. Cell Differentiation / genetics. Mast Cells / cytology. Proto-Oncogene Proteins / genetics
  • [MeSH-minor] Animals. Cell Count. Cells, Cultured. Erythroid Cells / cytology. GATA2 Transcription Factor / genetics. Humans. Leukemia / genetics. Macrophages / cytology. Megakaryocytes / cytology. Mice. Mice, Inbred C57BL. Mice, Transgenic. Stem Cells / cytology. Transfection. Up-Regulation


20. Hall MA, Slater NJ, Begley CG, Salmon JM, Van Stekelenburg LJ, McCormack MP, Jane SM, Curtis DJ: Functional but abnormal adult erythropoiesis in the absence of the stem cell leukemia gene. Mol Cell Biol; 2005 Aug;25(15):6355-62
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  • [Title] Functional but abnormal adult erythropoiesis in the absence of the stem cell leukemia gene.
  • Previous studies have indicated that the stem cell leukemia gene (SCL) is essential for both embryonic and adult erythropoiesis.
  • We have examined erythropoiesis in conditional SCL knockout mice for at least 6 months after loss of SCL function and report that SCL was important but not essential for the generation of mature red blood cells.
  • The unexpected finding that SCL-independent erythropoiesis can proceed in the adult suggests that alternate factors can replace the essential functions of SCL and raises the possibility that similar mechanisms also explain the relatively minor defects previously observed in SCL-null hematopoietic stem cells.

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  • (PMID = 16024775.001).
  • [ISSN] 0270-7306
  • [Journal-full-title] Molecular and cellular biology
  • [ISO-abbreviation] Mol. Cell. Biol.
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / P01 HL053749; United States / NHLBI NIH HHS / HL / R01 HL069232; United States / NHLBI NIH HHS / HL / P01 HL53749-03; United States / NHLBI NIH HHS / HL / R01 HL69232-01
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / DNA-Binding Proteins; 0 / Proto-Oncogene Proteins; 0 / Tal1 protein, mouse; 0 / Transcription Factors
  • [Other-IDs] NLM/ PMC1190361
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21. Silberstein L, Sánchez MJ, Socolovsky M, Liu Y, Hoffman G, Kinston S, Piltz S, Bowen M, Gambardella L, Green AR, Göttgens B: Transgenic analysis of the stem cell leukemia +19 stem cell enhancer in adult and embryonic hematopoietic and endothelial cells. Stem Cells; 2005 Oct;23(9):1378-88
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  • [Title] Transgenic analysis of the stem cell leukemia +19 stem cell enhancer in adult and embryonic hematopoietic and endothelial cells.
  • Appropriate transcriptional regulation is critical for the biological functions of many key regulatory genes, including the stem cell leukemia (SCL) gene.
  • As part of a systematic dissection of SCL transcriptional regulation, we have previously identified a 5,245-bp SCL +18/19 enhancer that targeted embryonic endothelium together with embryonic and adult hematopoietic progenitors and stem cells (HSCs).
  • This enhancer is proving to be a powerful tool for manipulating hematopoietic progenitors and stem cells, but the design and interpretation of such transgenic studies require a detailed understanding of enhancer activity in vivo.
  • Moreover, activity in a proportion of thymocytes and other SCL-negative cell types suggests the existence of a silencer elsewhere in the SCL locus.
  • [MeSH-major] Basic Helix-Loop-Helix Transcription Factors / genetics. Enhancer Elements, Genetic / genetics. Hematopoietic Stem Cells / cytology. Proto-Oncogene Proteins / genetics
  • [MeSH-minor] Animals. Bone Marrow Cells / cytology. Cell Lineage. Endothelial Cells / cytology. Endothelial Cells / enzymology. Female. Gene Expression Regulation, Developmental / genetics. Gene Expression Regulation, Enzymologic / genetics. Male. Mast Cells / cytology. Mast Cells / enzymology. Megakaryocytes / cytology. Megakaryocytes / enzymology. Mice. Mice, Inbred C57BL. Mice, Inbred CBA. Mice, Transgenic. beta-Galactosidase / biosynthesis. beta-Galactosidase / blood. beta-Galactosidase / genetics

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  • (PMID = 16051983.001).
  • [ISSN] 1066-5099
  • [Journal-full-title] Stem cells (Dayton, Ohio)
  • [ISO-abbreviation] Stem Cells
  • [Language] eng
  • [Grant] United Kingdom / Wellcome Trust / /
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / Proto-Oncogene Proteins; 0 / Tal1 protein, mouse; EC 3.2.1.23 / beta-Galactosidase
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22. Schlaeger TM, Mikkola HK, Gekas C, Helgadottir HB, Orkin SH: Tie2Cre-mediated gene ablation defines the stem-cell leukemia gene (SCL/tal1)-dependent window during hematopoietic stem-cell development. Blood; 2005 May 15;105(10):3871-4
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  • [Title] Tie2Cre-mediated gene ablation defines the stem-cell leukemia gene (SCL/tal1)-dependent window during hematopoietic stem-cell development.
  • The stem-cell leukemia gene (SCL/tal1) is essential for the formation of all blood lineages.
  • SCL is first expressed in mesodermal cells that give rise to embryonic blood cells, and continues to be expressed in fetal and adult hematopoietic stem cells (HSCs).
  • However, SCL is not required for the maintenance of established long-term repopulating (LTR) HSCs in the adult.
  • The time point at which HSC development becomes SCL independent has not been defined.
  • [MeSH-major] Cell Differentiation. DNA-Binding Proteins / metabolism. Hematopoietic Stem Cells / cytology. Hematopoietic Stem Cells / metabolism. Integrases / metabolism. Proto-Oncogene Proteins / metabolism. Receptor, TIE-2 / metabolism. Transcription Factors / metabolism. Viral Proteins / metabolism

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  • (PMID = 15677556.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / DNA-Binding Proteins; 0 / Proto-Oncogene Proteins; 0 / Tal1 protein, mouse; 0 / Transcription Factors; 0 / Viral Proteins; EC 2.7.10.1 / Receptor, TIE-2; EC 2.7.7.- / Cre recombinase; EC 2.7.7.- / Integrases
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23. Pimanda JE, Silberstein L, Dominici M, Dekel B, Bowen M, Oldham S, Kallianpur A, Brandt SJ, Tannahill D, Göttgens B, Green AR: Transcriptional link between blood and bone: the stem cell leukemia gene and its +19 stem cell enhancer are active in bone cells. Mol Cell Biol; 2006 Apr;26(7):2615-25
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  • [Title] Transcriptional link between blood and bone: the stem cell leukemia gene and its +19 stem cell enhancer are active in bone cells.
  • The stem cell leukemia gene (SCL/tal 1) encodes a basic helix-loop-helix transcription factor that is essential for the normal development of blood progenitors and blood vessels.
  • We have previously characterized a panel of SCL enhancers including the +19 element, which directs expression to hematopoietic stem cells and endothelium.
  • Despite consistent expression in cells of the osteogenic lineage, SCL protein is not required for bone specification of embryonic stem cells.
  • A 644-bp fragment containing the SCL +19 core enhancer was active in both blood and bone cell lines and was bound in vivo by a common array of Ets and GATA transcription factors.

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  • (PMID = 16537906.001).
  • [ISSN] 0270-7306
  • [Journal-full-title] Molecular and cellular biology
  • [ISO-abbreviation] Mol. Cell. Biol.
  • [Language] ENG
  • [Grant] United Kingdom / Wellcome Trust / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / DNA-Binding Proteins; 0 / ELF1 protein, human; 0 / Elf1 protein, mouse; 0 / Fli1 protein, mouse; 0 / GATA2 Transcription Factor; 0 / Gata2 protein, mouse; 0 / Nuclear Proteins; 0 / Proto-Oncogene Protein c-fli-1; 0 / Proto-Oncogene Proteins; 0 / Tal1 protein, mouse; 0 / Transcription Factors
  • [Other-IDs] NLM/ PMC1430329
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24. Yoshida K, Hirabayashi Y, Wada S, Watanabe F, Watanabe K, Aizawa S, Inoue T: p53 (TRP53) deficiency-mediated antiapoptosis escape after 5 Gy X irradiation still induces stem cell leukemia in C3H/He mice: comparison between whole-body assay and bone marrow transplantation (BMT) assay. Radiat Res; 2007 Jun;167(6):703-10
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  • [Title] p53 (TRP53) deficiency-mediated antiapoptosis escape after 5 Gy X irradiation still induces stem cell leukemia in C3H/He mice: comparison between whole-body assay and bone marrow transplantation (BMT) assay.
  • Interestingly, the present study showed a high frequency of stem cell leukemia, i.e., leukemias characterized by a lack of differentiation due also to p53 deficiency, even after 5 Gy irradiation.
  • The frequencies of stem cell leukemias (and those of total hematopoietic malignancies) were 16% (24%) at 1 Gy and 45% (75%) at 3 Gy.
  • Furthermore, markedly high incidences of stem cell leukemias were observed at 5 Gy in p53(+/-) mice, i.e., 87% (100%) in the transplantation assay and 60% (83.3%) in the whole-body assay, whereas a conventional whole-body assay induced only 14% in wild-type mice.
  • The high incidence of stem cell leukemias observed in this study using heterozygous p53-deficient mice agrees with results of a previous study of homozygous p53-deficient mice and is consistent with the high frequency of loss of heterozygosity in the p53 wild-type allele observed in leukemias.
  • This suggests that the target cells for radiation-induced stem cell leukemias may be p53-deficient hematopoietic stem cells.
  • [MeSH-major] Apoptosis / radiation effects. Bone Marrow Transplantation / methods. Leukemia, Radiation-Induced / physiopathology. Leukemia, Radiation-Induced / surgery. Stem Cells / radiation effects. Tumor Suppressor Protein p53 / deficiency


25. Heuser M, Sly LM, Argiropoulos B, Kuchenbauer F, Lai C, Weng A, Leung M, Lin G, Brookes C, Fung S, Valk PJ, Delwel R, Löwenberg B, Krystal G, Humphries RK: Modeling the functional heterogeneity of leukemia stem cells: role of STAT5 in leukemia stem cell self-renewal. Blood; 2009 Nov 5;114(19):3983-93
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  • [Title] Modeling the functional heterogeneity of leukemia stem cells: role of STAT5 in leukemia stem cell self-renewal.
  • Although the cancer stem cell (CSC) concept implies that CSCs are rare, recent reports suggest that CSCs may be frequent in some cancers.
  • We hypothesized that the proportion of leukemia stem cells would vary as a function of the number of dysregulated pathways.
  • Leukemia-initiating cell (LIC) number and in vitro expansion potential of LICs were functionally assessed by limiting dilution analyses.
  • LIC expansion potential was 132-fold increased in the 2- compared with the 1-oncogene model, although phenotypically, both leukemias were similar.
  • Interestingly, in 201 acute myeloid leukemia (AML) patients, coexpression of MN1 and HOXA9 was restricted to patients with the poorest prognosis and was associated with highly active STAT signaling.
  • Our data demonstrate the functional heterogeneity of LICs and show that STAT signaling is critical for leukemia stem cell self-renewal in MN1- and HOXA9-expressing leukemias.
  • [MeSH-major] Leukemia, Experimental / metabolism. Leukemia, Experimental / pathology. Models, Biological. Neoplastic Stem Cells / metabolism. Neoplastic Stem Cells / pathology. STAT5 Transcription Factor / metabolism
  • [MeSH-minor] Animals. Cell Proliferation / drug effects. Disease Models, Animal. Female. Granulocyte-Macrophage Colony-Stimulating Factor / pharmacology. Homeodomain Proteins / genetics. Homeodomain Proteins / metabolism. Humans. In Vitro Techniques. Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / metabolism. Leukemia, Myeloid, Acute / pathology. MAP Kinase Signaling System / drug effects. Male. Mice. Mice, Inbred BALB C. Mice, Inbred C57BL. Mice, Knockout. Neoplasm Proteins / genetics. Neoplasm Proteins / metabolism. Oncogene Proteins / genetics. Oncogene Proteins / metabolism. Oncogenes. Recombinant Proteins. STAT1 Transcription Factor / deficiency. STAT1 Transcription Factor / genetics. STAT1 Transcription Factor / metabolism. Signal Transduction / drug effects

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  • [CommentIn] Blood. 2009 Nov 5;114(19):3976-7 [19892722.001]
  • (PMID = 19667399.001).
  • [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 / Homeodomain Proteins; 0 / Mn1 protein, mouse; 0 / Neoplasm Proteins; 0 / Oncogene Proteins; 0 / Recombinant Proteins; 0 / STAT1 Transcription Factor; 0 / STAT5 Transcription Factor; 0 / Stat1 protein, mouse; 0 / Stat5b protein, mouse; 0 / homeobox protein HOXA9; 83869-56-1 / Granulocyte-Macrophage Colony-Stimulating Factor
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26. Wong P, Iwasaki M, Somervaille TC, Ficara F, Carico C, Arnold C, Chen CZ, Cleary ML: The miR-17-92 microRNA polycistron regulates MLL leukemia stem cell potential by modulating p21 expression. Cancer Res; 2010 May 1;70(9):3833-42
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  • [Title] The miR-17-92 microRNA polycistron regulates MLL leukemia stem cell potential by modulating p21 expression.
  • Despite advances in defining the critical molecular determinants for leukemia stem cell (LSC) generation and maintenance, little is known about the roles of microRNAs in LSC biology.
  • Here, we identify microRNAs that are differentially expressed in LSC-enriched cell fractions (c-kit(+)) in a mouse model of MLL leukemia.
  • Expression of miR-17 family microRNAs was substantially reduced concomitant with leukemia cell differentiation and loss of self-renewal, whereas forced expression of a polycistron construct encoding miR-17-19b miRNAs significantly shortened the latency for MLL leukemia development.
  • Leukemias expressing increased levels of the miR-17-19b construct displayed a higher frequency of LSCs, more stringent block of differentiation, and enhanced proliferation associated with reduced expression of p21, a cyclin-dependent kinase inhibitor previously implicated as a direct target of miR-17 microRNAs.
  • Knockdown of p21 in MLL-transformed cells phenocopied the overexpression of the miR-17 polycistron, including a significant decrease in leukemia latency, validating p21 as a biologically relevant and direct in vivo target of the miR-17 polycistron in MLL leukemia.
  • Thus, microRNAs quantitatively regulate LSC self-renewal in MLL-associated leukemia in part by modulating the expression of p21, a known regulator of normal stem cell function.

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  • [Copyright] (c)2010 AACR.
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  • (PMID = 20406979.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / R01 HL081612; United States / NCI NIH HHS / CA / R01 CA116606; United States / NCI NIH HHS / CA / CA55029; United States / NCI NIH HHS / CA / R01 CA055029-18; United States / NHLBI NIH HHS / HL / R01 HL081612-05; United States / NCI NIH HHS / CA / CA116606-05; United States / NCI NIH HHS / CA / R01 CA055029; United States / NCI NIH HHS / CA / CA116606; United States / NHLBI NIH HHS / HL / R01 HL081612-04; United States / NIH HHS / OD / DP1 OD006435; United States / NCI NIH HHS / CA / CA055029-18; United States / NCI NIH HHS / CA / R01 CA116606-05
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cdkn1a protein, mouse; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / MicroRNAs; 0 / Mirn17 microRNA, mouse; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein
  • [Other-IDs] NLM/ NIHMS185039; NLM/ PMC2862107
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27. Wilson NK, Miranda-Saavedra D, Kinston S, Bonadies N, Foster SD, Calero-Nieto F, Dawson MA, Donaldson IJ, Dumon S, Frampton J, Janky R, Sun XH, Teichmann SA, Bannister AJ, Göttgens B: The transcriptional program controlled by the stem cell leukemia gene Scl/Tal1 during early embryonic hematopoietic development. Blood; 2009 May 28;113(22):5456-65
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  • [Title] The transcriptional program controlled by the stem cell leukemia gene Scl/Tal1 during early embryonic hematopoietic development.
  • The basic helix-loop-helix transcription factor Scl/Tal1 controls the development and subsequent differentiation of hematopoietic stem cells (HSCs).
  • In this study, we have used ChIP-Seq technology (coupling chromatin immunoprecipitation with deep sequencing) to generate a genome-wide catalog of Scl-binding events in a stem/progenitor cell line, followed by validation using primary fetal liver cells and comprehensive transgenic mouse assays.
  • By coupling ChIP-Seq in model cell lines with in vivo transgenic validation and sophisticated bioinformatic analysis, we have identified a widely applicable strategy for the reconstruction of stem cell regulatory networks in which biologic material is otherwise limiting.
  • Moreover, in addition to revealing multiple previously unrecognized links to known HSC regulators, as well as novel links to genes not previously implicated in HSC function, comprehensive transgenic analysis of regulatory elements provided substantial new insights into the transcriptional control of several important hematopoietic regulators, including Cbfa2t3h/Eto2, Cebpe, Nfe2, Zfpm1/Fog1, Erg, Mafk, Gfi1b, and Myb.


