Medizinische Universität Graz Austria/Österreich - Forschungsportal - Medical University of Graz
Lind Karin |
** = Publikationen gelistet in SCI/SSCI/Pubmed
2023
Abstract (Zeitschrift)
** Lyssy, F; Lind, K; Zöscher, F; Zebisch, A; Wölfler, A; Pabst, G; Fosselteder, J; Reinisch, A; Sill, H; Dutta, S
Modelling drug resistance conferred by mono- and bi-allelic TP53 aberrations using isogenic AML cell lines
ONCOL RES TREAT. 2023; 46: 188-189.
[Poster]
Web of Science
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2022
Originalarbeit (Zeitschrift)
** Dutta, S; Moritz, J; Pregartner, G; Thallinger, GG; Brandstätter, I; Lind, K; Rezania, S; Lyssy, F; Reinisch, A; Zebisch, A; Berghold, A; Wölfler, A; Sill, H
Comparison of acute myeloid leukemia and myelodysplastic syndromes with TP53 aberrations.
Ann Hematol. 2022; 101(4):837-846
Doi: 10.1007/s00277-022-04766-2
[OPEN ACCESS]
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Kurzbericht/Letter
** Meszaros, N; Lind, K; Sehlke, R; Vilagos, B; Krall, N; Vladimer, GI; Sill, H
Influence of cryopreservation on drug responses and gene expression of AML cells: Implications for the use of biobanked tissues
BRIT J HAEMATOL. 2022;
Doi: 10.1111/bjh.18557
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2020
Kurzbericht/Letter
** Pabst, G; Lind, K; Graf, R; Zebisch, A; Stölzel, F; Döhner, K; Heitzer, E; Reinisch, A; Sill, H
TP53 mutated AML subclones exhibit engraftment in a humanized bone marrow ossicle mouse model.
Ann Hematol. 2020; 99(3):653-655
Doi: 10.1007/s00277-020-03920-y
[OPEN ACCESS]
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2019
Originalarbeit (Zeitschrift)
** Aigner, P; Mizutani, T; Horvath, J; Eder, T; Heber, S; Lind, K; Just, V; Moll, HP; Yeroslaviz, A; Fischer, MJM; Kenner, L; Győrffy, B; Sill, H; Grebien, F; Moriggl, R; Casanova, E; Stoiber, D
STAT3β is a tumor suppressor in acute myeloid leukemia.
Blood Adv. 2019; 3(13): 1989-2002.
Doi: 10.1182/bloodadvances.2018026385
[OPEN ACCESS]
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2018
Kurzbericht/Letter
** Kashofer, K; Gornicec, M; Lind, K; Caraffini, V; Schauer, S; Beham-Schmid, C; Wölfler, A; Hoefler, G; Sill, H; Zebisch, A
Detection of prognostically relevant mutations and translocations in myeloid sarcoma by next generation sequencing.
Leuk Lymphoma. 2018; 59(2):501-504
Doi: 10.1080/10428194.2017.1339879
[OPEN ACCESS]
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** Schulz, E; Lind, K; Renner, W; Petersen, BS; Quehenberger, F; Dill, C; Hofer, S; Lal, R; Hoefler, G; Schlenke, P; Ehninger, G; Schetelig, J; Middeke, JM; Stölzel, F; Sill, H
The TP53 Pro72Arg SNP in de novo acute myeloid leukaemia - results of two cohort studies involving 215 patients and 3759 controls.
Br J Haematol. 2018; 181(1):148-151
Doi: 10.1111/bjh.14527
[OPEN ACCESS]
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2017
Originalarbeit (Zeitschrift)
** Lal, R; Lind, K; Heitzer, E; Ulz, P; Aubell, K; Kashofer, K; Middeke, JM; Thiede, C; Schulz, E; Rosenberger, A; Hofer, S; Feilhauer, B; Rinner, B; Svendova, V; Schimek, MG; Rücker, FG; Hoefler, G; Döhner, K; Zebisch, A; Wölfler, A; Sill, H
Somatic TP53 mutations characterize preleukemic stem cells in acute myeloid leukemia.
Blood. 2017; 129(18): 2587-2591.
