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4. Evidence for Recombinant GRP78, CALR, PDIA3 and GPI as Mediators of Genetic Instability in Human CD34+ Cells

Author

Fabarius, Alice, primary, Samra, Vanessa, additional, Drews, Oliver, additional, Mörz, Handan, additional, Bierbaum, Miriam, additional, Darwich, Ali, additional, Weiss, Christel, additional, Brendel, Susanne, additional, Kleiner, Helga, additional, Seifarth, Wolfgang, additional, Greffrath, Wolfgang, additional, Hofmann, Wolf-Karsten, additional, Schmitt, Clemens A., additional, and Popp, Henning D., additional

Published
2022
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5. Antibody Response to Vaccination with BNT162b2, mRNA-1273, and ChADOx1 in Patients with Myeloid and Lymphoid Neoplasms

Author

Rotterdam, Jil, primary, Thiaucourt, Margot, additional, Schwaab, Juliana, additional, Reiter, Andreas, additional, Kreil, Sebastian, additional, Steiner, Laurenz, additional, Popp, Henning D., additional, Hofmann, Wolf-Karsten, additional, Bonatz, Karin, additional, Gerhards, Catharina, additional, Neumaier, Michael, additional, Jawhar, Mohamad, additional, and Saussele, Susanne, additional

Published
2021
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7. Proteins Marking the Sequence of Genotoxic Signaling from Irradiated Mesenchymal Stromal Cells to CD34+ Cells

Author

Kohl, Vanessa, primary, Drews, Oliver, additional, Costina, Victor, additional, Bierbaum, Miriam, additional, Jawhar, Ahmed, additional, Roehl, Henning, additional, Weiss, Christel, additional, Brendel, Susanne, additional, Kleiner, Helga, additional, Flach, Johanna, additional, Spiess, Birgit, additional, Seifarth, Wolfgang, additional, Nowak, Daniel, additional, Hofmann, Wolf-Karsten, additional, Fabarius, Alice, additional, and Popp, Henning D., additional

Published
2021
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8. Genotoxic Bystander Signals from Irradiated Human Mesenchymal Stromal Cells Mainly Localize in the 10–100 kDa Fraction of Conditioned Medium

Author

Kohl, Vanessa, primary, Fabarius, Alice, additional, Drews, Oliver, additional, Bierbaum, Miriam, additional, Jawhar, Ahmed, additional, Darwich, Ali, additional, Weiss, Christel, additional, Flach, Johanna, additional, Brendel, Susanne, additional, Kleiner, Helga, additional, Seifarth, Wolfgang, additional, Hofmann, Wolf-Karsten, additional, and Popp, Henning D., additional

Published
2021
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9. Adverse Prognostic Impact of the KIT D816V Transcriptional Activity in Advanced Systemic Mastocytosis

Author

Naumann, Nicole, primary, Lübke, Johannes, additional, Baumann, Sofie, additional, Schwaab, Juliana, additional, Hoffmann, Oliver, additional, Kreil, Sebastian, additional, Dangelo, Vito, additional, Reiter, Lukas, additional, Bugert, Peter, additional, Kristensen, Thomas, additional, Sotlar, Karl, additional, Haselmann, Verena, additional, Schneider, Sven, additional, Metzgeroth, Georgia, additional, Weiss, Christel, additional, Popp, Henning D., additional, Fabarius, Alice, additional, Hofmann, Wolf-Karsten, additional, Cross, Nicholas C. P., additional, Reiter, Andreas, additional, and Jawhar, Mohamad, additional

Published
2021
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10. Genotoxic bystander signals from irradiated human mesenchymal stromal cells mainly localize in the 10 – 100 kDa fraction of conditioned medium

Author

Popp, Henning D., primary, Kohl, Vanessa, additional, Fabarius, Alice, additional, Drews, Oliver, additional, Bierbaum, Miriam, additional, Jawhar, Ahmed, additional, Darwich, Ali, additional, Weiss, Christel, additional, Flach, Johanna, additional, Brendel, Susanne, additional, Kleiner, Helga, additional, Seifarth, Wolfgang, additional, and Hofmann, Wolf-Karsten, additional