28. Chao MP, Seita J, Weissman IL: Establishment of a normal hematopoietic and leukemia stem cell hierarchy. Cold Spring Harb Symp Quant Biol; 2008;73:439-49
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Establishment of a normal hematopoietic and leukemia stem cell hierarchy.
  • Many types of adult tissues, especially for high turnover tissues such as the blood and intestinal system, stand on a hierarchical tissue-specific stem cell system.
  • Tissue-specific stem cells concurrently have self-renewal capacity and potential to give rise to all types of mature cells in their tissue.
  • The differentiation process of the tissue-specific stem cell is successive restriction of these capacities.
  • The first progeny of tissue-specific stem cells are multipotent progenitors (MPPs) that lose long-term self-renewal capacity yet have full lineage potential.
  • In this chapter, we review our findings and other key experiments that have led to the establishment of the current cellular stem and progenitor hierarchy in the blood-forming systems of mice and humans for both normal and leukemic hematopoiesis.
  • We also review select signaling pathways intrinsic to normal hematopoietic and leukemic stem cell populations as well our recent findings elucidating the possible origin of the leukemia stem cell.
  • [MeSH-major] Hematopoiesis / physiology. Hematopoietic Stem Cells / cytology. Leukemia, Myeloid / pathology. Neoplastic Stem Cells / pathology
  • [MeSH-minor] Adult. Adult Stem Cells / cytology. Animals. Apoptosis. Cell Differentiation. Cell Movement. Cell Proliferation. Humans. Mice. Models, Biological. Multipotent Stem Cells / cytology. Species Specificity

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  • (PMID = 19022770.001).
  • [ISSN] 1943-4456
  • [Journal-full-title] Cold Spring Harbor symposia on quantitative biology
  • [ISO-abbreviation] Cold Spring Harb. Symp. Quant. Biol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01CA86017
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Number-of-references] 104
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29. Kim J, Lee SG, Song J, Kim SJ, Rha SY, Lee KA, Park TS, Choi JR: Molecular characterization of alternative SET-NUP214 fusion transcripts in a case of acute undifferentiated leukemia. Cancer Genet Cytogenet; 2010 Sep;201(2):73-80
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  • [Title] Molecular characterization of alternative SET-NUP214 fusion transcripts in a case of acute undifferentiated leukemia.
  • The SET-NUP214 fusion gene has been rarely reported in acute myeloid leukemia, acute undifferentiated leukemia, and recurrently in T-cell acute lymphoblastic leukemia.
  • Herein we present a novel case of acute undifferentiated leukemia with SET-NUP214 rearrangement due to the cryptic deletion of the 9q34 region producing two different types of fusion transcripts by alternative splicing and molecular characterization of the fusion transcripts by fluorescence in situ hybridization, reverse transcriptase-polymerase chain reaction, and array comparative genomic hybridization analyses.
  • [MeSH-major] Leukemia / genetics. Oncogene Proteins, Fusion / genetics
  • [MeSH-minor] Acute Disease. Adult. Comparative Genomic Hybridization. Female. Gene Deletion. Humans. Immunophenotyping. In Situ Hybridization, Fluorescence. Male. Sequence Analysis, RNA. Translocation, Genetic

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  • [Copyright] 2010 Elsevier Inc. All rights reserved.
  • (PMID = 20682390.001).
  • [ISSN] 1873-4456
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Oncogene Proteins, Fusion; 0 / SET-CAN fusion protein, human
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30. López-Jiménez J, Martín-Ballesteros E, Sureda A, Uralburu C, Lorenzo I, del Campo R, Fernández C, Calbacho M, García-Belmonte D, Fernández G: Chemotherapy-induced nausea and vomiting in acute leukemia and stem cell transplant patients: results of a multicenter, observational study. Haematologica; 2006 Jan;91(1):84-91
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  • [Title] Chemotherapy-induced nausea and vomiting in acute leukemia and stem cell transplant patients: results of a multicenter, observational study.
  • DESIGN AND METHODS: This was a multicenter, prospective, observational follow-up study including: (i) acute myeloid leukemia patients treated with moderately to highly emetogenic chemotherapy and (ii) hematopoietic stem cell transplant recipients, without reduced intensity conditioning.
  • RESULTS: One hundred consecutive transplant and 77 acute myeloid leukemia patients were studied.
  • Transplant conditioning was the most important risk factor for CINV: complete response occurred in only 20% of transplant patients (vs. 47% for leukemia patients).
  • Among patients with emesis, the mean percentage of days with emesis and the mean (+/-SD) total number of emetic episodes were 61% and 9.4+/-8.9 (transplant recipients), and 53.6% and 6.2+/-7.3 (leukemia patients), respectively.
  • CINV control was lower in the delayed than in the acute phase.
  • [MeSH-minor] Acute Disease. Female. Follow-Up Studies. Hematopoietic Stem Cell Transplantation / adverse effects. Hematopoietic Stem Cell Transplantation / methods. Humans. Leukemia / complications. Leukemia / therapy. Male. Middle Aged. Prospective Studies. Serotonin Antagonists / therapeutic use. Transplantation Conditioning / adverse effects. Transplantation Conditioning / methods

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  • (PMID = 16434375.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Serotonin Antagonists
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31. Batlle M, Vall-Llovera F, Bechini J, Camps I, Marcos P, Vives S, Oriol A, Ribera JM: [Neutropenic enterocolitis in adult patients with acute leukemia or stem cell transplant recipients: study of 7 cases]. Med Clin (Barc); 2007 Nov 10;129(17):660-3
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  • [Title] [Neutropenic enterocolitis in adult patients with acute leukemia or stem cell transplant recipients: study of 7 cases].
  • [Transliterated title] Enterocolitis neutropénica en adultos con leucemia aguda o receptores de un trasplante de progenitores hematopoyéticos: estudio de 7 casos.
  • BACKGROUND AND OBJECTIVE: Neutropenic enterocolitis (NE) is a complication arising in neutropenic patients with acute leukemia or solid tumours while treated with intensive chemotherapy.
  • The optimal therapeutic procedures have not been well established.
  • Acute myeloblastic leukemia was the most frequent diagnosis (5 cases).
  • Two other patients had received an stem cell transplantation.
  • CONCLUSIONS: NE is a severe complication of patients with hematologic malignancies submitted to intensive chemotherapy or receiving stem cell transplantation.
  • [MeSH-major] Enterocolitis, Neutropenic / etiology. Leukemia, Myeloid, Acute / complications. Stem Cell Transplantation / adverse effects

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  • (PMID = 18005634.001).
  • [ISSN] 0025-7753
  • [Journal-full-title] Medicina clínica
  • [ISO-abbreviation] Med Clin (Barc)
  • [Language] spa
  • [Publication-type] Case Reports; Comparative Study; English Abstract; Journal Article
  • [Publication-country] Spain
  • [Chemical-registry-number] 0 / Anti-Bacterial Agents; 0 / Antineoplastic Agents
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32. Abrahamsson AE, Geron I, Gotlib J, Dao KH, Barroga CF, Newton IG, Giles FJ, Durocher J, Creusot RS, Karimi M, Jones C, Zehnder JL, Keating A, Negrin RS, Weissman IL, Jamieson CH: Glycogen synthase kinase 3beta missplicing contributes to leukemia stem cell generation. Proc Natl Acad Sci U S A; 2009 Mar 10;106(10):3925-9
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  • [Title] Glycogen synthase kinase 3beta missplicing contributes to leukemia stem cell generation.
  • Recent evidence suggests that a rare population of self-renewing cancer stem cells (CSC) is responsible for cancer progression and therapeutic resistance.
  • Chronic myeloid leukemia (CML) represents an important paradigm for understanding the genetic and epigenetic events involved in CSC production.
  • CML progresses from a chronic phase (CP) in hematopoietic stem cells (HSC) that harbor the BCR-ABL translocation, to blast crisis (BC), characterized by aberrant activation of beta-catenin within granulocyte-macrophage progenitors (GMP).
  • Here we show that BC CML myeloid progenitors, in particular GMP, serially transplant leukemia in immunocompromised mice and thus are enriched for leukemia stem cells (LSC).
  • Notably, cDNA sequencing of Wnt/beta-catenin pathway regulatory genes, including adenomatous polyposis coli, GSK3beta, axin 1, beta-catenin, lymphoid enhancer factor-1, cyclin D1, and c-myc, revealed a novel in-frame splice deletion of the GSK3beta kinase domain in the GMP of BC samples that was not detectable by sequencing in blasts or normal progenitors.

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  • (PMID = 19237556.001).
  • [ISSN] 1091-6490
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / 2P01CA49605; United States / NCI NIH HHS / CA / R01 CA086017; United States / NCI NIH HHS / CA / CA86017; United States / NHLBI NIH HHS / HL / K23 HL004409; United States / NHLBI NIH HHS / HL / K23 HL04409; United States / NCI NIH HHS / CA / P01 CA049605; United States / NCI NIH HHS / CA / R01 CA086065; United States / NCI NIH HHS / CA / CA086065
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] EC 2.7.11.1 / glycogen synthase kinase 3 beta; EC 2.7.11.26 / Glycogen Synthase Kinase 3
  • [Other-IDs] NLM/ PMC2646624
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33. Carter BZ, Mak DH, Cortes J, Andreeff M: The elusive chronic myeloid leukemia stem cell: does it matter and how do we eliminate it? Semin Hematol; 2010 Oct;47(4):362-70
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  • [Title] The elusive chronic myeloid leukemia stem cell: does it matter and how do we eliminate it?
  • Chronic myeloid leukemia (CML) is a clonal multistep myeloproliferative disease originating from and ultimately sustained by a rare population of BCR-ABL(+) cells with multilineage stem cell properties.
  • Despite this achievement, CML is often not curable, largely due to the innate insensitivity of CML stem cells, particularly when in a quiescent state.
  • This failure of not only imatinib but also the second-generation tyrosine kinase inhibitors (TKIs) frequently leads to relapse upon drug discontinuation.
  • Thus, any curative therapy must eliminate CML stem cells.
  • A comprehensive understanding of the biological properties of CML stem cells and an elucidation of the molecular mechanisms and signaling pathways enabling these CML stem cells to self-renew, combined with insight into the regulation of apoptosis signaling and the mechanisms governing the interaction of CML stem cells with their bone marrow microenvironment, will facilitate the development of therapies for targeting these cells.
  • Here, we discuss the biological properties of CML stem cells and potential strategies to eliminate them.

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  • (PMID = 20875553.001).
  • [ISSN] 1532-8686
  • [Journal-full-title] Seminars in hematology
  • [ISO-abbreviation] Semin. Hematol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P01 CA049639; United States / NCI NIH HHS / CA / P30 CA016672; United States / NCI NIH HHS / CA / CA16672; United States / NCI NIH HHS / CA / P01 CA49639
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Interferon-alpha; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate
  • [Other-IDs] NLM/ NIHMS219537; NLM/ PMC2948413
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34. Li F, Zhang L, Li C, Ni B, Wu Y, Huang Y, Zhang G, Wang L, Zhang A, He Y, Fu T, Tong W, Liu B: Adenovirus-mediated stem cell leukemia gene transfer induces rescue of interstitial cells of Cajal in ICC-loss mice. Int J Colorectal Dis; 2010 May;25(5):557-66
MedlinePlus Health Information. consumer health - Stem Cells.

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  • [Title] Adenovirus-mediated stem cell leukemia gene transfer induces rescue of interstitial cells of Cajal in ICC-loss mice.
  • OBJECTIVE: Interaction of c-Kit and its ligand stem cell factor (SCF) is necessary for appropriate development and survival of interstitial cells of Cajal (ICC) in the intestine.
  • Stem cell leukemia (SCL) gene acts as a positive regulator of upstream transcription of c-Kit expression.
  • [MeSH-major] Adenoviridae / genetics. Basic Helix-Loop-Helix Transcription Factors / metabolism. Gene Transfer Techniques. Interstitial Cells of Cajal / pathology. Leukemia / pathology. Stem Cells / metabolism
  • [MeSH-minor] Animals. Cell Shape. Colon / pathology. Colon / ultrastructure. Disease Models, Animal. HeLa Cells. Humans. Mice. Mice, Inbred BALB C. Proto-Oncogene Proteins c-kit / metabolism. Recombination, Genetic. Reproducibility of Results. Staining and Labeling

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  • (PMID = 20165856.001).
  • [ISSN] 1432-1262
  • [Journal-full-title] International journal of colorectal disease
  • [ISO-abbreviation] Int J Colorectal Dis
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Basic Helix-Loop-Helix Transcription Factors; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit
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35. Terme JM, Lhermitte L, Asnafi V, Jalinot P: TGF-beta induces degradation of TAL1/SCL by the ubiquitin-proteasome pathway through AKT-mediated phosphorylation. Blood; 2009 Jun 25;113(26):6695-8
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  • T-cell acute lymphoblastic leukemia 1 (TAL1), also known as stem cell leukemia (SCL), plays important roles in differentiation of hematopoietic and endothelial cells and is deregulated in a high percentage of T-cell acute lymphoblastic leukemia (T-ALL).

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  • (PMID = 19406989.001).
  • [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 / Androstadienes; 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / Leupeptins; 0 / Neoplasm Proteins; 0 / Proteasome Inhibitors; 0 / Proto-Oncogene Proteins; 0 / TCF Transcription Factors; 0 / TCF7L1 protein, human; 0 / Transcription Factor 7-Like 1 Protein; 0 / Transforming Growth Factor beta1; 0 / Ubiquitin; 1114-81-4 / Phosphothreonine; 133407-82-6 / benzyloxycarbonylleucyl-leucyl-leucine aldehyde; 135471-20-4 / TAL1 protein, human; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.11.1 / AKT1 protein, human; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 3.4.25.1 / Proteasome Endopeptidase Complex; EC 6.3.2.19 / STUB1 protein, human; EC 6.3.2.19 / Ubiquitin-Protein Ligases; XVA4O219QW / wortmannin
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36. Webert KE, Cook RJ, Couban S, Carruthers J, Lee KA, Blajchman MA, Lipton JH, Brandwein JM, Heddle NM: A multicenter pilot-randomized controlled trial of the feasibility of an augmented red blood cell transfusion strategy for patients treated with induction chemotherapy for acute leukemia or stem cell transplantation. Transfusion; 2008 Jan;48(1):81-91
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  • [Title] A multicenter pilot-randomized controlled trial of the feasibility of an augmented red blood cell transfusion strategy for patients treated with induction chemotherapy for acute leukemia or stem cell transplantation.
  • Patients with acute leukemia receiving induction chemotherapy or those undergoing stem cell transplantation were assigned to one of two treatment groups: standard transfusion strategy (transfusion of 2 units of red blood cells [RBCs] when their Hb level was less than 80 g/L) or an augmented transfusion strategy (transfusion of 2 units of RBCs when their Hb level was less than 120 g/L).
  • The proportions of patients experiencing clinically significant bleeding and the time to first bleed were not significantly different between the control and experimental groups.
  • The proportion of patient-days with platelet (PLT) transfusions was not different between the experimental and control groups.
  • The mean number of donor exposures (PLT and RBC transfusions) was not different between experimental and control groups.
  • [MeSH-major] Erythrocyte Transfusion / methods. Hemorrhage / etiology. Leukemia / complications. Leukemia / therapy
  • [MeSH-minor] Acute Disease. Adult. Aged. Antineoplastic Agents / therapeutic use. Feasibility Studies. Female. Hematopoietic Stem Cell Transplantation. Hemoglobins / analysis. Humans. Male. Middle Aged. Pilot Projects

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  • (PMID = 17894791.001).
  • [ISSN] 0041-1132
  • [Journal-full-title] Transfusion
  • [ISO-abbreviation] Transfusion
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Hemoglobins
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37. Zhang L, Liu BH, Tong WD, Li CX: [Distribution and efficiency of recombinant adenovirus mediated human stem cell leukemia gene transfer in mice with interstitial cells of Cajal loss]. Zhonghua Wei Chang Wai Ke Za Zhi; 2007 Mar;10(2):119-23
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  • [Title] [Distribution and efficiency of recombinant adenovirus mediated human stem cell leukemia gene transfer in mice with interstitial cells of Cajal loss].
  • OBJECTIVE: To investigate the construction of the green fluorescent protein (GFP) labeled recombinant adenovirus containing human stem cell leukemia (hSCL) and its distribution and efficiency in mice with interstitial cells of Cajal (ICC) loss.
  • [MeSH-major] Adenoviridae / genetics. Genetic Therapy. Green Fluorescent Proteins / genetics. Leukemia, Myeloid, Acute / genetics

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  • (PMID = 17380448.001).
  • [ISSN] 1671-0274
  • [Journal-full-title] Zhonghua wei chang wai ke za zhi = Chinese journal of gastrointestinal surgery
  • [ISO-abbreviation] Zhonghua Wei Chang Wai Ke Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 147336-22-9 / Green Fluorescent Proteins
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38. Ozbek U, Kandilci A, van Baal S, Bonten J, Boyd K, Franken P, Fodde R, Grosveld GC: SET-CAN, the product of the t(9;9) in acute undifferentiated leukemia, causes expansion of early hematopoietic progenitors and hyperproliferation of stomach mucosa in transgenic mice. Am J Pathol; 2007 Aug;171(2):654-66
SciCrunch. Marmoset Gene list: Data: Gene Annotation .

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  • [Title] SET-CAN, the product of the t(9;9) in acute undifferentiated leukemia, causes expansion of early hematopoietic progenitors and hyperproliferation of stomach mucosa in transgenic mice.
  • Leukemia-specific chromosome translocations involving the nucleoporin CAN/NUP214 lead to expression of different fusion genes including DEK-CAN, CAN-ABL, and SET-CAN.
  • DEK-CAN and CAN-ABL1 are associated with acute myeloid leukemia and T-cell acute lymphoblastic leukemia, respectively, whereas SET-CAN was identified in a patient with acute undifferentiated leukemia.
  • Although SET-CAN mice showed expansion of an early progenitor cell pool and partial depletion of lymphocytes, the animals were not leukemia-prone and did not show shortening of disease latency after retroviral tagging.
  • This suggests that SET-CAN expression in acute undifferentiated leukemia might determine the primitive phenotype of the disease, whereas secondary genetic lesions are necessary for disease development.