Doi: 10.1182/blood-2016-11-751008
[OPEN ACCESS]
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** Stefanzl, G; Berger, D; Cerny-Reiterer, S; Blatt, K; Eisenwort, G; Sperr, WR; Hoermann, G; Lind, K; Hauswirth, AW; Bettelheim, P; Sill, H; Melo, JV; Jager, U; Valent, P
The pan-BCL-2-blocker obatoclax (GX15-070) and the PI3-kinase/mTOR-inhibitor BEZ235 produce cooperative growth-inhibitory effects in ALL cells
ONCOTARGET. 2017; 8(40): 67709-67722.
Doi: 10.18632/oncotarget.18810
[OPEN ACCESS]
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2016
Originalarbeit (Zeitschrift)
** Zebisch, A; Lal, R; Müller, M; Lind, K; Kashofer, K; Girschikofsky, M; Fuchs, D; Wölfler, A; Geigl, JB; Sill, H
Acute myeloid leukemia with TP53 germ line mutations.
Blood. 2016; 128(18): 2270-2272.
Doi: 10.1182/blood-2016-08-732610
[OPEN ACCESS]
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Abstract (Zeitschrift)
** Olipitz, W; Lind, K; Monsberger, N; Katschnig, A; Mangerich, A; Rankl, J; Hofer, S; Mueller, M; Schulz, E; Quehenberger, F; Schlembach, D; Robier, C; Woelfler, A; Zebisch, A; Sill, H
IMPAIRED BASE EXCISION REPAIR GLYCOSYLASE/AP ENDONUCLEASE ACTIVITY CONTRIBUTES TO CYTARABINE RESISTANCE IN ACUTE MYELOID LEUKEMIA
HAEMATOLOGICA. 2016; 101: 211-212.
[Poster]
Web of Science
** Schulz, E; Lind, K; Renner, W; Petersen, BS; Dill, C; Hofer, S; Lal, R; Quehenberger, F; Stolzel, F; Sill, H
THE HOMOZYGOUS TP53 P72R SNP IS ASSOCIATED WITH NON-FAVORABLE CYTOGENETIC RISK GROUPS IN ACUTE MYELOID LEUKEMIA
HAEMATOLOGICA. 2016; 101: 383-383.
[Poster]
Web of Science
** Zebisch, A; Lal, R; Muller, M; Lind, K; Sill, H
TP53 germline mutations occur in acute myeloid leukemia and are associated with therapy-related cases following ionizing radiation
WIEN KLIN WOCHENSCHR. 2016; 128: S385-S386.
[Poster]
Web of Science
2015
Kurzbericht/Letter
** Hackl, H; Steinleitner, K; Lind, K; Hofer, S; Tosic, N; Pavlovic, S; Suvajdzic, N; Sill, H; Wieser, R
A gene expression profile associated with relapse of cytogenetically normal acute myeloid leukemia is enriched for leukemia stem cell genes.
Leuk Lymphoma. 2015; 56(4):1126-1128
Doi: 10.3109/10428194.2014.944523
[OPEN ACCESS]
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2014
Abstract (Zeitschrift)
** Olipitz, W; Lind, K; Monsberger, N; Katschnig, A; Mangerich, A; Hofer, S; Schulz, E; Quehenberger, F; Schlembach, D; Robier, C; Woelfler, A; Zebisch, A; Sill, H
Base Excision Repair Glycosylase Activity Is Impaired in a Subgroup of Acute Myeloid Leukemia Resulting in Increased Levels of Oxidative Base Lesions
BLOOD. 2014; 124(21):-56th Annual Meeting of the American-Society-of-Hematology; DEC 06-09, 2014; San Francisco, CA.
[Poster]
Web of Science
** Olipitz, W; Lind, K; Monsberger, N; Katschnig, A; Mangerich, A; Hofer, S; Schulz, E; Quehenberger, F; Schlembach, D; Robier, C; Wölfler, A; Zebisch, A; Sill, H
Base excision repair glycosylase activity is impaired in a subgroup of acute myeloid leukemia resulting in increased levels of oxidative base lesions
Oncol Res Treat. 2014; 37(S5):49-49.-Annual Meeting of the German, Austrian and Swiss Associations of Hematology and Medical Oncology; OCT 10-14; Hamburg, GERMANY. (ISBN: 978-3-318-02811-9 )
[Poster]
Web of Science
2012
Originalarbeit (Zeitschrift)
** Fried, I; Bodner, C; Pichler, MM; Lind, K; Beham-Schmid, C; Quehenberger, F; Sperr, WR; Linkesch, W; Sill, H; Wölfler, A
Frequency, onset and clinical impact of somatic DNMT3A mutations in therapy-related and secondary acute myeloid leukemia.