Published
2020
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11. Irradiated mesenchymal stromal cells induce genetic instability in human CD34+ cells

Author

Kohl, Vanessa, primary, Drews, Oliver, additional, Costina, Victor, additional, Bierbaum, Miriam, additional, Jawhar, Ahmed, additional, Roehl, Henning, additional, Weiss, Christel, additional, Brendel, Susanne, additional, Kleiner, Helga, additional, Flach, Johanna, additional, Spiess, Birgit, additional, Seifarth, Wolfgang, additional, Nowak, Daniel, additional, Hofmann, Wolf-Karsten, additional, Fabarius, Alice, additional, and Popp, Henning D., additional

Published
2020
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12. Antileukemic Efficacy in Vitro of Talazoparib and APE1 Inhibitor III Combined with Decitabine in Myeloid Malignancies

Author

Kohl, Vanessa, Flach, Johanna, Naumann, Nicole, Brendel, Susanne, Kleiner, Helga, Weiss, Christel, Seifarth, Wolfgang, Nowak, Daniel, Hofmann, Wolf-Karsten, Fabarius, Alice, and Popp, Henning D.

Subjects
ape1 inhibitor iii, hemic and lymphatic diseases, chronic myelomonocytic leukemia, poly(adp ribose) polymerase 1/2, acute myeloid leukemia, talazoparib, lcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogens, apurinic/apyrimidinic endonuclease 1, lcsh:RC254-282, Article, myelodysplastic syndrome
Abstract

Malignant hematopoietic cells of myelodysplastic syndromes (MDS)/chronic myelomonocytic leukemias (CMML) and acute myeloid leukemias (AML) may be vulnerable to inhibition of poly(ADP ribose) polymerase 1/2 (PARP1/2) and apurinic/apyrimidinic endonuclease 1 (APE1). PARP1/2 and APE1 are critical enzymes involved in single-strand break repair and base excision repair, respectively. Here, we investigated the cytotoxic efficacy of talazoparib and APE1 inhibitor III, inhibitors of PARP1/2 and APE1, in primary CD34+ MDS/CMML cell samples (n = 8; 4 MDS and 4 CMML) and in primary CD34+ or CD34− AML cell samples (n = 18) in comparison to healthy CD34+ donor cell samples (n = 8). Strikingly, talazoparib and APE1 inhibitor III demonstrated critical antileukemic efficacy in selected MDS/CMML and AML cell samples. Low doses of talazoparib and APE1 inhibitor III further increased the cytotoxic efficacy of decitabine in MDS/CMML and AML cells. Moreover, low doses of APE1 inhibitor III increased the cytotoxic efficacy of talazoparib in MDS/CMML and AML cells. In summary, talazoparib and APE1 inhibitor III demonstrated substantial antileukemic efficacy as single agents, in combination with decitabine, and combined with each other. Hence, our findings support further investigation of these agents in sophisticated clinical trials.

Published
2019

15. Comparison of RNA-Based Versus DNA-Based Quantitative KIT D816V Mutation Analysis Reveals Significant Disparity in Patients with Advanced Systemic Mastocytosis

Author

Jawhar, Mohamad, primary, Naumann, Nicole, additional, Lübke, Johannes, additional, Schwaab, Juliana, additional, Hofmann, Oliver, additional, Kristensen, Thomas Kielsgaard, additional, Sotlar, Karl, additional, Haselmann, Verena, additional, Schneider, Sven, additional, Metzgeroth, Georgia, additional, Popp, Henning D., additional, Fabarius, Alice, additional, Bugert, Peter, additional, Hofmann, Wolf-Karsten, additional, and Reiter, Andreas, additional

Published
2019
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16. Accumulation of DNA damage and alteration of the DNA damage response in monoclonal B-cell lymphocytosis and chronic lymphocytic leukemia

Author

Popp, Henning D., primary, Flach, Johanna, additional, Brendel, Susanne, additional, Ruppenthal, Sabrina, additional, Kleiner, Helga, additional, Seifarth, Wolfgang, additional, Schneider, Sven, additional, Schulze, Torsten J., additional, Weiss, Christel, additional, Wenz, Frederik, additional, Hofmann, Wolf-Karsten, additional, and Fabarius, Alice, additional