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  • (PMID = 17569777.001).
  • [ISSN] 0002-9440
  • [Journal-full-title] The American journal of pathology
  • [ISO-abbreviation] Am. J. Pathol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P30 CA021765; United States / NCI NIH HHS / CA / CA-21765; United States / NCI NIH HHS / CA / CA-76480
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Chromosomal Proteins, Non-Histone; 0 / Ki-67 Antigen; 0 / Nuclear Pore Complex Proteins; 0 / Nup214 protein, mouse; 0 / Oncogene Proteins, Fusion
  • [Other-IDs] NLM/ PMC1934515
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39. Juarez MA, Su F, Chun S, Kiel MJ, Lyons SE: Distinct roles for SCL in erythroid specification and maturation in zebrafish. J Biol Chem; 2005 Dec 16;280(50):41636-44
ZFIN. ZFIN .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The stem cell leukemia (SCL) transcription factor is essential for vertebrate hematopoiesis.
  • Although all hematopoietic functions were rescued by wild-type Scl mRNA, an Scl DNA binding mutant rescued primitive and definitive hematopoiesis but did not rescue primitive erythroid maturation.
  • [MeSH-minor] Alternative Splicing. Animals. Cell Differentiation. Cell Lineage. DNA / chemistry. DNA-Binding Proteins. Electrophoresis, Agar Gel. Erythroid-Specific DNA-Binding Factors / metabolism. Hematopoiesis. In Situ Hybridization. Models, Genetic. Mutation. Phenotype. Protein Structure, Tertiary. RNA / chemistry. RNA, Antisense / chemistry. RNA, Messenger / metabolism. RNA, Small Interfering / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Stem Cells. Transcription Factors. Zebrafish

  • Gene Ontology. gene/protein/disease-specific - Gene Ontology annotations from this paper .
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  • (PMID = 16210319.001).
  • [ISSN] 0021-9258
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / K22-CA095024-02
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / DNA-Binding Proteins; 0 / Erythroid-Specific DNA-Binding Factors; 0 / Proto-Oncogene Proteins; 0 / RNA, Antisense; 0 / RNA, Messenger; 0 / RNA, Small Interfering; 0 / Transcription Factors; 0 / Zebrafish Proteins; 0 / tal1 protein, zebrafish; 63231-63-0 / RNA; 9007-49-2 / DNA
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40. Smith AM, Sanchez MJ, Follows GA, Kinston S, Donaldson IJ, Green AR, Göttgens B: A novel mode of enhancer evolution: the Tal1 stem cell enhancer recruited a MIR element to specifically boost its activity. Genome Res; 2008 Sep;18(9):1422-32
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A novel mode of enhancer evolution: the Tal1 stem cell enhancer recruited a MIR element to specifically boost its activity.
  • The stem cell leukemia TAL1 (also known as SCL) transcription factor is essential for the normal development of blood stem cells and we have previously shown that the Tal1 +19 enhancer directs expression to hematopoietic stem cells, hematopoietic progenitors, and to endothelium.
  • Here we demonstrate that an adjacent region 1 kb upstream (+18 element) is in an open chromatin configuration and carries active histone marks but does not function as an enhancer in transgenic mice.
  • Instead, it boosts activity of the +19 enhancer both in stable transfection assays and during differentiation of embryonic stem (ES) cells carrying single-copy reporter constructs targeted to the Hprt locus.

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  • (PMID = 18687876.001).
  • [ISSN] 1088-9051
  • [Journal-full-title] Genome research
  • [ISO-abbreviation] Genome Res.
  • [Language] ENG
  • [Grant] United Kingdom / Wellcome Trust / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / Proto-Oncogene Proteins; 0 / Tal1 protein, mouse; 135471-20-4 / TAL1 protein, human
  • [Other-IDs] NLM/ PMC2527711
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41. Sahin F, Sercan Z, Ertan Y, Ocakci S, Ay E, Vural F, Yuksel E, Tombuloglu M, Saydam G: Rapid transformation of atypical myeloproliferative disorder with consistent t(8;13) to B-cell acute lymphoblastic leukemia: a case report. Hematology; 2007 Dec;12(6):489-92
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Rapid transformation of atypical myeloproliferative disorder with consistent t(8;13) to B-cell acute lymphoblastic leukemia: a case report.
  • 8p11 myeloproliferative syndrome (EMS; also known as the stem cell leukemia syndrome-SCLL) is a rare atypical myeloproliferative disorder associated with chromosomal abnormalities involving the 8p11 chromosomal band.
  • Disease phenotype associated with this translocation has some typical features such as poor prognosis, and transformation to mainly acute leukemia and non-Hodgkin lymphoma; commonly with a T-cell phenotype in which obtaining and maintenance of remission is difficult by conventional chemotherapy.
  • We hereby present a case diagnosed as atypical chronic myeloproliferative disease with consistent t(8;13)(p12;q12) and transformed rapidly to pre-B-cell acute lymphoblastic leukemia which is a rare clinical presentation.
  • [MeSH-major] Burkitt Lymphoma / etiology. Cell Transformation, Neoplastic. Myeloproliferative Disorders / pathology. Translocation, Genetic

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
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  • (PMID = 17852454.001).
  • [ISSN] 1607-8454
  • [Journal-full-title] Hematology (Amsterdam, Netherlands)
  • [ISO-abbreviation] Hematology
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
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42. Deshpande AJ, Buske C: Knocking the Wnt out of the sails of leukemia stem cell development. Cell Stem Cell; 2007 Dec 13;1(6):597-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Knocking the Wnt out of the sails of leukemia stem cell development.
  • Tumor propagation by cancer stem cells (CSCs) requires their ability to self-renew, and yet the signal pathways involved in this process remain poorly defined.
  • In the December issue of Cancer Cell, Zhao et al. (2007) provide compelling evidence that Wnt/beta-catenin signaling is crucial for the maintenance of chronic myelogenous leukemia (CML) stem cells.
  • [MeSH-major] Leukemia. Stem Cells / physiology. Wnt Proteins / genetics. Wnt Proteins / physiology. beta Catenin / physiology

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  • (PMID = 18371398.001).
  • [ISSN] 1875-9777
  • [Journal-full-title] Cell stem cell
  • [ISO-abbreviation] Cell Stem Cell
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Wnt Proteins; 0 / beta Catenin
  • [Number-of-references] 10
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43. Wong P, Iwasaki M, Somervaille TC, So CW, Cleary ML: Meis1 is an essential and rate-limiting regulator of MLL leukemia stem cell potential. Genes Dev; 2007 Nov 1;21(21):2762-74
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Meis1 is an essential and rate-limiting regulator of MLL leukemia stem cell potential.
  • Oncogenic mutations of the MLL histone methyltransferase confer an unusual ability to transform non-self-renewing myeloid progenitors into leukemia stem cells (LSCs) by mechanisms that remain poorly defined.
  • Misregulation of Hox genes is likely to be critical for LSC induction and maintenance but alone it does not recapitulate the phenotype and biology of MLL leukemias, which are clinically heterogeneous--presumably reflecting differences in LSC biology and/or frequency.
  • TALE (three-amino-acid loop extension) class homeodomain proteins of the Pbx and Meis families are also misexpressed in this context, and we thus employed knockout, knockdown, and dominant-negative genetic techniques to investigate the requirements and contributions of these factors in MLL oncoprotein-induced acute myeloid leukemia.

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  • (PMID = 17942707.001).
  • [ISSN] 0890-9369
  • [Journal-full-title] Genes & development
  • [ISO-abbreviation] Genes Dev.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA055029; United States / NCI NIH HHS / CA / R37 CA042971; United States / NCI NIH HHS / CA / CA42971; United States / NCI NIH HHS / CA / CA55029
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / Homeodomain Proteins; 0 / Neoplasm Proteins; 0 / Pbx2 protein, mouse; 0 / Proto-Oncogene Proteins; 0 / Repressor Proteins; 0 / Tgif protein, mouse; 0 / myeloid ecotropic viral integration site 1 protein; 146150-81-4 / proto-oncogene protein Pbx3; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein
  • [Other-IDs] NLM/ PMC2045130
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44. Li X, Xiong JW, Shelley CS, Park H, Arnaout MA: The transcription factor ZBP-89 controls generation of the hematopoietic lineage in zebrafish and mouse embryonic stem cells. Development; 2006 Sep;133(18):3641-50
ZFIN. ZFIN .

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  • [Title] The transcription factor ZBP-89 controls generation of the hematopoietic lineage in zebrafish and mouse embryonic stem cells.
  • Hematopoietic development is closely linked to that of blood vessels and the two processes are regulated in large part by transcription factors that control cell fate decisions and cellular differentiation.
  • Both blood and blood vessels derive from a common progenitor, termed the hemangioblast, but the factor(s) specifying the development and differentiation of this stem cell population into the hematopoietic and vascular lineages remain ill defined.
  • Injection of ZBP-89 mRNA into cloche zebrafish embryos, which lack both the hematopoietic and endothelial lineages, rescues hematopoiesis but not vasculogenesis.
  • Injection of mRNA for Stem Cell Leukemia (SCL), a transcription factor that directs hemangioblast development into blood cell precursors, rescues the bloodless phenotype in ZBP-89 zebrafish morphants.
  • Forced expression of ZBP-89 induces the expansion of hematopoietic progenitors in wild-type zebrafish and in mouse embryonic stem cell cultures but inhibits angiogenesis in vivo and in vitro.

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  • (PMID = 16914492.001).
  • [ISSN] 0950-1991
  • [Journal-full-title] Development (Cambridge, England)
  • [ISO-abbreviation] Development
  • [Language] ENG
  • [Grant] United States / NIA NIH HHS / AG / AG019676-04; United States / NIDDK NIH HHS / DK / R01 DK081920; United States / NIA NIH HHS / AG / AG19676; United States / NIA NIH HHS / AG / K01 AG019676-04
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / Transcription Factors; 0 / ZBP-89 protein, zebrafish; 0 / Zebrafish Proteins; 0 / Zfp148 protein, mouse
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45. Stubbs MC, Armstrong SA: Therapeutic implications of leukemia stem cell development. Clin Cancer Res; 2007 Jun 15;13(12):3439-42
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  • [Title] Therapeutic implications of leukemia stem cell development.
  • Acute myelogenous leukemias, and perhaps many other cancers, are maintained by a population of cancer stem cells that can regenerate themselves as well as give rise to more differentiated and less proliferative cells that constitute the bulk of the disease.
  • Recent discoveries have shed light on both the nature of leukemia stem cells (LSC) and their cells of origin.
  • [MeSH-major] Cell Transformation, Neoplastic / metabolism. Hematopoietic Stem Cells / physiology. Leukemia / physiopathology. Neoplastic Stem Cells / physiology
  • [MeSH-minor] Animals. Cell Differentiation. Cell Lineage. Humans

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  • (PMID = 17575205.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 23
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46. Dekel B, Metsuyanim S, Garcia AM, Quintero C, Sanchez MJ, Izraeli S: Organ-injury-induced reactivation of hemangioblastic precursor cells. Leukemia; 2008 Jan;22(1):103-13
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Early in mammalian development, the stem cell leukemia (SCL/TAL1) gene and its distinct 3' enhancer (SCL 3'En) specify bipotential progenitor cells that give rise to blood and endothelium, thus termed hemangioblasts.
  • [MeSH-major] Endothelium, Vascular / cytology. Hematopoietic Stem Cells / metabolism. Kidney Diseases / metabolism. Reperfusion Injury / metabolism. Vascular Endothelial Growth Factor Receptor-2 / genetics

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  • (PMID = 17898790.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD31; 0 / Antigens, CD34; 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / Proto-Oncogene Proteins; 0 / RNA, Messenger; 0 / Tal1 protein, mouse; EC 2.7.10.1 / Flt1 protein, mouse; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-1; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-2; EC 3.1.3.48 / Antigens, CD45
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47. Ichijo T, Chrousos GP, Kino T: Activated glucocorticoid receptor interacts with the INHAT component Set/TAF-Ibeta and releases it from a glucocorticoid-responsive gene promoter, relieving repression: implications for the pathogenesis of glucocorticoid resistance in acute undifferentiated leukemia with Set-Can translocation. Mol Cell Endocrinol; 2008 Feb 13;283(1-2):19-31
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  • [Title] Activated glucocorticoid receptor interacts with the INHAT component Set/TAF-Ibeta and releases it from a glucocorticoid-responsive gene promoter, relieving repression: implications for the pathogenesis of glucocorticoid resistance in acute undifferentiated leukemia with Set-Can translocation.
  • Set/template-activating factor (TAF)-Ibeta, part of the Set-Can oncogene product found in acute undifferentiated leukemia, is a component of the inhibitor of acetyltransferases (INHAT) complex.
  • Set-Can fusion protein, on the other hand, did not interact with GR, was constitutively co-precipitated with GREs and suppressed GRIP1-induced enhancement of GR transcriptional activity and histone acetylation.
  • Thus, Set/TAF-Ibeta acts as a ligand-activated GR-responsive transcriptional repressor, while Set-Can does not retain physiologic responsiveness to ligand-bound GR, possibly contributing to the poor responsiveness of Set-Can-harboring leukemic cells to glucocorticoids.
  • [MeSH-major] Chromosomal Proteins, Non-Histone / metabolism. Glucocorticoids / pharmacology. Leukemia / pathology. Oncogene Proteins, Fusion / metabolism. Promoter Regions, Genetic / genetics. Receptors, Glucocorticoid / metabolism. Transcription Factors / metabolism. Translocation, Genetic

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  • (PMID = 18096310.001).
  • [ISSN] 0303-7207
  • [Journal-full-title] Molecular and cellular endocrinology
  • [ISO-abbreviation] Mol. Cell. Endocrinol.
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / / Z01 HD008732-06
  • [Publication-type] Journal Article; Research Support, N.I.H., Intramural
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Chromosomal Proteins, Non-Histone; 0 / Glucocorticoids; 0 / Histone Chaperones; 0 / Ligands; 0 / Nuclear Proteins; 0 / Oncogene Proteins, Fusion; 0 / Phosphoproteins; 0 / Receptors, Glucocorticoid; 0 / Repressor Proteins; 0 / SET protein, human; 0 / SET-CAN fusion protein, human; 0 / Transcription Factors; EC 2.3.1.48 / Histone Acetyltransferases
  • [Other-IDs] NLM/ NIHMS42142; NLM/ PMC2350211
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48. Nicholson E, Holyoake T: The chronic myeloid leukemia stem cell. Clin Lymphoma Myeloma; 2009;9 Suppl 4:S376-81
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  • [Title] The chronic myeloid leukemia stem cell.
  • Chronic myeloid leukemia (CML) is a clonal stem cell disorder that is characterized by the acquired chromosomal translocation BCR-ABL.
  • This gives rise to a constitutively active tyrosine kinase deregulation of the normal mechanisms of cell cycle control.
  • In the normal hematopoietic system, hematopoietic stem cells (HSC) self-renew to form identical daughter cells but also differentiate to mature blood cells.
  • Leukemic stem cells (LSC) share these properties of self-renewal and also differentiate to mature leukemic cells.
  • LSC have been isolated from patients with CML: these cells give rise to leukemia following transplantation into NOD-SCID mice models.
  • Further characterization of CML stem cells has demonstrated that a small percentage of these cells are quiescent despite culture with growth factors.
  • The CML stem cell arises from a normal HSC that has acquired the Philadelphia chromosome.
  • Quiescent stem cells are resistant to treatment with imatinib in vitro and are thought also to show resistance in vivo.
  • The properties of the stem cells that lead to this drug resistance are still being characterized.
  • Newer molecular therapies are in development that act to specifically target and eradicate the stem cell pool.
  • [MeSH-major] Hematopoietic Stem Cells / pathology. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / diagnosis. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / therapy. Neoplastic Stem Cells / pathology


49. Kong KY, Williamson EA, Rogers JH, Tran T, Hromas R, Dahl R: Expression of Scl in mesoderm rescues hematopoiesis in the absence of Oct-4. Blood; 2009 Jul 2;114(1):60-3

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  • In embryonic stem cells, Oct-4 concentration is critical in determining the development of endoderm, mesoderm, and trophectoderm.
  • However, hematopoiesis can be rescued in the absence of Oct-4 after mesoderm specification if the essential hematopoietic transcription factor stem cell leukemia is expressed.