Haematologica. 2012; 97(2):246-250
Doi: 10.3324/haematol.2011.051581
[OPEN ACCESS]
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** Schulz, E; Valentin, A; Ulz, P; Beham-Schmid, C; Lind, K; Rupp, V; Lackner, H; Wölfler, A; Zebisch, A; Olipitz, W; Geigl, J; Berghold, A; Speicher, MR; Sill, H
Germline mutations in the DNA damage response genes BRCA1, BRCA2, BARD1 and TP53 in patients with therapy related myeloid neoplasms.
J Med Genet. 2012; 49(7):422-428
Doi: 10.1136/jmedgenet-2011-100674
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** Zebisch, A; Wölfler, A; Fried, I; Wolf, O; Lind, K; Bodner, C; Haller, M; Drasche, A; Pirkebner, D; Matallanas, D; Rath, O; Blyth, K; Delwel, R; Taskesen, E; Quehenberger, F; Kolch, W; Troppmair, J; Sill, H
Frequent loss of RAF kinase inhibitor protein expression in acute myeloid leukemia.
Leukemia. 2012; 26(8):1842-1849
Doi: 10.1038/leu.2012.61
[OPEN ACCESS]
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Abstract (Zeitschrift)
** Schulz, E; Valentin, A; Ulz, P; Beham-Schmid, C; Lind, K; Rupp, V; Lackner, H; Wolfler, A; Zebisch, A; Olipitz, W; Geigl, JB; Berghold, A; Speicher, MR; Sill, H
Germ-line mutations in cancer predisposing genes BRCA1, BRCA2, BARD1 and TP53 in patients with therapy-related myeloid neoplasms.
ONKOLOGIE. Onkologie. 2012; 35: 117-117.-Annual Meeting of the German, Austrian and Swiss Associations of Hematology and Medical Oncology; OCT 19-23, 2012; Stuttgart, GERMANY.
[Poster]
Web of Science
2011
Kurzbericht/Letter
** Pichler, MM; Bodner, C; Fischer, C; Deutsch, AJ; Hiden, K; Beham-Schmid, C; Linkesch, W; Guelly, C; Sill, H; Wölfler, A
Evaluation of mutations in the isocitrate dehydrogenase genes in therapy-related and secondary acute myeloid leukaemia identifies a patient with clonal evolution to IDH2 R172K homozygosity due to uniparental disomy.
Br J Haematol. 2011; 152(5): 669-672.
Doi: 10.1111/j.1365-2141.2010.08404.x
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Abstract (Konferenzband)
** Zebisch, A; Wölfler, A; Hiden K; Bodner, C; Quehenberger, F; Drasche, A; Pirkebner, D; Haller, M; Matallanas, D; Fried, I; Rath, O; Blyth, K; Taskesen, E; Kolch, W; Troppmair, J; Sill, H
RAF kinase inhibitor protein ist ein neuer Tumor-Suppressor bei der akuten myeloischen Leukämie
Onkologie. 2011; 34(S6):209-209.-Jahrestagung der Deutschen, Österreichischen und Schweizerischen Gesellschaften für Hämatologie und Onkologie; SEP 30-OCT 4, 2011; Basel, Switzerland. (ISBN: 978-3-8055-9922-1 )
[Oral Communication]
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2010
Übersichtsarbeit
** Wieser, R; Scheideler, M; Hackl, H; Engelmann, M; Schneckenleithner, C; Hiden, K; Papak, C; Trajanoski, Z; Sill, H; Fonatsch, C
microRNAs in acute myeloid leukemia: expression patterns, correlations with genetic and clinical parameters, and prognostic significance.
Genes Chromosomes Cancer. 2010; 49(3):193-203
Doi: 10.1002/gcc.20740
Web of Science
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Abstract (Zeitschrift)
** Haller, M; Zebisch, A; Hiden, K; Hoefler, G; Sill, H; Troppmair, J
Loss of RAF kinase inhibitor protein is a somatic event in the pathogenesis of therapy-related acute myeloid leukemias with C-RAF germline mutations
FEBS J. 2010; 277: 127-127.