Published
2018
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17. Incidence and prognostic impact of cytogenetic aberrations in patients with systemic mastocytosis

Author

Naumann, Nicole, primary, Jawhar, Mohamad, additional, Schwaab, Juliana, additional, Kluger, Sebastian, additional, Lübke, Johannes, additional, Metzgeroth, Georgia, additional, Popp, Henning D., additional, Khaled, Nada, additional, Horny, Hans‐Peter, additional, Sotlar, Karl, additional, Valent, Peter, additional, Haferlach, Claudia, additional, Göhring, Gudrun, additional, Schlegelberger, Brigitte, additional, Meggendorfer, Manja, additional, Hofmann, Wolf‐Karsten, additional, Cross, Nicholas C.P., additional, Reiter, Andreas, additional, and Fabarius, Alice, additional

Published
2018
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19. Erratum: Cumulative radiation exposure from imaging procedures and associated lifetime cancer risk for patients with lymphoma

Author

Fabritius, Grete, primary, Brix, Gunnar, additional, Nekolla, Elke, additional, Klein, Stefan, additional, Popp, Henning D., additional, Meyer, Mathias, additional, Glatting, Gerhard, additional, Hagelstein, Claudia, additional, Hofmann, Wolf K., additional, Schoenberg, Stefan O., additional, and Henzler, Thomas, additional

Published
2017
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20. Accumulation of DNA damage and alteration of the DNA damage response in monoclonal B-cell lymphocytosis and chronic lymphocytic leukemia.

Author

Popp, Henning D., Flach, Johanna, Brendel, Susanne, Ruppenthal, Sabrina, Kleiner, Helga, Seifarth, Wolfgang, Schneider, Sven, Schulze, Torsten J., Weiss, Christel, Wenz, Frederik, Hofmann, Wolf-Karsten, and Fabarius, Alice

Subjects
*LYMPHOCYTOSIS, *CHRONIC lymphocytic leukemia, *DNA damage, *DOUBLE-strand DNA breaks, *DNA repair, *MANNOSE-binding lectins
Abstract

Accumulation of DNA damage and alteration of the DNA damage response (DDR) are critical features of genetic instability that is presumed to be implicated in the pathogenesis of monoclonal B-cell lymphocytosis (MBL) and chronic lymphocytic leukemia (CLL). Here, we show increased numbers of γH2AX foci, a marker of DNA double-strand breaks (DSB), in CD19+ cells of CLL patients as compared to CD19+ cells of MBL patients and healthy individuals. Furthermore, numerous γH2AX/53BP1 foci in CLL cells suggest activation of error-prone non-homologous end-joining repair mechanisms. Signatures of DDR proteins further indicate alterations of the DDR in CLL in contrast to a largely regular activation in MBL and healthy controls. In summary, our results provide evidence for the stepwise accumulation of DNA damage in the progression of MBL towards CLL and suggest increased DNA damage, error-prone DNA repair and altered DDR signaling to be critical mechanisms of clonal evolution in MBL and CLL. [ABSTRACT FROM AUTHOR]

Published
2019
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21. Incidence and Prognostic Impact of Cytogenetics in Combination with Molecular Aberrations in Patients with Systemic Mastocytosis

Author

Naumann, Nicole, primary, Jawhar, Mohamad, additional, Schwaab, Juliana, additional, Metzgeroth, Georgia, additional, Popp, Henning D, additional, Khaled, Nada, additional, Horny, Hans-Peter, additional, Sotlar, Karl, additional, Valent, Peter, additional, Haferlach, Claudia, additional, Göhring, Gudrun, additional, Schlegelberger, Brigitte, additional, Meggendorfer, Manja, additional, Cross, Nicholas C.P., additional, Hofmann, Wolf-Karsten, additional, Reiter, Andreas, additional, and Fabarius, Alice, additional

Published
2016
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25. DNA Damage and DNA Damage Response in Chronic Myeloid Leukemia.