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  • (PMID = 19321862.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA102283; United States / NHLBI NIH HHS / HL / R01 HL075783; United States / NCI NIH HHS / CA / CA102283; United States / NHLBI NIH HHS / HL / HL075783
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / Octamer Transcription Factor-3; 0 / Pou5f1 protein, mouse; 0 / Proto-Oncogene Proteins; 0 / Recombinant Proteins; 0 / Tal1 protein, mouse
  • [Other-IDs] NLM/ PMC2710954
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50. Feller N, Kelder A, Westra G, Ossenkoppele GJ, Schuurhuis GJ: Positive selection for CD90 as a purging option in acute myeloid leukemia stem cell transplants. Cytometry B Clin Cytom; 2008 Jan;74(1):9-16
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Positive selection for CD90 as a purging option in acute myeloid leukemia stem cell transplants.
  • BACKGROUND: Several studies showed the benefit of purging of acute myeloid leukemia (AML) stem cell transplants.
  • We reported previously that purging by positive selection of CD34+ and CD133+ cells resulted in a 3-4 log tumor cell reduction (TCR) in CD34- and/or CD133- AML, but has been shown to be potentially applicable in only about 50% of cases.
  • Similar to CD34 and CD133, CD90 marks the hematopoietic CD34 positive stem cells capable of full hematopoietic recovery after myeloablative chemotherapy, and therefore, in the present study, we explored whether a similar purging approach is possible using CD90.
  • METHODS: CD90 expression was established by flowcytometry in diagnosis AML on the clonogenic AML CD34+ blast population by flow cytometry.
  • For the calculation of the efficacy of TCR by positive selection, AML blasts were recognized by either prelabeling diagnosis blasts with CD45-FITC in spiking model experiments or using expression of leukemia associated marker combinations both in spiking experiments and in real transplants.
  • [MeSH-major] Antigens, Thy-1 / immunology. Bone Marrow Purging / methods. Flow Cytometry. Leukemia, Myeloid, Acute / therapy. Peripheral Blood Stem Cell Transplantation / methods
  • [MeSH-minor] Antigens, CD34 / immunology. Antigens, CD34 / metabolism. Biomarkers, Tumor / immunology. Female. Hematopoietic Stem Cells / cytology. Hematopoietic Stem Cells / immunology. Hematopoietic Stem Cells / metabolism. Humans. Immunophenotyping. Male. Middle Aged

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  • [Copyright] (c) 2007 Clinical Cytometry Society
  • (PMID = 18061946.001).
  • [ISSN] 1552-4957
  • [Journal-full-title] Cytometry. Part B, Clinical cytometry
  • [ISO-abbreviation] Cytometry B Clin Cytom
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD34; 0 / Antigens, Thy-1; 0 / Biomarkers, Tumor
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51. Göthert JR, Brake RL, Smeets M, Dührsen U, Begley CG, Izon DJ: NOTCH1 pathway activation is an early hallmark of SCL T leukemogenesis. Blood; 2007 Nov 15;110(10):3753-62
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  • The acquired activation of stem cell leukemia (SCL) during T lymphopoiesis is a common event in T-cell acute lymphoblastic leukemia (T-ALL).
  • Here, we generated tamoxifen (TAM)-inducible transgenic mice (lck-ER(T2)-SCL) to study the consequences of acquired SCL activation during T-cell development.
  • Aberrant activation of SCL in thymocytes resulted in the accumulation of immature CD4(+)CD8(+) (double-positive, DP) cells by preventing normal surface expression of the T-cell receptor alphabeta (TCRalphabeta) complex.
  • Strikingly, NOTCH1 target gene up-regulation was already observed after short-term SCL induction, implying that enhanced NOTCH signaling is mediated by SCL and is not dependent on secondary genetic events.
  • [MeSH-major] Basic Helix-Loop-Helix Transcription Factors / genetics. Cell Transformation, Neoplastic / metabolism. Leukemia, T-Cell / genetics. Proto-Oncogene Proteins / genetics. Receptor, Notch1 / metabolism
  • [MeSH-minor] Animals. CD4-Positive T-Lymphocytes / cytology. CD8-Positive T-Lymphocytes / cytology. Cell Survival. Genes, T-Cell Receptor beta. Mice. Mice, Transgenic. Models, Biological. Organ Culture Techniques. Signal Transduction / physiology. Thymus Gland / cytology. Thymus Gland / embryology

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  • (PMID = 17698635.001).
  • [ISSN] 0006-4971
  • [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 / Basic Helix-Loop-Helix Transcription Factors; 0 / Notch1 protein, mouse; 0 / Proto-Oncogene Proteins; 0 / Receptor, Notch1; 0 / Tal1 protein, mouse
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52. Sumanas S, Lin S: Ets1-related protein is a key regulator of vasculogenesis in zebrafish. PLoS Biol; 2006 Jan;4(1):e10
ZFIN. ZFIN .

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  • During embryonic development, multiple signaling pathways control specification, migration, and differentiation of the vascular endothelial cell precursors, angioblasts.
  • No single gene responsible for the commitment of mesenchymal cells to the angioblast cell fate has been identified as yet.
  • Angioblasts in etsrp-morpholino-injected embryos (morphants) failed to undergo migration and differentiation and did not coalesce into functional blood vessels.
  • Expression of all vascular endothelial molecular markers tested was severely reduced in etsrp morphants, whereas hematopoietic markers were not affected.
  • Overexpression of etsrp RNA caused multiple cell types to express vascular endothelial markers. etsrp RNA restored expression of vascular markers in cloche mutants, defective in hematopoietic and endothelial cell formation, arguing that etsrp functions downstream of cloche in angioblast formation. etsrp gene function was also required for endothelial marker induction by the vascular endothelial growth factor (vegf) and stem cell leukemia (scl/tal1).

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  • [CommentIn] PLoS Biol. 2006 Jan;4(1):e24 [16535776.001]
  • (PMID = 16336046.001).
  • [ISSN] 1545-7885
  • [Journal-full-title] PLoS biology
  • [ISO-abbreviation] PLoS Biol.
  • [Language] ENG
  • [Databank-accession-numbers] GENBANK/ DQ021472
  • [Grant] United States / NIDDK NIH HHS / DK / R01 DK054508; United States / NHLBI NIH HHS / HL / T32 HL069766; United States / NIDDK NIH HHS / DK / R01 DK54508
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / Etsrp protein, zebrafish; 0 / GATA1 Transcription Factor; 0 / Proto-Oncogene Proteins; 0 / Zebrafish Proteins; 0 / gata1 protein, zebrafish; 0 / tal1 protein, zebrafish; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-2
  • [Other-IDs] NLM/ PMC1310653
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53. Bockamp E, Antunes C, Liebner S, Schmitt S, Cabezas-Wallscheid N, Heck R, Ohnngemach S, Oesch-Bartlomowicz B, Rickert C, Sanchez MJ, Hengstler J, Kaina B, Wilson A, Trumpp A, Eshkind L: In vivo fate mapping with SCL regulatory elements identifies progenitors for primitive and definitive hematopoiesis in mice. Mech Dev; 2009 Oct;126(10):863-72
Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • One of the principal issues facing biomedical research is to elucidate developmental pathways and to establish the fate of stem and progenitor cells in vivo.
  • Hematopoiesis, the process of blood cell formation, provides a powerful experimental system for investigating this process.
  • Here, we employ transcriptional regulatory elements from the stem cell leukemia (SCL) gene to selectively label primitive and definitive hematopoiesis.
  • The distinct lineage-restricted potential of SCL-labelled early progenitors demonstrates that primitive erythroid cell fate specification is initiated during mid gastrulation.
  • [MeSH-major] Basic Helix-Loop-Helix Transcription Factors / physiology. Cell Lineage. Hematopoiesis. Proto-Oncogene Proteins / physiology. Stem Cells / cytology

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  • (PMID = 19631738.001).
  • [ISSN] 1872-6356
  • [Journal-full-title] Mechanisms of development
  • [ISO-abbreviation] Mech. Dev.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / Proto-Oncogene Proteins; 0 / Tal1 protein, mouse
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54. Jin H, Xu J, Qian F, Du L, Tan CY, Lin Z, Peng J, Wen Z: The 5' zebrafish scl promoter targets transcription to the brain, spinal cord, and hematopoietic and endothelial progenitors. Dev Dyn; 2006 Jan;235(1):60-7
ZFIN. ZFIN .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The stem cell leukemia (SCL) gene encodes a basic helix-loop-helix transcription factor and is essential for embryonic angiogenesis, hematopoietic stem cell specification, and erythrocyte maturation.
  • Detailed analysis of the stable transgenic fish reveals that this 5-kb upstream sequence is sufficient to direct the EGFP transcription to the brain, spinal cord, and hematopoietic-endothelial progenitors, possibly the hemangioblast, but not primitive erythrocyte, suggesting that the zebrafish scl transcription in hematopoietic-endothelial progenitors and erythrocyte is regulated by distinct cis element(s).
  • [MeSH-major] Basic Helix-Loop-Helix Transcription Factors / genetics. Brain / embryology. Endothelium / embryology. Hematopoietic Stem Cells / metabolism. Promoter Regions, Genetic. Proto-Oncogene Proteins / genetics. Spinal Cord / embryology. Zebrafish / genetics. Zebrafish Proteins / genetics

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  • [Copyright] 2005 Wiley-Liss, Inc.
  • (PMID = 16258937.001).
  • [ISSN] 1058-8388
  • [Journal-full-title] Developmental dynamics : an official publication of the American Association of Anatomists
  • [ISO-abbreviation] Dev. Dyn.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / Proto-Oncogene Proteins; 0 / Zebrafish Proteins; 0 / tal1 protein, zebrafish
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55. Guzman ML, Jordan CT: Lessons learned from the study of JunB: new insights for normal and leukemia stem cell biology. Cancer Cell; 2009 Apr 7;15(4):252-4
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  • [Title] Lessons learned from the study of JunB: new insights for normal and leukemia stem cell biology.
  • JunB is important in maintaining normal hematopoietic stem cell functions, but the mechanisms underlying its activity are not well understood.
  • In the current issue of Cancer Cell, a study by Santaguida et al. provides new insights into JunB's function and the genesis of myeloid disease.
  • [MeSH-major] Leukemia / pathology. Neoplastic Stem Cells / pathology. Proto-Oncogene Proteins c-jun / physiology
  • [MeSH-minor] Animals. Cell Differentiation

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  • [CommentOn] Cancer Cell. 2009 Apr 7;15(4):341-52 [19345332.001]
  • (PMID = 19345324.001).
  • [ISSN] 1878-3686
  • [Journal-full-title] Cancer cell
  • [ISO-abbreviation] Cancer Cell
  • [Language] eng
  • [Publication-type] Comment; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Proto-Oncogene Proteins c-jun
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56. Aikawa Y, Katsumoto T, Zhang P, Shima H, Shino M, Terui K, Ito E, Ohno H, Stanley ER, Singh H, Tenen DG, Kitabayashi I: PU.1-mediated upregulation of CSF1R is crucial for leukemia stem cell potential induced by MOZ-TIF2. Nat Med; 2010 May;16(5):580-5, 1p following 585
The Lens. Cited by Patents in .

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  • [Title] PU.1-mediated upregulation of CSF1R is crucial for leukemia stem cell potential induced by MOZ-TIF2.
  • Leukemias and other cancers possess self-renewing stem cells that help to maintain the cancer.
  • Cancer stem cell eradication is thought to be crucial for successful anticancer therapy.
  • Using an acute myeloid leukemia (AML) model induced by the leukemia-associated monocytic leukemia zinc finger (MOZ)-TIF2 fusion protein, we show here that AML can be cured by the ablation of leukemia stem cells.
  • Studies using PU.1-deficient mice showed that PU.1 is essential for the ability of MOZ-TIF2 to establish and maintain AML stem cells.
  • Cells expressing high amounts of CSF1R (CSF1R(high) cells), but not those expressing low amounts of CSF1R (CSF1R(low) cells), showed potent leukemia-initiating activity.
  • Moreover, induction of AML was suppressed in CSF1R-deficient mice and CSF1R inhibitors slowed the progression of MOZ-TIF2-induced leukemia.
  • Thus, in this subtype of AML, leukemia stem cells are contained within the CSF1R(high) cell population, and we suggest that targeting of PU.1-mediated upregulation of CSF1R expression might be a useful therapeutic approach.

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  • (PMID = 20418886.001).
  • [ISSN] 1546-170X
  • [Journal-full-title] Nature medicine
  • [ISO-abbreviation] Nat. Med.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA041456-24; United States / NCI NIH HHS / CA / R01 CA032551; United States / NCI NIH HHS / CA / P01 CA066996; United States / NCI NIH HHS / CA / 5P30-CA13330; United States / NCI NIH HHS / CA / CA041456-24; United States / NCI NIH HHS / CA / R01-CA41456; United States / NCI NIH HHS / CA / CA32551; United States / NCI NIH HHS / CA / R01 CA041456; United States / NCI NIH HHS / CA / P30 CA013330; United States / NHLBI NIH HHS / HL / R01 HL112719
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Colony-Stimulating Factors; 0 / NCOA2 protein, human; 0 / Nuclear Receptor Coactivator 2; 0 / Proto-Oncogene Proteins; 0 / Receptors, Colony-Stimulating Factor; 0 / Recombinant Fusion Proteins; 0 / Trans-Activators; 0 / proto-oncogene protein Spi-1; 81627-83-0 / Macrophage Colony-Stimulating Factor; EC 2.7.10.1 / Receptor, Macrophage Colony-Stimulating Factor
  • [Other-IDs] NLM/ NIHMS265702; NLM/ PMC3039870
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57. Williams BA, Wang XH, Keating A: Clonogenic assays measure leukemia stem cell killing not detectable by chromium release and flow cytometric cytotoxicity assays. Cytotherapy; 2010 Nov;12(7):951-60
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  • [Title] Clonogenic assays measure leukemia stem cell killing not detectable by chromium release and flow cytometric cytotoxicity assays.
  • BACKGROUND AIMS: NK-92, a permanent natural killer (NK) cell line, shows cytotoxicity against a variety of tumors and has been tested in a phase I trial.
  • We tested the toxicity of NK-92 and chemotherapy drugs against the stem cell capacity of the acute leukemia cell line, KG1.
  • METHODS: KG1 was assessed for stem cell frequency by serial dilution, single-cell sorting and colony growth in methylcellulose.
  • RESULTS: The culture-initiating cell frequency of whole KG1 was between 1 in 100 to 1000 by serial dilution and single-cell sorting.
  • The cumulative flow cytotoxicity assay was more sensitive than the chromium-release assay in detecting target cell killing.
  • At a 10:1 ratio NK-92 eliminated the clonogenic capacity of KG1, which was not predicted by the chromium-release assay.
  • CONCLUSIONS: Clonogenic assays provide a more sensitive means of assessing the effect of a cytotoxic agent against putative cancer stem cells within cell lines, provided that they grow well in liquid culture medium or methylcellulose.
  • [MeSH-major] Flow Cytometry. Killer Cells, Natural / metabolism. Leukemia / immunology. Neoplastic Stem Cells / metabolism. Tumor Stem Cell Assay
  • [MeSH-minor] Antigens, CD34 / biosynthesis. Antigens, CD38 / biosynthesis. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cell Culture Techniques. Cell Line, Tumor. Cell Separation. Chromium Isotopes / metabolism. Cytarabine / pharmacology. Cytarabine / therapeutic use. Cytotoxicity Tests, Immunologic / methods. Cytotoxicity, Immunologic. Daunorubicin / pharmacology. Daunorubicin / therapeutic use. Humans. Sensitivity and Specificity

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  • (PMID = 20230219.001).
  • [ISSN] 1477-2566
  • [Journal-full-title] Cytotherapy
  • [ISO-abbreviation] Cytotherapy
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD34; 0 / Chromium Isotopes; 04079A1RDZ / Cytarabine; EC 3.2.2.5 / Antigens, CD38; ZS7284E0ZP / Daunorubicin
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58. Sausville J, Molinolo AA, Cheng X, Frampton J, Takebe N, Gutkind JS, Feldman RA: RCAS/SCL-TVA animal model allows targeted delivery of polyoma middle T oncogene to vascular endothelial progenitors in vivo and results in hemangioma development. Clin Cancer Res; 2008 Jun 15;14(12):3948-55
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

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  • PURPOSE: To recapitulate the generation of cancer stem cells in the context of an intact animal using a retroviral vector capable of in vivo delivery of oncogenes to primitive endothelial and hematopoietic stem cells.
  • EXPERIMENTAL DESIGN: Targeting of these progenitors was achieved using transgenic mice in which the avian TVA retroviral receptor was placed under the control of the stem cell leukemia (scl/tal-1) gene promoter and SCL +19 enhancer.
  • RESULTS: Injection of an avian retrovirus encoding polyoma middle T (PyMT), an oncogene that transforms endothelial cells, caused rapid lethality in all SCL-TVA mice but not in control TVA(-) littermates.
  • The presence of TVA(+) cells in the lesions suggests that the cells originally infected by PyMT retained stem cell characteristics.
  • This animal model should allow the generation of endothelial cancer stem cells in the natural environment of an immunocompetent animal, thereby enabling the recapitulation of genetic alterations that are responsible for the initiation and progression of human malignancies of endothelial origin.
  • [MeSH-minor] Animals. Cell Transformation, Neoplastic / genetics. Cells, Cultured. Chickens. Mice. Mice, Inbred C57BL. Mice, Transgenic. Models, Animal. NIH 3T3 Cells. Oncogenes / physiology. Stem Cells / metabolism. Transgenes

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  • (PMID = 18559617.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, Polyomavirus Transforming; 0 / Avian Proteins; 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / Proto-Oncogene Proteins; 0 / Receptors, Virus; 0 / Tva receptor; 135471-20-4 / TAL1 protein, human
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59. Bockamp E, Antunes C, Maringer M, Heck R, Presser K, Beilke S, Ohngemach S, Alt R, Cross M, Sprengel R, Hartwig U, Kaina B, Schmitt S, Eshkind L: Tetracycline-controlled transgenic targeting from the SCL locus directs conditional expression to erythrocytes, megakaryocytes, granulocytes, and c-kit-expressing lineage-negative hematopoietic cells. Blood; 2006 Sep 1;108(5):1533-41
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  • The stem cell leukemia gene SCL, also known as TAL-1, encodes a basic helix-loop-helix transcription factor expressed in erythroid, myeloid, megakaryocytic, and hematopoietic stem cells.
  • Analysis of this mouse using different tetracycline-dependent reporter strains demonstrated that switchable transgene expression was restricted to erythrocytes, megakaryocytes, granulocytes, and, importantly, to the c-kit-expressing and lineage-negative cell fraction of the bone marrow.