[Poster]
Web of Science
** Zebisch, A; Woelfler, A; Hiden, K; Bodner, C; Quehenberger, F; Drasche, A; Pirkebner, D; Haller, M; Rath, O; Blyth, K; Taskesen, E; Kolch, W; Troppmair, J; Sill, H
Loss of RAF Kinase Inhibitor Protein Is a Frequent Event In Acute Myeloid Leukemia with a Monocytic Phenotype and Cooperates with Mutant RAS In Malignant Transformation
BLOOD. 2010; 116(21): 1702-1702.
[Poster]
Web of Science
** Zebisch, A; Woelfler, A; Hiden, K; Bodner, C; Quehenberger, F; Drasche, A; Pirkebner, D; Rath, O; Blyth, K; Delwel, R; Taskesen, E; Kolch, W; Troppmair, J; Sill, H
LOSS OF RKIP IN ACUTE MYELOID LEUKEMIA WITH A MONOCYTIC PHENOTYPE
HAEMATOL-HEMATOL J. 2010; 95: 0026 -Annual Meting of the European Haematology Association; June 2010; Barcelona.
[Poster]
Web of Science
2009
Originalarbeit (Zeitschrift)
** Zebisch, A; Haller, M; Hiden, K; Goebel, T; Hoefler, G; Troppmair, J; Sill, H
Loss of RAF kinase inhibitor protein is a somatic event in the pathogenesis of therapy-related acute myeloid leukemias with C-RAF germline mutations.
Leukemia. 2009; 23(6): 1049-1053.
Doi: 10.1038/leu.2009.68
[OPEN ACCESS]
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Abstract (Zeitschrift)
** Olipitz, W; Scheer, N; Quehenberger, F; Hiden, K; Rankl, J; Schlembach, D; Sill, H
Base Excision Repair Deficiency in Acute Myeloid Leukemia.
BLOOD. 2009; 114(22): 454-454.
[Poster]
Web of Science
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2006
Originalarbeit (Zeitschrift)
** Zebisch, A; Staber, PB; Delavar, A; Bodner, C; Hiden, K; Fischereder, K; Janakiraman, M; Linkesch, W; Auner, HW; Emberger, W; Windpassinger, C; Schimek, MG; Hoefler, G; Troppmair, J; Sill, H
Two transforming C-RAF germ-line mutations identified in patients with therapy-related acute myeloid leukemia.
Cancer Res. 2006; 66(7):3401-3408
Doi: 10.1158/0008-5472.CAN-05-0115
[OPEN ACCESS]
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2004
Originalarbeit (Zeitschrift)
** Auner, HW; Zebisch, A; Schimek, MG; Bodner, C; Hiden, K; Linkesch, W; Haas, OA; Beham-Schmid, C; Sill, H
High expression of the sister-chromatid separation regulator and proto-oncogene hSecurin occurs in a subset of myeloid leukaemias but is not implicated in the pathogenesis of aneuploidy.
Leukemia. 2004; 18(2):303-308
Doi: 10.1038/sj.leu.2403235
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Abstract (Zeitschrift)
** Zebisch, A; Staber, PB; Fischereder, K; Bodner, C; Hiden, K; Linkesch, W; Auner, HW; Emberger, W; Windpassinger, C; Schimek, MG; Hoefler, G; Troppmair, J; Sill, H
Two novel activating germline mutations of the C-RAF proto-oncogene predisposing to solid tbmors and therapy-related acute myeloid leukemia.
BLOOD 2004 104: 920A-920A.
Doi: 10.1182/blood.V104.11.3370.3370
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2002
Originalarbeit (Zeitschrift)
** Olipitz, W; Hopfinger, G; Aguiar, RC; Gunsilius, E; Girschikofsky, M; Bodner, C; Hiden, K; Linkesch, W; Hoefler, G; Sill, H
Defective DNA-mismatch repair: a potential mediator of leukemogenic susceptibility in therapy-related myelodysplasia and leukemia.
Genes Chromosomes Cancer. 2002; 34(2):243-248
Doi: 10.1002/gcc.10059
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2000
Abstract (Zeitschrift)
** Olipitz, W; Hopfinger, G; Hoefler, G; Girschikofsky, M; Bodner, C; Hiden, K; Aguiar, R; Linkesch, W; Sill, H
Microsatellite instability but lack of alternations of genes targeted by defective DNA-mismatch repair in therapy-related MDS and leukemia.
BLOOD 2000 96: 104A-104A.
Web of Science