Author

Popp, Henning D., Kohl, Vanessa, Naumann, Nicole, Flach, Johanna, Brendel, Susanne, Kleiner, Helga, Weiss, Christel, Seifarth, Wolfgang, Saussele, Susanne, Hofmann, Wolf-Karsten, and Fabarius, Alice

Subjects
*DNA repair, *CHRONIC myeloid leukemia, *DNA damage, *DASATINIB, *DOUBLE-strand DNA breaks, *BLOOD testing
Abstract

DNA damage and alterations in the DNA damage response (DDR) are critical sources of genetic instability that might be involved in BCR-ABL1 kinase-mediated blastic transformation of chronic myeloid leukemia (CML). Here, increased DNA damage is detected by γH2AX foci analysis in peripheral blood mononuclear cells (PBMCs) of de novo untreated chronic phase (CP)-CML patients (n = 5; 2.5 γH2AX foci per PBMC ± 0.5) and blast phase (BP)-CML patients (n = 3; 4.4 γH2AX foci per PBMC ± 0.7) as well as CP-CML patients with loss of major molecular response (MMR) (n = 5; 1.8 γH2AX foci per PBMC ± 0.4) when compared to DNA damage in PBMC of healthy donors (n = 8; 1.0 γH2AX foci per PBMC ± 0.1) and CP-CML patients in deep molecular response or MMR (n = 26; 1.0 γH2AX foci per PBMC ± 0.1). Progressive activation of erroneous non-homologous end joining (NHEJ) repair mechanisms during blastic transformation in CML is indicated by abundant co-localization of γH2AX/53BP1 foci, while a decline of the DDR is suggested by defective expression of (p-)ATM and (p-)CHK2. In summary, our data provide evidence for the accumulation of DNA damage in the course of CML and suggest ongoing DNA damage, erroneous NHEJ repair mechanisms, and alterations in the DDR as critical mediators of blastic transformation in CML. [ABSTRACT FROM AUTHOR]

Published
2020
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26. Comparison of RNA-Based Versus DNA-Based Quantitative KITD816V Mutation Analysis Reveals Significant Disparity in Patients with Advanced Systemic Mastocytosis

Author

Jawhar, Mohamad, Naumann, Nicole, Lübke, Johannes, Schwaab, Juliana, Hofmann, Oliver, Kristensen, Thomas Kielsgaard, Sotlar, Karl, Haselmann, Verena, Schneider, Sven, Metzgeroth, Georgia, Popp, Henning D., Fabarius, Alice, Bugert, Peter, Hofmann, Wolf-Karsten, and Reiter, Andreas