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  • (PMID = 16675709.001).
  • [ISSN] 0006-4971
  • [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 / Basic Helix-Loop-Helix Transcription Factors; 0 / DNA Primers; 0 / Proto-Oncogene Proteins; 0 / Recombinant Proteins; 0 / Tal1 protein, mouse; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit; F8VB5M810T / Tetracycline
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60. Qian F, Zhen F, Xu J, Huang M, Li W, Wen Z: Distinct functions for different scl isoforms in zebrafish primitive and definitive hematopoiesis. PLoS Biol; 2007 May;5(5):e132
ZFIN. ZFIN .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The stem-cell leukemia (SCL, also known as TAL1) gene encodes a basic helix-loop-helix transcription factor that is essential for the initiation of primitive and definitive hematopoiesis, erythrocyte and megakarocyte differentiation, angiogenesis, and astrocyte development.
  • Functional analysis reveals that while scl-alpha and -beta are redundant for the initiation of primitive hematopoiesis, these two isoforms exert distinct functions in the regulation of primitive erythroid differentiation and definitive hematopoietic stem cell specification.
  • [MeSH-major] Basic Helix-Loop-Helix Transcription Factors / metabolism. Gene Expression. Hematopoiesis / physiology. Hematopoietic Stem Cells / cytology. Proto-Oncogene Proteins / metabolism. Zebrafish / genetics. Zebrafish Proteins / metabolism
  • [MeSH-minor] Animals. Base Sequence. Blotting, Northern. Cell Differentiation / physiology. Cloning, Molecular. DNA Primers. Immunohistochemistry. In Situ Hybridization. Molecular Sequence Data. Protein Isoforms / metabolism. Sequence Alignment. Sequence Analysis, DNA

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  • (PMID = 17472439.001).
  • [ISSN] 1545-7885
  • [Journal-full-title] PLoS biology
  • [ISO-abbreviation] PLoS Biol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / DNA Primers; 0 / Protein Isoforms; 0 / Proto-Oncogene Proteins; 0 / Zebrafish Proteins; 0 / tal1 protein, zebrafish
  • [Other-IDs] NLM/ PMC1858710
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61. Vormoor HJ: Malignant stem cells in childhood acute lymphoblastic leukemia: the stem cell concept revisited. Cell Cycle; 2009 Apr 1;8(7):996-9
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  • [Title] Malignant stem cells in childhood acute lymphoblastic leukemia: the stem cell concept revisited.
  • We have recently shown that in childhood acute lymphoblastic leukemia (ALL) blasts at different stages of immunophenotypic maturation possess stem cell properties.
  • Here, we discuss our results in the context of previous investigations of ALL stem cells and recent studies highlighting specific limitations of the xenotransplantation models for human hematopoietic cells.
  • Leukemia-propagating stem cells in ALL may be more frequent than previously thought!
  • [MeSH-major] Hematopoietic Stem Cell Transplantation. Neoplastic Stem Cells / metabolism. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism

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  • (PMID = 19270513.001).
  • [ISSN] 1551-4005
  • [Journal-full-title] Cell cycle (Georgetown, Tex.)
  • [ISO-abbreviation] Cell Cycle
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD19; 0 / Antigens, CD20; 0 / Antigens, CD34
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62. Faber J, Armstrong SA: Mixed lineage leukemia translocations and a leukemia stem cell program. Cancer Res; 2007 Sep 15;67(18):8425-8
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  • [Title] Mixed lineage leukemia translocations and a leukemia stem cell program.
  • Cancer stem cells (CSC) may provide the self-renewal capacity required to sustain a tumor.
  • One possibility is that CSC arise from the stem cell counterparts in normal tissues.
  • In support of this idea, we showed recently that mixed lineage leukemia fusion oncoproteins can convert committed hematopoietic progenitors into leukemias, which include leukemia stem cells expressing a self-renewal associated program in the context of a differentiated myeloid cell.
  • [MeSH-major] Hematopoietic Stem Cells / pathology. Leukemia, Biphenotypic, Acute / pathology. Neoplastic Stem Cells / pathology
  • [MeSH-minor] Animals. Cell Transformation, Neoplastic / genetics. Cell Transformation, Neoplastic / metabolism. Cell Transformation, Neoplastic / pathology. Humans. Oncogene Proteins, Fusion / biosynthesis. Oncogene Proteins, Fusion / genetics. Translocation, Genetic

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  • (PMID = 17875678.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Oncogene Proteins, Fusion
  • [Number-of-references] 24
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63. Park DM, Zhuang Z, Chen L, Szerlip N, Maric I, Li J, Sohn T, Kim SH, Lubensky IA, Vortmeyer AO, Rodgers GP, Oldfield EH, Lonser RR: von Hippel-Lindau disease-associated hemangioblastomas are derived from embryologic multipotent cells. PLoS Med; 2007 Feb;4(2):e60
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • BACKGROUND: To determine the origin of the neoplastic cell in central nervous system (CNS) hemangioblastomas in von Hippel-Lindau disease (VHL) and its role in tumor formation and distribution, we characterized and differentiated neoplastic cells from hemangioblastomas removed from VHL patients.
  • Consistent with an embryologically derived hemangioblast, the neoplastic cells demonstrated coexpression of the mesodermal markers brachyury, Flk-1 (vascular endothelial growth factor-2), and stem cell leukemia (Scl).
  • The neoplastic cells also expressed hematopoietic stem cell antigens and receptors including CD133, CD34, c-kit, Scl, erythropoietin, and erythropoietin receptor.
  • CONCLUSIONS: The neoplastic cell of origin for CNS hemangioblastomas in VHL patients is the mesoderm-derived, embryologically arrested hemangioblast.
  • [MeSH-major] Cerebellar Neoplasms / pathology. Hemangioblastoma / pathology. Multipotent Stem Cells / pathology. von Hippel-Lindau Disease / complications
  • [MeSH-minor] Adolescent. Adult. Antigens, CD13 / genetics. Blotting, Western. Cell Degranulation. Female. Follow-Up Studies. Gene Expression Regulation, Neoplastic. Humans. Male. Middle Aged. RNA, Neoplasm / genetics. Retrospective Studies. Reverse Transcriptase Polymerase Chain Reaction. Tumor Cells, Cultured

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  • (PMID = 17298169.001).
  • [ISSN] 1549-1676
  • [Journal-full-title] PLoS medicine
  • [ISO-abbreviation] PLoS Med.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / RNA, Neoplasm; EC 3.4.11.2 / Antigens, CD13
  • [Other-IDs] NLM/ PMC1796910
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64. Cheng Y, Zhang Z, Slape C, Aplan PD: Cre-loxP-mediated recombination between the SIL and SCL genes leads to a block in T-cell development at the CD4- CD8- to CD4+ CD8+ transition. Neoplasia; 2007 Apr;9(4):315-21
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cre-loxP-mediated recombination between the SIL and SCL genes leads to a block in T-cell development at the CD4- CD8- to CD4+ CD8+ transition.
  • In the most common form of stem cell leukemia (SCL) gene rearrangement, an interstitial deletion of 82 kb brings SCL under the control of regulatory elements that normally govern expression of the ubiquitously expressed SCL interrupting locus (SIL) gene, which is located directly upstream of SCL.
  • To investigate the effect of this fusion in a mouse model, a bacterial artificial chromosome (BAC) clone containing both human SIL and SCL genes was isolated, and loxP sites were inserted into intron 1 of both the SIL and SCL genes, corresponding to the sites at which recombination occurs in human T-cell acute lymphocytic leukemia patients.
  • These results demonstrate that conditional activation of SCL under control of SIL regulatory elements can impair normal T-cell development.
  • [MeSH-major] Basic Helix-Loop-Helix Transcription Factors / genetics. CD4-Positive T-Lymphocytes / enzymology. CD8-Positive T-Lymphocytes / enzymology. Cell Differentiation / genetics. Extracellular Matrix Proteins / physiology. Gene Rearrangement, T-Lymphocyte / genetics. Integrases / genetics. Intracellular Signaling Peptides and Proteins / genetics. Protein-Lysine 6-Oxidase / physiology. Proto-Oncogene Proteins / genetics

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  • (PMID = 17460775.001).
  • [ISSN] 1476-5586
  • [Journal-full-title] Neoplasia (New York, N.Y.)
  • [ISO-abbreviation] Neoplasia
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / / Z01 SC010379-06
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Intramural
  • [Publication-country] Canada
  • [Chemical-registry-number] 0 / Antigens, CD4; 0 / Antigens, CD8; 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / Extracellular Matrix Proteins; 0 / Intracellular Signaling Peptides and Proteins; 0 / Proto-Oncogene Proteins; 0 / STIL protein, human; 135471-20-4 / TAL1 protein, human; 149137-54-2 / Lox protein, mouse; EC 1.4.3.13 / Protein-Lysine 6-Oxidase; EC 2.7.7.- / Cre recombinase; EC 2.7.7.- / Integrases
  • [Other-IDs] NLM/ PMC1854848
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65. Zhang Y, Payne KJ, Zhu Y, Price MA, Parrish YK, Zielinska E, Barsky LW, Crooks GM: SCL expression at critical points in human hematopoietic lineage commitment. Stem Cells; 2005 Jun-Jul;23(6):852-60
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  • The stem cell leukemia (SCL or tal-1) gene was initially identified as a translocation partner in a leukemia that possessed both lymphoid and myeloid differentiation potential.
  • Mice that lacked SCL expression showed a complete block in hematopoiesis; thus, SCL was associated with hematopoietic stem cell (HSC) function.
  • Using recently defined surface immunophenotypes, we fluorescence-activated cell-sorted (FACS) highly purified populations of primary human hematopoietic progenitors for reverse transcription-polymerase chain reaction (RT-PCR) analysis of SCL expression.
  • [MeSH-major] DNA-Binding Proteins / biosynthesis. DNA-Binding Proteins / physiology. Hematopoietic Stem Cells / metabolism. Proto-Oncogene Proteins / biosynthesis. Proto-Oncogene Proteins / physiology. Transcription Factors / biosynthesis. Transcription Factors / physiology
  • [MeSH-minor] Animals. Antigens, CD34 / biosynthesis. Basic Helix-Loop-Helix Transcription Factors. Bone Marrow Cells / cytology. Cell Differentiation. Cell Line. Cell Lineage. Cell Separation. Cells, Cultured. Down-Regulation. Flow Cytometry. Humans. Immunophenotyping. Mice. Models, Biological. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Stem Cells / cytology. Thymus Gland / metabolism. Time Factors

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  • (PMID = 15917481.001).
  • [ISSN] 1066-5099
  • [Journal-full-title] Stem cells (Dayton, Ohio)
  • [ISO-abbreviation] Stem Cells
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / K01 DK066163; United States / NCI NIH HHS / CA / P01CA59318; United States / NHLBI NIH HHS / HL / P50HL54850; United States / NHLBI NIH HHS / HL / R01HL77912
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD34; 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / DNA-Binding Proteins; 0 / Proto-Oncogene Proteins; 0 / RNA, Messenger; 0 / Transcription Factors; 135471-20-4 / TAL1 protein, human
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66. Göthert JR, Gustin SE, Hall MA, Green AR, Göttgens B, Izon DJ, Begley CG: In vivo fate-tracing studies using the Scl stem cell enhancer: embryonic hematopoietic stem cells significantly contribute to adult hematopoiesis. Blood; 2005 Apr 1;105(7):2724-32
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  • [Title] In vivo fate-tracing studies using the Scl stem cell enhancer: embryonic hematopoietic stem cells significantly contribute to adult hematopoiesis.
  • Evidence for the lineage relationship between embryonic and adult hematopoietic stem cells (HSCs) in the mouse is primarily indirect.
  • In order to study this relationship in a direct manner, we expressed the tamoxifen-inducible Cre-ER(T) recombinase under the control of the stem cell leukemia (Scl) stem-cell enhancer in transgenic mice (HSC-SCL-Cre-ER(T)).
  • Strikingly, the proportion of marked cells within the transplanted and the in vivo-remaining HSC compartment was not different, implying that no further HSC generation occurred during late fetal and neonatal stages of development.
  • [MeSH-major] Enhancer Elements, Genetic. Hematopoiesis / physiology. Hematopoietic Stem Cells / cytology. Hematopoietic Stem Cells / physiology. Integrases / genetics
  • [MeSH-minor] Age Factors. Animals. Antineoplastic Agents, Hormonal / pharmacology. Biomarkers. Cell Lineage. Gene Expression / drug effects. Hematopoietic Stem Cell Transplantation. Lac Operon. Mice. Mice, Inbred C57BL. Mice, Transgenic. Recombination, Genetic. Tamoxifen / pharmacology. Transgenes / physiology

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  • (PMID = 15598809.001).
  • [ISSN] 0006-4971
  • [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 / Antineoplastic Agents, Hormonal; 0 / Biomarkers; 094ZI81Y45 / Tamoxifen; EC 2.7.7.- / Cre recombinase; EC 2.7.7.- / Integrases
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67. Delabesse E, Ogilvy S, Chapman MA, Piltz SG, Gottgens B, Green AR: Transcriptional regulation of the SCL locus: identification of an enhancer that targets the primitive erythroid lineage in vivo. Mol Cell Biol; 2005 Jun;25(12):5215-25
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  • The stem cell leukemia (SCL) gene, also known as TAL-1, encodes a basic helix-loop-helix protein that is essential for the formation of all hematopoietic lineages, including primitive erythropoiesis.
  • However, it is not known whether these SCL enhancers also regulate neighboring genes within the SCL locus, and the erythroid expression of SCL remains unexplained.
  • Here, we have quantitated transcripts from SCL and neighboring genes in multiple hematopoietic cell types.
  • A systematic survey of histone H3 and H4 acetylation throughout the SCL locus in different hematopoietic cell types identified several peaks of histone acetylation between SIL and MAP17, all of which corresponded to previously characterized SCL enhancers or to the MAP17 promoter.
  • Downstream of MAP17 (and 40 kb downstream of SCL exon 1a), an additional peak of acetylation was identified in hematopoietic cells and was found to correlate with expression of SCL but not other neighboring genes.
  • This +40 region is conserved in human-dog-mouse-rat sequence comparisons, functions as an erythroid cell-restricted enhancer in vitro, and directs beta-galactosidase expression to primitive, but not definitive, erythroblasts in transgenic mice.

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  • (PMID = 15923636.001).
  • [ISSN] 0270-7306
  • [Journal-full-title] Molecular and cellular biology
  • [ISO-abbreviation] Mol. Cell. Biol.
  • [Language] ENG
  • [Grant] United Kingdom / Wellcome Trust / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / DNA-Binding Proteins; 0 / Histones; 0 / Membrane Proteins; 0 / Neoplasm Proteins; 0 / PDZK1IP1 protein, human; 0 / Pdzk1ip1 protein, mouse; 0 / Pdzk1ip1 protein, rat; 0 / Proto-Oncogene Proteins; 0 / Transcription Factors; 135471-20-4 / TAL1 protein, human
  • [Other-IDs] NLM/ PMC1140604
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68. Brandts CH, Berdel WE, Serve H: Oncogenic signaling in acute myeloid leukemia. Curr Drug Targets; 2007 Feb;8(2):237-46
Genetic Alliance. consumer health - Leukemia, Myeloid.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Oncogenic signaling in acute myeloid leukemia.
  • Acute myeloid leukemia (AML) is a malignant disease of the bone marrow.
  • It is increasingly recognized that AML represents a hierarchical disease, originating from a leukemia stem cell population.
  • [MeSH-major] Leukemia, Myeloid / genetics. Oncogenes. Signal Transduction
  • [MeSH-minor] Acute Disease. Animals. Cell Differentiation. Cell Proliferation. Humans. Models, Animal

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  • (PMID = 17305501.001).
  • [ISSN] 1873-5592
  • [Journal-full-title] Current drug targets
  • [ISO-abbreviation] Curr Drug Targets
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Netherlands
  • [Number-of-references] 135
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69. Unger C, Kärner E, Treschow A, Stellan B, Felldin U, Concha H, Wendel M, Hovatta O, Aints A, Ahrlund-Richter L, Dilber MS: Lentiviral-mediated HoxB4 expression in human embryonic stem cells initiates early hematopoiesis in a dose-dependent manner but does not promote myeloid differentiation. Stem Cells; 2008 Oct;26(10):2455-66

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Lentiviral-mediated HoxB4 expression in human embryonic stem cells initiates early hematopoiesis in a dose-dependent manner but does not promote myeloid differentiation.
  • The variation of HoxB4 expression levels might be a key regulatory mechanism in the differentiation of human embryonic stem cell (hESC)-derived hematopoietic stem cells (HSCs).
  • High levels of HoxB4 expression correlated to an improved yield of cells expressing CD34, CD38, the stem cell leukemia gene, and vascular epithelium-cadherin.
  • However, no improvement in myeloid cell maturation was observed, as determined by colony formation assays.
  • In contrast, hESCs with low HoxB4 levels did not show any elevated hematopoietic development.
  • These data suggest that HoxB4-induced effects on hESC-derived HSCs are concentration-dependent during in vitro development and reduce proliferation of other cell types in vitro and in vivo.
  • [MeSH-major] Cell Differentiation. Embryonic Stem Cells / cytology. Embryonic Stem Cells / metabolism. Hematopoiesis / genetics. Homeodomain Proteins / genetics. Lentivirus / genetics. Myeloid Cells / cytology. Transcription Factors / genetics
  • [MeSH-minor] Animals. Biomarkers / metabolism. Cell Proliferation. Colony-Forming Units Assay. Gene Expression Regulation, Developmental. Genetic Vectors / genetics. Green Fluorescent Proteins / metabolism. HeLa Cells. Humans. Male. Mice. Mice, SCID. Octamer Transcription Factor-3 / metabolism. Teratoma / pathology. Transduction, Genetic

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  • (PMID = 18617691.001).
  • [ISSN] 1549-4918
  • [Journal-full-title] Stem cells (Dayton, Ohio)
  • [ISO-abbreviation] Stem Cells
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers; 0 / HOXB4 protein, human; 0 / Homeodomain Proteins; 0 / Octamer Transcription Factor-3; 0 / POU5F1 protein, human; 0 / Transcription Factors; 0 / enhanced green fluorescent protein; 147336-22-9 / Green Fluorescent Proteins
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70. Kouroukis CT, Chia S, Verma S, Robson D, Desbiens C, Cripps C, Mikhael J: Canadian supportive care recommendations for the management of neutropenia in patients with cancer. Curr Oncol; 2008 Jan;15(1):9-23

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • We review existing international guidelines, the indications for primary and secondary prophylaxis, the importance of maintaining dose intensity, and the use of csfs in leukemia, stem-cell transplantation, and radiotherapy.
  • Finally, csf dosing and schedules, duration of therapy, and associated acute and potential chronic toxicities are examined.

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  • (PMID = 18317581.001).
  • [ISSN] 1198-0052
  • [Journal-full-title] Current oncology (Toronto, Ont.)
  • [ISO-abbreviation] Curr Oncol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Canada
  • [Other-IDs] NLM/ PMC2259432
  • [Keywords] NOTNLM ; Canadian recommendations / chemotherapy-induced neutropenia / colony-stimulating factors / febrile neutropenia / neutropenia / safety / supportive care
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71. Wu KF, Ma XT, Zheng GG, Song YH: [Leukemia stem cells and their microenvironment--editorial]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2007 Dec;15(6):1139-41
MedlinePlus Health Information. consumer health - Leukemia.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Leukemia stem cells and their microenvironment--editorial].
  • As pioneer of tumor stem cell research, leukemia stem cell research has not only important theoretical significance, but also clinical application potential.
  • The survival and development of stem cells are directly impacted by their microenvironment.
  • The research on leukemia stem cells and their microenvironment are now becoming a hot topic.
  • The author presumes that stem cells are a population with heterogenecity and hierarchy; any single cell from the population is difficult to form a clone; the interaction between the leukemia stem cell and its microenvironment can be described by the concept of leukemia stem cell niche.
  • In this article, the leukemia cell population with heterogenecity and hierarchy as well as leukemia stem cell niche were summarized and discussed.

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  • (PMID = 18088452.001).
  • [ISSN] 1009-2137
  • [Journal-full-title] Zhongguo shi yan xue ye xue za zhi
  • [ISO-abbreviation] Zhongguo Shi Yan Xue Ye Xue Za Zhi
  • [Language] CHI
  • [Publication-type] Editorial; English Abstract; Research Support, Non-U.S. Gov't
  • [Publication-country] China
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72. Funayama K, Murai F, Shimane M, Nomura H, Asano S: Adhesion-induced drug resistance in leukemia stem cells. Pharmacology; 2010;86(2):79-84
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Adhesion-induced drug resistance in leukemia stem cells.
  • The co-culture of TF-1 leukemia cells and MS-5 stromal cells produces a cobblestone area which partially mimics the leukemia stem cell niche.
  • The adhering leukemia cells are shown to become less sensitive to cytarabine, etoposide and daunorubicin.
  • These changes are associated with an increased proportion of the G0/G1 phase, increased upregulation of cyclin-dependent kinase inhibitors, and increased levels of Bcl-2, but not with any change in the expression of BAX or drug transporters such as ABCG2 and MDR1, compared to monocultured leukemic cells.
  • These findings suggest that adhesion alone can lead to drug resistance in leukemic stem cells by various mechanisms.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Drug Resistance, Neoplasm. Leukemia / physiopathology. Neoplastic Stem Cells / drug effects. Neoplastic Stem Cells / physiology. Stem Cell Niche / physiopathology. Stromal Cells / physiology
  • [MeSH-minor] Bone Marrow Cells / physiology. Cell Adhesion. Cell Cycle. Cell Line, Tumor. Coculture Techniques. Cyclin-Dependent Kinase Inhibitor Proteins / genetics. Cyclin-Dependent Kinase Inhibitor Proteins / metabolism. Cytarabine / pharmacology. Daunorubicin / pharmacokinetics. Daunorubicin / pharmacology. Etoposide / pharmacology. Humans. Lysosomes / metabolism. Osmolar Concentration. Proto-Oncogene Proteins c-bcl-2 / genetics. Proto-Oncogene Proteins c-bcl-2 / metabolism. Up-Regulation. Vacuolar Proton-Translocating ATPases / genetics. Vacuolar Proton-Translocating ATPases / metabolism

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  • Hazardous Substances Data Bank. CYTARABINE .
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  • [Copyright] Copyright 2010 S. Karger AG, Basel.
  • [ErratumIn] Pharmacology. 2010;86(4):202
  • (PMID = 20689339.001).
  • [ISSN] 1423-0313
  • [Journal-full-title] Pharmacology
  • [ISO-abbreviation] Pharmacology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Cyclin-Dependent Kinase Inhibitor Proteins; 0 / Proto-Oncogene Proteins c-bcl-2; 04079A1RDZ / Cytarabine; 6PLQ3CP4P3 / Etoposide; EC 3.6.1.- / Vacuolar Proton-Translocating ATPases; ZS7284E0ZP / Daunorubicin
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73. Wang Z, Iwasaki M, Ficara F, Lin C, Matheny C, Wong SH, Smith KS, Cleary ML: GSK-3 promotes conditional association of CREB and its coactivators with MEIS1 to facilitate HOX-mediated transcription and oncogenesis. Cancer Cell; 2010 Jun 15;17(6):597-608
The Lens. Cited by Patents in .

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  • Acute leukemias induced by MLL chimeric oncoproteins are among the subset of cancers distinguished by a paradoxical dependence on GSK-3 kinase activity for sustained proliferation.
  • We demonstrate here that GSK-3 maintains the MLL leukemia stem cell transcriptional program by promoting the conditional association of CREB and its coactivators TORC and CBP with homedomain protein MEIS1, a critical component of the MLL-subordinate program, which in turn facilitates HOX-mediated transcription and transformation.
  • This mechanism also applies to hematopoietic cells transformed by other HOX genes, including CDX2, which is highly expressed in a majority of acute myeloid leukemias, thus providing a molecular approach based on GSK-3 inhibitory strategies to target HOX-associated transcription in a broad spectrum of leukemias.

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  • [Copyright] Copyright 2010 Elsevier Inc. All rights reserved.
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  • (PMID = 20541704.001).
  • [ISSN] 1878-3686
  • [Journal-full-title] Cancer cell
  • [ISO-abbreviation] Cancer Cell
  • [Language] ENG
  • [Databank-accession-numbers] GEO/ GSE21842
  • [Grant] United States / NCI NIH HHS / CA / T32 CA009151; United States / NCI NIH HHS / CA / R01 CA116606; United States / NCI NIH HHS / CA / T32 CA009151-37; United States / NCI NIH HHS / CA / CA116606-05; United States / NCI NIH HHS / CA / T32 CA09151; United States / NCI NIH HHS / CA / CA009151-37; United States / NCI NIH HHS / CA / CA116606; United States / NCI NIH HHS / CA / R01 CA116606-05
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CRTC1 protein, human; 0 / CRTC2 protein, human; 0 / Cdx4 protein, mouse; 0 / Cyclic AMP Response Element-Binding Protein; 0 / DNA-Binding Proteins; 0 / HOXB1 homeodomain protein; 0 / Homeodomain Proteins; 0 / Hoxb4 protein, mouse; 0 / Indoles; 0 / Maleimides; 0 / Neoplasm Proteins; 0 / Oncogene Proteins, Fusion; 0 / Pbx1 protein, mouse; 0 / Proto-Oncogene Proteins; 0 / Proto-Oncogene Proteins c-fos; 0 / SB 216763; 0 / Transcription Factors; 0 / homeobox protein HOXA9; 0 / myeloid ecotropic viral integration site 1 protein; 0 / pbx1 protein, human; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.3.1.48 / CREB-Binding Protein; EC 2.7.11.26 / Glycogen Synthase Kinase 3
  • [Other-IDs] NLM/ NIHMS203816; NLM/ PMC2919232
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74. Jamieson CH, Barroga CF, Vainchenker WP: Miscreant myeloproliferative disorder stem cells. Leukemia; 2008 Nov;22(11):2011-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Miscreant myeloproliferative disorder stem cells.
  • Myeloproliferative disorders (MPDs), typified by robust marrow and extramedullary hematopoiesis, have a propensity to progress to acute leukemia.
  • Although the hematopoietic stem cell (HSC) origin of MPDs was suggested over 30 years ago, only recently the HSC-specific effects of MPD molecular mutations have been investigated.
  • The pivotal role of BCR-ABL in chronic myeloid leukemia (CML) development provided the rationale for targeted therapy, which greatly reduced mortality rates.
  • Although JAK2 activation appears to be central to BCR-ABL-negative MPD pathogenesis, its effects may be cell type and context specific.
  • Recent evidence suggests that acquired mutations misdirect differentiation and survival of the MPD-initiating stem cell resulting in the production of aberrant self-renewing progenitors that subvert the microenvironment leading to leukemia stem cell generation and leukemic transformation.
  • Thus, combined therapies targeting aberrant molecular pathways may be required to redirect miscreant MPD stem cells.
  • [MeSH-major] Fusion Proteins, bcr-abl / genetics. Myeloid Progenitor Cells / pathology. Myeloproliferative Disorders / etiology. Myeloproliferative Disorders / pathology. Neoplastic Stem Cells / pathology
  • [MeSH-minor] Cell Differentiation. Humans

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  • (PMID = 18923436.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] EC 2.7.10.2 / Fusion Proteins, bcr-abl
  • [Number-of-references] 30
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75. Chan WI, Huntly BJ: Leukemia stem cells in acute myeloid leukemia. Semin Oncol; 2008 Aug;35(4):326-35
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Leukemia stem cells in acute myeloid leukemia.
  • At the apex of these hierarchies sit so-called cancer stem cells or cancer-initiating cells, which are wholly responsible for the continued growth and propagation of the tumor.
  • The first such cancer stem cells were described in acute myeloid leukemia (AML).
  • Following treatment, the majority of tumors, including leukemias, initially respond.
  • A likely explanation for this is that leukemia stem cells are relatively insensitive to current therapies and that tumor bulk reduction reflects the death of leukemic blasts that lack tumor initiation potential.
  • This review will focus on what is known of the molecular and cellular biology of the leukemia stem cell and the leukemia stem cell niche in AML and then will identify molecular pathways critical for leukemia stem cells.
  • Finally, we will identify current and prospective therapeutic targets to facilitate eradication of leukemia stem cells.
  • It is hoped that, in defining the biology of cancer stem cells and how they differ from their adult tissue stem cell counterpart, we should identify therapeutic targets to improve treatment outcomes in leukemia and other malignant diseases.
  • [MeSH-major] Leukemia, Myeloid, Acute / pathology. Neoplastic Stem Cells / pathology
  • [MeSH-minor] Apoptosis. Cell Differentiation. Cell Lineage. Drug Delivery Systems. Humans. Signal Transduction

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  • (PMID = 18692683.001).
  • [ISSN] 0093-7754
  • [Journal-full-title] Seminars in oncology
  • [ISO-abbreviation] Semin. Oncol.
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / G116/187
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 64
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76. Niebuhr B, Fischer M, Täger M, Cammenga J, Stocking C: Gatekeeper function of the RUNX1 transcription factor in acute leukemia. Blood Cells Mol Dis; 2008 Mar-Apr;40(2):211-8
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Gatekeeper function of the RUNX1 transcription factor in acute leukemia.
  • The RUNX1 gene encodes the alpha subunit of the core binding factor (CBF) and is a common target of genetic mutations in acute leukemia.
  • This pool of "escaped" cells is the target of secondary mutations, accumulating over time to induce the aggressive manifestation of acute leukemia.
  • Evidence from patient and animal studies supports the concept that RUNX1 mutations are the initiating event in different leukemia subtypes, but also suggests that diverse mechanisms are used to subvert RUNX1 function.
  • A number of different approaches have led to the identification of secondary events that lead to the overt acute phase; however, the majority is unknown.
  • Finally, the concept of the "leukemia stem cell" and its therapeutic importance is discussed in light of the RUNX1 gatekeeper function.
  • [MeSH-major] Core Binding Factor Alpha 2 Subunit / metabolism. Leukemia, Myeloid, Acute / metabolism. Oncogene Proteins, Fusion / metabolism. Transcription Factors / metabolism
  • [MeSH-minor] Animals. Cell Differentiation / genetics. Cell Transformation, Neoplastic. Hematopoiesis / genetics. Humans. Mutation. Neoplastic Stem Cells / metabolism. Transcription, Genetic

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  • (PMID = 17920312.001).
  • [ISSN] 1079-9796
  • [Journal-full-title] Blood cells, molecules & diseases
  • [ISO-abbreviation] Blood Cells Mol. Dis.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / Oncogene Proteins, Fusion; 0 / RUNX1 protein, human; 0 / Transcription Factors
  • [Number-of-references] 81
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77. Wojiski S, Guibal FC, Kindler T, Lee BH, Jesneck JL, Fabian A, Tenen DG, Gilliland DG: PML-RARalpha initiates leukemia by conferring properties of self-renewal to committed promyelocytic progenitors. Leukemia; 2009 Aug;23(8):1462-71
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] PML-RARalpha initiates leukemia by conferring properties of self-renewal to committed promyelocytic progenitors.
  • Acute promyelocytic leukemia (APL) is characterized by hyperproliferation of promyelocytes, progenitors that are committed to terminal differentiation into granulocytes, making it an ideal disease in which to study the transforming potential of less primitive cell types.
  • We utilized a murine model of APL in which the PML-RARalpha oncogene is expressed from the endogenous cathepsin G promoter to test the hypothesis that leukemia stem cell (LSC) activity resides within the differentiated promyelocyte compartment.
  • Progression to acute leukemia was associated with an expansion of the promyelocyte compartment at the expense of other stem, progenitor and terminally differentiated populations.
  • Leukemic promyelocytes exhibited properties of self-renewal, and were capable of engendering leukemia in secondary recipient mice.
  • These findings are consistent with the hypothesis that cancer stem cells may arise from committed progenitors that lack stem cell properties, provided that the initiating mutation in cancer progression activates programs that confer properties of self-renewal.

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  • (PMID = 19322209.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA66996; United States / NCI NIH HHS / CA / P01 CA066996-130011; United States / NIDDK NIH HHS / DK / DK50654; United States / NCI NIH HHS / CA / CA066996-130011; United States / NCI NIH HHS / CA / P01 CA066996; United States / NIDDK NIH HHS / DK / DK050654-060004; United States / NCI NIH HHS / CA / P01 CA066996-120009; United States / Howard Hughes Medical Institute / / ; United States / NIDDK NIH HHS / DK / P01 DK050654; United States / NIDDK NIH HHS / DK / P01 DK050654-060004; United States / NCI NIH HHS / CA / CA066996-120009
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Oncogene Proteins, Fusion; 0 / Recombinant Fusion Proteins; 0 / promyelocytic leukemia-retinoic acid receptor alpha fusion oncoprotein; 5688UTC01R / Tretinoin; EC 3.4.- / Cathepsins; EC 3.4.21.- / Serine Endopeptidases; EC 3.4.21.20 / CTSG protein, human; EC 3.4.21.20 / Cathepsin G; EC 3.4.21.20 / Ctsg protein, mouse
  • [Other-IDs] NLM/ NIHMS222020; NLM/ PMC2914549
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78. Panagopoulos I, Kerndrup G, Carlsen N, Strömbeck B, Isaksson M, Johansson B: Fusion of NUP98 and the SET binding protein 1 (SETBP1) gene in a paediatric acute T cell lymphoblastic leukaemia with t(11;18)(p15;q12). Br J Haematol; 2007 Jan;136(2):294-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Fusion of NUP98 and the SET binding protein 1 (SETBP1) gene in a paediatric acute T cell lymphoblastic leukaemia with t(11;18)(p15;q12).
  • Three NUP98 chimaeras have previously been reported in T cell acute lymphoblastic leukaemia (T-ALL): NUP98/ADD3, NUP98/CCDC28A, and NUP98/RAP1GDS1.
  • Nested polymerase chain reaction did not amplify the reciprocal SETBP1/NUP98, suggesting that NUP98/SETBP1 transcript is pathogenetically important.
  • SETBP1 has previously not been implicated in leukaemias; however, it encodes a protein that specifically interacts with SET, fused to NUP214 in a case of acute undifferentiated leukaemia.
  • [MeSH-major] Carrier Proteins / genetics. Chromosomes, Human, Pair 11. Chromosomes, Human, Pair 18. Leukemia-Lymphoma, Adult T-Cell / genetics. Nuclear Pore Complex Proteins / genetics. Nuclear Proteins / genetics. Oncogene Proteins, Fusion / genetics. Translocation, Genetic

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  • (PMID = 17233820.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Carrier Proteins; 0 / Nuclear Pore Complex Proteins; 0 / Nuclear Proteins; 0 / Oncogene Proteins, Fusion; 0 / SETBP1 protein, human; 0 / nuclear pore complex protein 98
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79. Vaiselbuh SR, Edelman M, Lipton JM, Liu JM: Ectopic human mesenchymal stem cell-coated scaffolds in NOD/SCID mice: an in vivo model of the leukemia niche. Tissue Eng Part C Methods; 2010 Dec;16(6):1523-31
MedlinePlus Health Information. consumer health - Leukemia.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Ectopic human mesenchymal stem cell-coated scaffolds in NOD/SCID mice: an in vivo model of the leukemia niche.
  • Human mesenchymal stem cells form the supportive structure in which the functional cells of a differentiated tissue reside.
  • We describe the creation of ectopic niches within polyurethane scaffolds coated with human mesenchymal stem cells.
  • When implanted subcutaneously in NOD/SCID mice, these niches supported engraftment of primary human acute myeloid leukemia cells.
  • The chemokine stromal-derived factor-1 (SDF-1 or CXCL12) and its receptor CXCR4 are critical for homing and migration of acute myeloid leukemia.
  • We believe that these scaffold niches provide a new and powerful tool to study the leukemia stem cell microenvironment and may be useful for identification of novel drug targets.
  • [MeSH-major] Choristoma / pathology. Leukemia / pathology. Mesenchymal Stromal Cells / cytology. Stem Cell Niche / pathology. Tissue Scaffolds
  • [MeSH-minor] Animals. Cells, Cultured. Coated Materials, Biocompatible / chemistry. Coated Materials, Biocompatible / pharmacology. Disease Models, Animal. Humans. Mesenchymal Stem Cell Transplantation. Mice. Mice, Inbred NOD. Mice, SCID. Neoplastic Stem Cells / cytology. Neoplastic Stem Cells / pathology. Transplantation, Heterologous. Tumor Microenvironment / physiology

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  • (PMID = 20586611.001).
  • [ISSN] 1937-3392
  • [Journal-full-title] Tissue engineering. Part C, Methods
  • [ISO-abbreviation] Tissue Eng Part C Methods
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Coated Materials, Biocompatible
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80. Zhou J, Zhang H, Gu P, Bai J, Margolick JB, Zhang Y: NF-kappaB pathway inhibitors preferentially inhibit breast cancer stem-like cells. Breast Cancer Res Treat; 2008 Oct;111(3):419-27
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] NF-kappaB pathway inhibitors preferentially inhibit breast cancer stem-like cells.
  • Accumulating evidence indicates that breast cancer is caused by cancer stem cells and cure of breast cancer requires eradication of breast cancer stem cells.
  • Previous studies with leukemia stem cells have shown that NF-kappaB pathway is important for leukemia stem cell survival.
  • In this study, by using MCF7 sphere cells as model of breast cancer stem-like cells, we evaluated the effect of NF-kappaB pathway specific inhibitors on human breast cancer MCF7 sphere cells.
  • Three inhibitors including parthenolide (PTL), pyrrolidinedithiocarbamate (PDTC) and its analog diethyldithiocarbamate (DETC) were found to preferentially inhibit MCF7 sphere cell proliferation.
  • These compounds also showed preferential inhibition in term of proliferation and colony formation on MCF7 side population (SP) cells, a small fraction of MCF7 cells known to enrich in breast cancer stem-like cells.
  • This study suggests that breast cancer stem-like cells could be selectively inhibited by targeting signaling pathways important for breast cancer stem-like cells.