Abstract

Systemic mastocytosis (SM) is characterized by activating mutations in KIT, usually KITD816V in >90% of patients. According to the WHO classification, detection of KITD816V is a minor diagnostic criterion. Moreover, a reduction of the RNA-based KITD816V expressed allele burden (EAB) of ≥25% at month 6 is a favorable marker for improved survival in midostaurin-treated advanced SM (AdvSM) patients. However, only limited data exist upon the comparison between RNA-based and DNA-based quantitative KITD816V mutation analyses. We therefore collected peripheral blood samples from 161 SM patients (indolent SM [ISM], n=40; AdvSM, n=121) at time of referral. We applied a real time reverse-transcriptase polymerase chain reaction (qRT-PCR) assay for assessment of the KITD816V EAB and a chip-based digital PCR (dPCR) for the quantification of the DNA-based KITD816V variant allele frequency (VAF, QuantStudio 3D dPCR System, ThermoFisher Scientific, Massachusetts, USA). The limit of detection (LOD) was assessed through serial dilution experiments with DNA from healthy individuals and DNA from a SM patient with a KITD816V VAF of approximately 50%. All samples were analyzed in two independent dPCR runs. In an inital round-robin test for an inter-laboratory (n=4) comparison on 30 DNA samples (ISM, n=7; AdvSM, n=19), we found a very good correlation between 3 different chip-based digital PCR systems (dPCR; droplet-based dPCR, ddPCR, BioRad Laboratories, California, USA; quantitative real-time PCR, qPCR, California, USA; dPCR vs. ddPCR r=0.99, R2=0.99; dPCR vs. qPCR r=0.99, R2=0.98). In ISM patients, the comparison between EAB and VAF revealed a strong linear relationship with a correlation (r) of 0.91 and a coefficient of determination (R2) of 0.84, which was significantly inferior (r=0.71; R2=0.5) in AdvSM patients. In 45/121 (37%) and 76/121 (63%) of AdvSM patients, the EAB/VAF ratio was ≤2 (cohort A) or >2 (cohort B). To confirm the significant disparity between EAB and VAF in individual patients, serial analyses of at least 3 samples in 12 patients revealed a stable EAB/VAF ratio during follow-up. The comparison between cohort A and cohort B revealed significant differences in terms of a higher median hemoglobin level (p=0.006), a lower percentage of patients with hemoglobin <10g/dL (p=0.02), a lower median monocyte level (p=0.01), a lower median alkaline phosphatase level (p=0.03), and a lower number of patients with a high risk molecular profile (at least one gene mutation in SRSF2, ASXL1, and/or RUNX1, S/A/R, p=0.02) in cohort A. Moreover, patients of cohort A had a significantly better overall survival (OS) (median OS 12.9 versus 3.3 years; hazard ratio 2.1; 95% confidence interval 1.2-3.5; p=0.005; Figure). We conclude that a) KITD816V EAB and VAF are significantly different in AdvSM patients but not in ISM and b) AdvSM patients with an EAB/VAF ratio >2 present with an aggressive phenotype and adverse prognosis as compared to patients with EAB/VAF ratio ≤2. We therefore recommend to routinely determine KITD816V EAB and VAF in AdvSM patients.

Published
2019
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27. Increase of DNA Damage and Alteration of the DNA Damage Response in Monoclonal B-Cell Lymphocytosis and Chronic Lymphocytic Leukemia

Author

Popp, Henning D., Brendel, Susanne, Ruppenthal, Sabrina, Kleiner, Helga, Schneider, Sven, Schulze, Torsten, Weiss, Christel, Wenz, Frederik, Hofmann, Wolf-Karsten, and Fabarius, Alice

Abstract

The increase of DNA damage and the alteration of the DNA damage response (DDR) are critical features of genetic instability presumably implicated in the pathogenesis of monoclonal B-cell lymphocytosis (MBL) and chronic lymphocytic leukemia (CLL). Immunofluorescence microscopy of γH2AX and 53BP1 was performed for the analysis of DNA double-strand breaks (DSB) in CD19+ lymphocytes of 6 healthy individuals, 6 MBL patients, 21 CLL patients and in cells of the CLL cell line HG-3. In addition, immunoblotting of p-ATM, p-ATR, p-CHK1, p-CHK2 and p-TP53 was used for the analysis of the DNA damage response (DDR). As compared to the γH2AX foci levels in healthy individuals (0.1 focus per CD19+ lymphocyte ± 0.0; mean ± standard error of mean) increased γH2AX foci levels were detected in MBL patients (0.3 focus per CD19+ lymphocyte ± 0.1), CLL patients (1.3 foci per CD19+ lymphocyte ± 0.3) and in cells of the cell line HG-3 (1.0 focus per cell). Particularly high γH2AX foci levels were observed in immunoglobulin heavy-chain variable-region (IGHV)-unmutated, 11q-deficient, 17p-deficient and TP53-mutated CLL. Co-localization of γH2AX and 53BP1 indicated promotion of 53BP1-mediated nonhomologous end-joining (NHEJ) repair mechanisms at sites of DSB. Absent expression of p-CHK1 and p-TP53 suggested impaired G2/M checkpoint control and impaired apoptosis signaling in MBL and CLL. In summary, our results provide evidence for a continuous increase of DNA damage across the spectrum from MBL to CLL in conjunction with an impaired DDR. Particularly high γH2AX foci levels were detected in IGHV-unmutated, 11q-deficient, 17p-deficient and TP53-mutated CLL. Moreover, abundant γH2AX/53BP1 foci suggested a critical role for (in)effective NHEJ repair mechanisms at sites of DSB in MBL and CLL.

Published
2017
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