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  • (PMID = 17965935.001).
  • [ISSN] 0167-6806
  • [Journal-full-title] Breast cancer research and treatment
  • [ISO-abbreviation] Breast Cancer Res. Treat.
  • [Language] ENG
  • [Grant] United States / NIAID NIH HHS / AI / P30 AI042855-03; United States / NIAID NIH HHS / AI / R01 AI044063; United States / NIAID NIH HHS / AI / AI44063
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / NF-kappa B; 0 / Pyrrolidines; 0 / Sesquiterpenes; 0 / Thiocarbamates; 25769-03-3 / pyrrolidine dithiocarbamic acid; 2RDB26I5ZB / parthenolide; 99Z2744345 / Ditiocarb; P88XT4IS4D / Paclitaxel
  • [Other-IDs] NLM/ NIHMS365443; NLM/ PMC3320112
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81. Patterson LJ, Gering M, Patient R: Scl is required for dorsal aorta as well as blood formation in zebrafish embryos. Blood; 2005 May 01;105(9):3502-11
ZFIN. ZFIN .

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  • The transcription factor, Scl/Tal1 (stem cell leukemia protein), is essential for hematopoiesis but thought to be required only for remodeling of endothelium in mouse embryos.
  • We conclude that scl is especially critical for the development of arteries where adult hematopoietic stem cells emerge, implicating scl in the formation of hemogenic endothelium.
  • [MeSH-minor] Animals. Basic Helix-Loop-Helix Transcription Factors. Blood Circulation / genetics. Embryo, Nonmammalian. Endothelium, Vascular / cytology. Endothelium, Vascular / embryology. Endothelium, Vascular / growth & development. Gene Expression Regulation, Developmental. Hematopoietic Stem Cells / cytology. Mice. Neovascularization, Physiologic. Zebrafish

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  • (PMID = 15644413.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / MC/ U137981013
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / DNA-Binding Proteins; 0 / Proto-Oncogene Proteins; 0 / Transcription Factors; 0 / Zebrafish Proteins; 0 / tal1 protein, zebrafish
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82. Fukukawa C, Shima H, Tanuma N, Okada T, Kato N, Adachi Y, Kikuchi K: The oncoprotein I-2PP2A/SET negatively regulates the MEK/ERK pathway and cell proliferation. Int J Oncol; 2005 Mar;26(3):751-6
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  • [Title] The oncoprotein I-2PP2A/SET negatively regulates the MEK/ERK pathway and cell proliferation.
  • I-2PP2A/SET, the translocation breakpoint-encoded protein expressed in acute undifferentiated leukemia, was identified as an inhibitor of protein phosphatase 2A (PP2A).
  • Induction of exogenous I-2PP2A/SET at a ratio of 1:1 to the endogenous protein resulted in suppression of cell proliferation.
  • In contrast, siRNA-mediated depletion of I-2PP2A/SET resulted in enhanced cell proliferation.
  • To examine the mode of action by which I-2PP2A/SET suppresses cell proliferation, we determined the effect of over-expressed I-2PP2A/SET on ERK activation.
  • I-2PP2A/SET suppressed activation of ERK following EGF stimulation but did not affect activation levels of stress kinases, JNK and p38.
  • These data suggest that I-2PP2A/SET negatively regulates cell growth by inhibiting the G1/S transition and inhibiting the MEK/ERK pathway stimulated by external stimuli.
  • [MeSH-major] Cell Proliferation. Chromosomal Proteins, Non-Histone / genetics. Chromosomal Proteins, Non-Histone / pharmacology. Extracellular Signal-Regulated MAP Kinases / pharmacology. MAP Kinase Kinase Kinases / pharmacology. Phosphoprotein Phosphatases / genetics. Phosphoprotein Phosphatases / pharmacology. Transcription Factors / genetics. Transcription Factors / pharmacology
  • [MeSH-minor] Cell Cycle. Gene Expression Profiling. HeLa Cells. Histone Chaperones. Humans. Protein Phosphatase 2

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  • (PMID = 15703833.001).
  • [ISSN] 1019-6439
  • [Journal-full-title] International journal of oncology
  • [ISO-abbreviation] Int. J. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Chromosomal Proteins, Non-Histone; 0 / Histone Chaperones; 0 / SET protein, human; 0 / Transcription Factors; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases; EC 2.7.11.25 / MAP Kinase Kinase Kinases; EC 3.1.3.16 / Phosphoprotein Phosphatases; EC 3.1.3.16 / Protein Phosphatase 2
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83. Schuringa JJ, Schepers H: Ex vivo assays to study self-renewal and long-term expansion of genetically modified primary human acute myeloid leukemia stem cells. Methods Mol Biol; 2009;538:287-300
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  • [Title] Ex vivo assays to study self-renewal and long-term expansion of genetically modified primary human acute myeloid leukemia stem cells.
  • With the emergence of the concept of the leukemia stem cell, assays to study them remain pivotal in understanding (leukemic) stem cell biology.
  • Although the in vivo NOD-SCID xenotransplantation model is still the favored model of choice in most cases, this system has some limitations as well, such as its cost-effectiveness, duration, and the lack of engraftability of cells from subsets of acute myeloid leukemia (AML) patients.
  • Here, we have described an ex vivo bone marrow stromal coculture system in which CD34(+) cells, but not CD34(-) cells, from the bone marrow or peripheral blood of AML patients can give rise to long-term cultures (LTC) that can be maintained for over 20 weeks.
  • Self-renewal within these L-CAs can be determined by sequential passaging of these L-CAs onto new MS5 stromal layers, which results in the generation of second, third, and fourth L-CAs that are able to sustain long-term expansion and generate high numbers of immature undifferentiated suspension cells.
  • Together, these tools should allow a further molecular elucidation of derailed signal transduction in AML stem cells.
  • [MeSH-major] Biological Assay / methods. Cell Culture Techniques / methods. Leukemia, Myeloid, Acute / pathology. Neoplastic Stem Cells / pathology. Transduction, Genetic / methods
  • [MeSH-minor] Animals. Antigens, CD34 / metabolism. Bone Marrow Cells / metabolism. Bone Marrow Cells / pathology. Cell Line, Tumor. Cells, Cultured. Coculture Techniques. Humans. Lentivirus / genetics. Mice. Neoplasm Proteins. Stromal Cells / metabolism. Stromal Cells / pathology

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  • (PMID = 19277587.001).
  • [ISSN] 1064-3745
  • [Journal-full-title] Methods in molecular biology (Clifton, N.J.)
  • [ISO-abbreviation] Methods Mol. Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD34; 0 / Neoplasm Proteins
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84. Faber J, Armstrong SA: Defining leukemia stem cells in MLL-translocated leukemias: implications for novel therapeutic strategies. Klin Padiatr; 2007 Nov-Dec;219(6):306-11
MedlinePlus Health Information. consumer health - Leukemia.

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  • [Title] Defining leukemia stem cells in MLL-translocated leukemias: implications for novel therapeutic strategies.
  • Hematological malignancies and probably many other tumors are dependent on highly proliferating and self-renewing cancer stem cells.
  • An important question in the development of novel, less toxic antileukemic strategies specifically targeting leukemia stem cells is how closely leukemia stem cells are related to normal hematopoietic stem cells.
  • It has been recently demonstrated that leukemia stem cells can be derived from different stages in normal hematopoiesis and have unique phenotypic and genetic features.
  • Introduction of Mixed-lineage leukemia ( MLL)-fusion oncoproteins, frequently found in infant leukemias and therapy-related leukemias, into differentiated hematopoietic progenitor cells results in the generation of leukemias with a high frequency of leukemia stem cells.
  • The progenitor-derived leukemia stem cells ectopically express a limited stem cell program while maintaining the global identity of differentiated myeloid cells.
  • Development of therapeutic strategies that specifically target the leukemia stem cell program while sparing normal hematopoietic stem cells may represent a novel therapeutic approach in human leukemias with high efficacy yet less side effects.
  • [MeSH-major] Leukemia / therapy. Leukemia, Biphenotypic, Acute. Myeloid-Lymphoid Leukemia Protein / genetics. Neoplastic Stem Cells
  • [MeSH-minor] Child. Hematopoietic Stem Cells. Histone-Lysine N-Methyltransferase. Humans. Infant. Oncogene Proteins, Fusion. Phenotype

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  • (PMID = 18050039.001).
  • [ISSN] 0300-8630
  • [Journal-full-title] Klinische Pädiatrie
  • [ISO-abbreviation] Klin Padiatr
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Review
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / MLL protein, human; 0 / Oncogene Proteins, Fusion; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
  • [Number-of-references] 62
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85. Xia ZB, Popovic R, Chen J, Theisler C, Stuart T, Santillan DA, Erfurth F, Diaz MO, Zeleznik-Le NJ: The MLL fusion gene, MLL-AF4, regulates cyclin-dependent kinase inhibitor CDKN1B (p27kip1) expression. Proc Natl Acad Sci U S A; 2005 Sep 27;102(39):14028-33
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  • MLL, involved in many chromosomal translocations associated with acute myeloid and lymphoid leukemia, has >50 known partner genes with which it is able to form in-frame fusions.
  • Characterizing important downstream target genes of MLL and of MLL fusion proteins may provide rational therapeutic strategies for the treatment of MLL-associated leukemia.
  • To this end, we developed inducible MLL-AF4 fusion cell lines in different backgrounds.
  • Overexpression of MLL-AF4 does not lead to increased proliferation in either cell line, but rather, cell growth was slowed compared with similar cell lines inducibly expressing truncated MLL.
  • We found that in the MLL-AF4-induced cell lines, the expression of the cyclin-dependent kinase inhibitor gene CDKN1B was dramatically changed at both the RNA and protein (p27kip1) levels.
  • Further, we confirmed CDKN1B promoter binding by ChIP in MLL-AF4 as well as in MLL-AF9 leukemia cell lines.
  • Our results suggest that CDKN1B is a downstream target of MLL and of MLL-AF4, and that, depending on the background cell type, MLL-AF4 inhibits or activates CDKN1B expression.
  • This finding may have implications in terms of leukemia stem cell resistance to chemotherapy in MLL-AF4 leukemias.

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  • (PMID = 16169901.001).
  • [ISSN] 0027-8424
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA40046; United States / NCI NIH HHS / CA / CA104300; United States / NCI NIH HHS / CA / P01 CA040046; United States / NCI NIH HHS / CA / CA78438; United States / NCI NIH HHS / CA / R01 CA104300; United States / NCI NIH HHS / CA / CA81269
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CDKN1B protein, human; 0 / Intracellular Signaling Peptides and Proteins; 0 / MLL-AF4 fusion protein, human; 0 / Oncogene Proteins, Fusion; 147604-94-2 / Cyclin-Dependent Kinase Inhibitor p27; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein
  • [Other-IDs] NLM/ PMC1236570
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86. van Gosliga D, Schepers H, Rizo A, van der Kolk D, Vellenga E, Schuringa JJ: Establishing long-term cultures with self-renewing acute myeloid leukemia stem/progenitor cells. Exp Hematol; 2007 Oct;35(10):1538-49
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Establishing long-term cultures with self-renewing acute myeloid leukemia stem/progenitor cells.
  • OBJECTIVE: With the emergence of the concept of the leukemia stem cell, assays to study them remain pivotal in understanding (leukemic) stem cell biology.
  • METHODS: We have cultured acute myeloid leukemia CD34(+) cells on bone marrow stroma.
  • RESULTS: A strong expansion was observed in about 75% of the acute myeloid leukemia cases (n = 30) and long-term cultures could be maintained for up to 24 weeks on MS5 bone marrow stromal cells.
  • Self-renewal within these L-CAs was determined by sequential passaging of these L-CAs onto new MS5 stromal layers, which resulted in the generation of second, third, and fourth L-CAs, which were able to sustain long-term expansion and generated high numbers of immature undifferentiated suspension cells.
  • CONCLUSION: We present a novel long-term leukemic stem/progenitor assay in which new drugs can be tested and in which genes can be overexpressed or downmodulated using a lentiviral approach in order to obtain more insight into the process of leukemic transformation and self-renewal.
  • [MeSH-major] Bone Marrow Cells / pathology. Cell Line, Tumor / pathology. Leukemia, Myeloid, Acute / pathology. Neoplastic Stem Cells / pathology. Tumor Stem Cell Assay

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  • (PMID = 17889721.001).
  • [ISSN] 0301-472X
  • [Journal-full-title] Experimental hematology
  • [ISO-abbreviation] Exp. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antigens, CD34; 0 / BMI1 protein, human; 0 / Homeodomain Proteins; 0 / Neoplasm Proteins; 0 / Nuclear Proteins; 0 / Proto-Oncogene Proteins; 0 / Repressor Proteins; 0 / homeobox protein HOXA9; 0 / myeloid ecotropic viral integration site 1 protein; EC 6.3.2.19 / Polycomb Repressive Complex 1
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87. Atallah E, Cortes J: Optimal initial therapy for patients with newly diagnosed chronic myeloid leukemia in chronic phase. Curr Opin Hematol; 2007 Mar;14(2):138-44
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Optimal initial therapy for patients with newly diagnosed chronic myeloid leukemia in chronic phase.
  • PURPOSE OF REVIEW: Imatinib mesylate, a tyrosine kinase inhibitor, has revolutionized the therapy of newly diagnosed patients with chronic myeloid leukemia.
  • Prior to imatinib, treatment algorithms for chronic myeloid leukemia patients recommended stem cell transplantation for patients less than 50 years old who had a donor and could undergo stem cell transplantation.
  • Other than stem cell transplantation, interferon was the only drug that could induce cytogenetic remissions in minority of patients.
  • The use of imatinib before stem cell transplant did not have an effect on mortality or morbidity posttransplant.
  • SUMMARY: Currently, imatinib is considered first line therapy in all patients with early chronic phase chronic myeloid leukemia with stem cell transplant reserved for patients who have disease resistant to imatinib therapy.
  • Our aim is to review current recommendations for initial therapy of patients with early chronic phasechronic myeloid leukemia, current areas of controversy and future directions.
  • [MeSH-major] Leukemia, Myeloid, Chronic-Phase / therapy
  • [MeSH-minor] Benzamides. Disease Management. Humans. Imatinib Mesylate. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / therapy. Piperazines / therapeutic use. Pyrimidines / therapeutic use

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  • (PMID = 17255791.001).
  • [ISSN] 1065-6251
  • [Journal-full-title] Current opinion in hematology
  • [ISO-abbreviation] Curr. Opin. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate
  • [Number-of-references] 53
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88. Ren M, Li X, Cowell JK: Genetic fingerprinting of the development and progression of T-cell lymphoma in a murine model of atypical myeloproliferative disorder initiated by the ZNF198-fibroblast growth factor receptor-1 chimeric tyrosine kinase. Blood; 2009 Aug 20;114(8):1576-84
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  • [Title] Genetic fingerprinting of the development and progression of T-cell lymphoma in a murine model of atypical myeloproliferative disorder initiated by the ZNF198-fibroblast growth factor receptor-1 chimeric tyrosine kinase.
  • A mouse model of human ZNF198-fibroblast growth factor receptor-1 (FGFR1) stem cell leukemia lymphoma has been developed to investigate mechanisms of oncogenesis and progression.
  • Using array-based comparative genomic hybridization, we followed disease progression after serial transplantation of ZNF198-FGFR1-transformed stem cells that give rise to a distinct myeloproliferative disorder and T-lymphoblastic leukemia.
  • A consistent, frequently homozygous, chr14:53880459-55011545 deletion, containing the T-cell receptor alpha and delta genes, was identified in the bone marrow, spleen, and lymph nodes in all cases.
  • The absence of cell-surface T-cell receptor alpha in tumor cells precludes CD3 recruitment, resulting in loss of a functional T-cell receptor complex, supporting the idea that prevention of maturation of CD4(+)/CD8(+) double-positive immature T cells is important in ZNF198-FGFR1 disease development.
  • Up-regulation of the B-cell line 2, interleukin 7 receptor alpha and interleuking 2 receptor alpha prosurvival genes in these undifferentiated tumor precursor cells suggests one mechanism that allows them to escape apoptosis in the thymus.
  • Thus, we have defined an important event in the process of ZNF198-FGFR1-induced T-cell leukemia.

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  • (PMID = 19506298.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA076167; United States / NCI NIH HHS / CA / CA076167
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Carrier Proteins; 0 / DNA-Binding Proteins; 0 / Recombinant Fusion Proteins; 0 / Transcription Factors; 0 / Zmym2 protein, mouse; EC 2.7.10.1 / Receptor, Fibroblast Growth Factor, Type 1
  • [Other-IDs] NLM/ PMC2731638
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89. Buzzai M, Licht JD: New molecular concepts and targets in acute myeloid leukemia. Curr Opin Hematol; 2008 Mar;15(2):82-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] New molecular concepts and targets in acute myeloid leukemia.
  • PURPOSE OF REVIEW: Most patients with acute myeloid leukemia treated with chemotherapy relapse.
  • It is increasingly recognized that the cause of chemoresistance and relapse resides within the leukemia stem cell population.
  • Successful eradication of leukemia stem cells would require a comprehensive profile of both the acquired molecular lesions and intrinsic features of leukemia stem cells.
  • This review describes recent work identifying molecular markers that may lead to development of novel therapeutics, ultimately aiming to eradicate leukemia stem cells in acute myeloid leukemia.
  • RECENT FINDINGS: In recent years, novel specific cell surface antigens have allowed identification of leukemia stem cells and permitted their distinction from normal hematopoietic stem cells.
  • Novel concepts of leukemia stem cells and niche interaction have elucidated the mechanisms that control leukemia stem cell survival and chemoresistance.
  • Recent detection of genetic aberrations affecting regulators of HOX gene expression and chromatin modifying enzymes, such as CDX2 and hDOT1L, respectively, elucidates new key players in stem cell self-renewal and leukemic transformation.
  • SUMMARY: The discovery of novel markers and survival pathways for leukemia stem cells has increased our potential to specifically target and eliminate the leukemic stem cell compartment, which is likely to improve clinical outcomes in acute myeloid leukemia.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Hematopoietic Stem Cells / drug effects. Leukemia, Myeloid, Acute

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  • (PMID = 18300752.001).
  • [ISSN] 1065-6251
  • [Journal-full-title] Current opinion in hematology
  • [ISO-abbreviation] Curr. Opin. Hematol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA59936
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Immunoconjugates; 0 / NCR2 protein, human; 0 / Natural Cytotoxicity Triggering Receptor 2; 0 / Receptors, Immunologic; 0 / Receptors, Interleukin-3
  • [Number-of-references] 51
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90. Krivtsov AV, Wang Y, Feng Z, Armstrong SA: Gene expression profiling of leukemia stem cells. Methods Mol Biol; 2009;538:231-46
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Gene expression profiling of leukemia stem cells.
  • Characterization of gene expression programs and pathways important for normal and cancer stem cells has become an active area of investigation.
  • Microarray analysis of various cell populations provides an opportunity to assess genomewide expression programs to define cellular identity and to potentially identify pathways activated in various stem cells.
  • Here we describe methods to isolate a leukemia stem cell population, amplify RNA, and perform microarray analyses.
  • [MeSH-major] Flow Cytometry / methods. Gene Expression Profiling. Granulocyte-Macrophage Progenitor Cells / metabolism. Leukemia, Myeloid, Acute / genetics. Neoplastic Stem Cells / metabolism. Oligonucleotide Array Sequence Analysis / methods
  • [MeSH-minor] Animals. Leukemia, Experimental / genetics. Leukemia, Experimental / metabolism. Leukemia, Experimental / pathology. Mice. Mice, Inbred C57BL. Myeloid-Lymphoid Leukemia Protein / genetics. Oncogene Proteins, Fusion / genetics. RNA, Messenger / analysis. RNA, Messenger / genetics. RNA, Messenger / metabolism

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  • (PMID = 19277590.001).
  • [ISSN] 1064-3745
  • [Journal-full-title] Methods in molecular biology (Clifton, N.J.)
  • [ISO-abbreviation] Methods Mol. Biol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P01 CA066996; United States / NCI NIH HHS / CA / P01 CA066996-15
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / MLL-AF9 fusion protein, human; 0 / Oncogene Proteins, Fusion; 0 / RNA, Messenger; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein
  • [Other-IDs] NLM/ NIHMS369625; NLM/ PMC3339407
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91. Attar EC, De Angelo DJ, Supko JG, D'Amato F, Zahrieh D, Sirulnik A, Wadleigh M, Ballen KK, McAfee S, Miller KB, Levine J, Galinsky I, Trehu EG, Schenkein D, Neuberg D, Stone RM, Amrein PC: Phase I and pharmacokinetic study of bortezomib in combination with idarubicin and cytarabine in patients with acute myelogenous leukemia. Clin Cancer Res; 2008 Mar 1;14(5):1446-54
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Phase I and pharmacokinetic study of bortezomib in combination with idarubicin and cytarabine in patients with acute myelogenous leukemia.
  • PURPOSE: Proteasome inhibition results in cytotoxicity to the leukemia stem cell in vitro.
  • We conducted this phase I study to determine if the proteasome inhibitor bortezomib could be safely added to induction chemotherapy in patients with acute myelogenous leukemia (AML).
  • Pharmacokinetic studies revealed that the total body clearance of bortezomib decreased significantly (P < 0.01, N = 26) between the first (mean +/- SD, 41.9 +/- 17.1 L/h/m(2)) and third (18.4 +/- 7.0 L/h/m(2)) doses.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / pharmacokinetics. Leukemia, Myeloid, Acute / metabolism

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  • (PMID = 18316568.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P01 CA066996
  • [Publication-type] Clinical Trial, Phase I; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Boronic Acids; 0 / Pyrazines; 04079A1RDZ / Cytarabine; 69G8BD63PP / Bortezomib; ZRP63D75JW / Idarubicin
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92. Cheng QS, Wang XB: [CD47 and leukemia stem cells]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2010 Aug;18(4):1088-91
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  • [Title] [CD47 and leukemia stem cells].
  • The expression of CD47 on normal hematopoietic stem cells (HSCs) is useful for maintaining the stability of HSCs in body, but the high expression of CD47 existed on leukemia stem cell (LSCs) of AML patients which can reduce the macrophage-induced phagocytosis to LSCs and decrease the clearance of innate immune system of organism to LSCs.

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  • (PMID = 20723335.001).
  • [ISSN] 1009-2137
  • [Journal-full-title] Zhongguo shi yan xue ye xue za zhi
  • [ISO-abbreviation] Zhongguo Shi Yan Xue Ye Xue Za Zhi
  • [Language] CHI
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antigens, CD47
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93. Ren X, Gomez GA, Zhang B, Lin S: Scl isoforms act downstream of etsrp to specify angioblasts and definitive hematopoietic stem cells. Blood; 2010 Jul 1;115(26):5338-46
ZFIN. ZFIN .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Scl isoforms act downstream of etsrp to specify angioblasts and definitive hematopoietic stem cells.
  • Recent lineage studies suggest that hematopoietic stem cells (HSCs) may be derived from endothelial cells.
  • We report here that zebrafish ets1-related protein (etsrp), which is essential for vascular endothelial development, also plays a critical role in the initiation of definitive hematopoiesis by controlling the expression of 2 stem cell leukemia (scl) isoforms (scl-alpha and scl-beta) in angioblasts.
  • Furthermore, both scl isoforms partially rescue runx1 but not ephrinb2a expression in embryos deficient in Vegf signaling.

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  • (PMID = 20185582.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / DK054508-13; United States / NHLBI NIH HHS / HL / F31 HL091713; United States / NIDDK NIH HHS / DK / R01 DK054508; United States / NIDDK NIH HHS / DK / Z01 DK054508; United States / NHLBI NIH HHS / HL / 5F31HL091713-02
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / Core Binding Factor Alpha 2 Subunit; 0 / Etsrp protein, zebrafish; 0 / Protein Isoforms; 0 / Proto-Oncogene Protein c-fli-1; 0 / Proto-Oncogene Proteins; 0 / Zebrafish Proteins; 0 / runx1 protein, zebrafish; 0 / tal1 protein, zebrafish
  • [Other-IDs] NLM/ PMC2902133
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94. Jordan CT: The potential of targeting malignant stem cells as a treatment for leukemia. Future Oncol; 2005 Apr;1(2):205-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The potential of targeting malignant stem cells as a treatment for leukemia.
  • Malignant stem cells have recently been described as the source of several types of human cancer.
  • These unique cell types are typically rare and possess properties that are distinct from most other tumor cells.
  • In leukemia, the natural properties of cancer stem cells indicate that current chemotherapy drugs will not be effective.
  • Consequently, new strategies are required that specifically and preferentially target the cancer stem cell population, whilst sparing normal stem cells.
  • This perspective article summarizes recent findings in the leukemia stem cell field and discusses new directions for therapy.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Antineoplastic Agents / therapeutic use. Apoptosis / drug effects. Leukemia / drug therapy. Neoplastic Stem Cells / drug effects

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  • (PMID = 16555992.001).
  • [ISSN] 1479-6694
  • [Journal-full-title] Future oncology (London, England)
  • [ISO-abbreviation] Future Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antineoplastic Agents
  • [Number-of-references] 22
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95. Neghina R, Neghina AM, Merkler C, Marincu I, Moldovan R, Iacobiciu I: Intestinal schistosomiasis, importation of a neglected tropical disease in Romania. Case report of a traveler to endemic regions. Travel Med Infect Dis; 2009 Jan;7(1):49-51
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  • CONCLUSIONS: Final diagnosis was established with difficulty in this case.
  • Failure to associate a febrile prolonged syndrome or chronic diarrhea with a history of travel can cause a delayed diagnosis.
  • [MeSH-major] Anthelmintics / therapeutic use. Intestinal Diseases, Parasitic / diagnosis. Praziquantel / therapeutic use. Schistosomiasis / diagnosis. Travel
  • [MeSH-minor] Adult. Diagnosis, Differential. Feces / parasitology. Humans. Male. Parasite Egg Count / veterinary. Retrospective Studies. Romania / epidemiology. Treatment Outcome

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  • (PMID = 19174302.001).
  • [ISSN] 1477-8939
  • [Journal-full-title] Travel medicine and infectious disease
  • [ISO-abbreviation] Travel Med Infect Dis
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Anthelmintics; 6490C9U457 / Praziquantel
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96. Fenk R, Schneider P, Kropff M, Huenerlituerkoglu AN, Steidl U, Aul C, Hildebrandt B, Haas R, Heyll A, Kobbe G, West German Myeloma Study Group: High-dose idarubicin, cyclophosphamide and melphalan as conditioning for autologous stem cell transplantation increases treatment-related mortality in patients with multiple myeloma: results of a randomised study. Br J Haematol; 2005 Aug;130(4):588-94
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  • [Title] High-dose idarubicin, cyclophosphamide and melphalan as conditioning for autologous stem cell transplantation increases treatment-related mortality in patients with multiple myeloma: results of a randomised study.
  • We conducted a randomised trial comparing an intensified versus a standard conditioning regimen for high-dose chemotherapy followed by autologous stem-cell transplantation in patients with multiple myeloma.
  • Acute toxicity, mainly because of infections, was higher in the intensified treatment arm with a treatment-related mortality of 20% versus 0% in the standard arm.
  • Response rates did not differ significantly between both treatment arms {intensified versus standard: complete response+near complete remission 50% [95% confidence interval (CI) 26-74%] vs. 33% (95% CI 17-55%), partial remission 35% (95% CI 16-61%) vs. 50% (95% CI 30-70%)}.
  • After a follow-up of 5 years, the median time-to-progression and overall survival were not significantly different between both patient groups.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / adverse effects. Multiple Myeloma / surgery. Stem Cell Transplantation / mortality. Transplantation Conditioning / adverse effects

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  • (PMID = 16098074.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Clinical Trial; Comparative Study; Journal Article; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 8N3DW7272P / Cyclophosphamide; Q41OR9510P / Melphalan; ZRP63D75JW / Idarubicin
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97. Giagounidis AA, Haase S, Heinsch M, Göhring G, Schlegelberger B, Aul C: Lenalidomide in the context of complex karyotype or interrupted treatment: case reviews of del(5q)MDS patients with unexpected responses. Ann Hematol; 2007 Feb;86(2):133-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Lenalidomide in the context of complex karyotype or interrupted treatment: case reviews of del(5q)MDS patients with unexpected responses.
  • Lenalidomide has particular activity in patients with transfusion-dependent del(5q) myelodysplastic syndromes (MDS), but mechanistic information is limited regarding the relationship between erythroid and cytogenetic responses.
  • We reviewed medical records from three distinct subgroups of del(5q) MDS patients who had unexpected effects with lenalidomide treatment: 1. two patients with complex karyotypes who achieved both cytogenetic remissions and transfusion independence; 2. two patients with 5q- syndrome who took lenalidomide for less than 12 weeks but remained transfusion independent for 15+ months still displaying del(5q) metaphases after 6 and 12 months; and 3. one patient who was a non-responder on lenalidomide during treatment but became transfusion independent for 13+ months after discontinuation.
  • All but the latter patient in this series had reduction of affected metaphases, suggesting that erythroid responses might be mediated by result from partial or complete suppression of the malignant clone, either directly or indirectly through modulation of the bone marrow microenvironment.
  • These clinical observations illustrate the heterogeneity of del(5q)MDS pathogenesis and the diversity of lenalidomide responses within this patient subset.
  • [MeSH-major] Chromosome Deletion. Myelodysplastic Syndromes / drug therapy. Myelodysplastic Syndromes / genetics. Thalidomide / analogs & derivatives
  • [MeSH-minor] Adult. Aged. Female. Humans. Karyotyping. Male. Middle Aged. Treatment Outcome

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  • (PMID = 17111142.001).
  • [ISSN] 1432-0584
  • [Journal-full-title] Annals of hematology
  • [ISO-abbreviation] Ann. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 4Z8R6ORS6L / Thalidomide; F0P408N6V4 / lenalidomide
  • [Other-IDs] NLM/ PMC1705486
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98. Xu Y, Leung CG, Lee DC, Kennedy BK, Crispino JD: MTB, the murine homolog of condensin II subunit CAP-G2, represses transcription and promotes erythroid cell differentiation. Leukemia; 2006 Jul;20(7):1261-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] MTB, the murine homolog of condensin II subunit CAP-G2, represses transcription and promotes erythroid cell differentiation.
  • In this report, we show that MTB (more than blood), which was initially isolated in a yeast two-hybrid screen for proteins that interact with the basic helix-loop-helix (bHLH) protein stem cell leukemia (SCL), and later identified as the murine homolog of the condensin II subunit CAP-G2, participates in erythroid cell development.
  • Consistent with the model that MTB may function together with SCL/E12 heterodimer during erythroid cell development, MTB is highly expressed in the erythroid lineage and is upregulated upon erythroid differentiation.
  • Moreover, overexpression of MTB promotes the terminal differentiation of the murine erythroleukemia erythroid cell line.

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  • (PMID = 16673016.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / DK061464-05; United States / NIDDK NIH HHS / DK / R01 DK061464; United States / NIDDK NIH HHS / DK / R01 DK-61464; United States / NIDDK NIH HHS / DK / R01 DK061464-05
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / DNA-Binding Proteins; 0 / Luzp5 protein, mouse; 0 / Multiprotein Complexes; 0 / Proteins; 0 / Proto-Oncogene Proteins; 0 / Repressor Proteins; 0 / TCF Transcription Factors; 0 / Tal1 protein, mouse; 0 / Tcf7l1 protein, mouse; 0 / Transcription Factor 7-Like 1 Protein; 0 / condensin complexes; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit; EC 3.6.1.- / Adenosine Triphosphatases
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99. Gekas C, Rhodes KE, Gereige LM, Helgadottir H, Ferrari R, Kurdistani SK, Montecino-Rodriguez E, Bassel-Duby R, Olson E, Krivtsov AV, Armstrong S, Orkin SH, Pellegrini M, Mikkola HK: Mef2C is a lineage-restricted target of Scl/Tal1 and regulates megakaryopoiesis and B-cell homeostasis. Blood; 2009 Apr 9;113(15):3461-71
Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Mef2C is a lineage-restricted target of Scl/Tal1 and regulates megakaryopoiesis and B-cell homeostasis.
  • The basic helix-loop-helix transcription factor stem cell leukemia gene (Scl) is a master regulator for hematopoiesis essential for hematopoietic specification and proper differentiation of the erythroid and megakaryocyte lineages.
  • Here, we identified a novel Scl target gene, transcription factor myocyte enhancer factor 2 C (Mef2C) from Scl(fl/fl) fetal liver progenitor cell lines.
  • Analysis of Mef2C(-/-) embryos showed that Mef2C, in contrast to Scl, is not essential for specification into primitive or definitive hematopoietic lineages.
  • Chromatin immunoprecipitation microarray hybridization analysis revealed that Mef2C is directly regulated by Scl in megakaryocytic cells, but not in erythroid cells.
  • In addition, an Scl-independent requirement for Mef2C in B-lymphoid homeostasis was observed in Mef2C-deficient mice, characterized as severe age-dependent reduction of specific B-cell progenitor populations reminiscent of premature aging.