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Book ; Thesis: Die Expression von CD66 auf neutrophilen Granulozyten

Hönig, Manfred

Vergleich nach Stimulation in vivo und in vitro und Einflüsse von Prostaglandinen der E-Serie

1997

Author's details	vorgelegt von Manfred Hönig
Language	German
Size	95 Bl. : graph. Darst.
Edition	[Mikrofiche-Ausg.]
Document type	Book ; Thesis
Thesis / German Habilitation thesis	Freiburg (Breisgau), Univ., Diss., 1998
Note	Mikrofiche-Ausg.: 2 Mikrofiches : 24x
HBZ-ID	HT009419272
Database	Catalogue ZB MED Medicine, Health

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Article: Hematopoietic Stem Cell Transplantation for Severe Combined Immunodeficiency (SCID).

Haddad, Elie / Hoenig, Manfred

Frontiers in pediatrics

2019 Volume 7, Page(s) 481

Abstract: Severe Combined Immunodeficiencies (SCID) are a heterogeneous group of monogenetic diseases. We describe the typical clinical presentation of patients with SCID as well as basic principles in diagnosis and therapy by hematopoietic stem cell ... ...

Abstract	Severe Combined Immunodeficiencies (SCID) are a heterogeneous group of monogenetic diseases. We describe the typical clinical presentation of patients with SCID as well as basic principles in diagnosis and therapy by hematopoietic stem cell transplantation. Therapeutic strategies may differ between subtypes and the inherent reduced capacity or inablility to reject a graft have to be considered.
Language	English
Publishing date	2019-11-19
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2711999-3
ISSN	2296-2360
ISSN	2296-2360
DOI	10.3389/fped.2019.00481
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Article ; Online: Chemotherapy for a secondary malignancy nearly restores complete chimerism in an SCID-patient after HSCT.

Maier, Felix I / Schulz, Ansgar / Furlan, Ingrid / Felgentreff, Kerstin / Jacobsen, Eva-Maria / Sirin, Mehtap / Schwarz, Klaus / Pannicke, Ulrich / Stursberg, Jana / Debatin, Klaus-Michael / Hönig, Manfred

Clinical immunology (Orlando, Fla.)

2024 Volume 259, Page(s) 109891

Abstract: For patients with inborn errors of immunity (IEI) and other inborn diseases, mixed donor chimerism is a well-accepted outcome of hematopoietic stem cell transplantation (HSCT). Cytoreductive chemotherapy for a secondary malignancy is a potential ... ...

Abstract	For patients with inborn errors of immunity (IEI) and other inborn diseases, mixed donor chimerism is a well-accepted outcome of hematopoietic stem cell transplantation (HSCT). Cytoreductive chemotherapy for a secondary malignancy is a potential challenge for the stability of the graft function after HSCT. We report on a boy with X-SCID who developed Ewing sarcoma ten years after HSCT which was successfully treated with cytoreductive chemotherapy, surgery and local radiation. Surprisingly, this treatment had a positive impact on mixed chimerism with an increase of donor-cell proportions from 40% for neutrophils and 75% for non-T-mononuclear cells (MNCs) to >90% for both. T-cell counts remained stable with 100% of donor origin. This is -to our knowledge- the first report on the impact of cytoreductive chemotherapy on post-HSCT mixed chimerism and provides an important first impression for future patients.
MeSH term(s)	Male ; Humans ; Chimerism ; Transplantation, Homologous ; Hematopoietic Stem Cell Transplantation ; Tissue Donors ; Neoplasms ; Graft vs Host Disease ; Transplantation Conditioning
Language	English
Publishing date	2024-01-05
Publishing country	United States
Document type	Journal Article
ZDB-ID	1459903-x
ISSN	1521-7035 ; 1521-6616
ISSN (online)	1521-7035
ISSN	1521-6616
DOI	10.1016/j.clim.2024.109891
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Article ; Online: Neugeborenenscreening auf schwere kombinierte Immundefekte (SCID) in Deutschland.

Ghosh, Sujal / Albert, Michael H / Hauck, Fabian / Hönig, Manfred / Schütz, Catharina / Schulz, Ansgar / Speckmann, Carsten

Bundesgesundheitsblatt, Gesundheitsforschung, Gesundheitsschutz

2023 Volume 66, Issue 11, Page(s) 1222–1231

Abstract: Patients with a severe combined immunodeficiency (SCID) harbor genetic mutations disrupting T cell immunity and hence suffer severe, life-threatening infections or manifestations of immune dysregulation within the first months of their life. The only ... ...

Title translation	Newborn screening for severe combined immunodeficiencies (SCID) in Germany.
Abstract	Patients with a severe combined immunodeficiency (SCID) harbor genetic mutations disrupting T cell immunity and hence suffer severe, life-threatening infections or manifestations of immune dysregulation within the first months of their life. The only cure is to correct their immune system, usually by means of hematopoietic stem cell transplantation (HSCT). Pilot studies and national programs in the United States and in European countries have shown that patients can be identified at an early asymptomatic stage through newborn screening. This allows treatment before the occurrence of severe complications, which improves the outcome of curative strategies like HSCT.After assessment by the Federal Joint Committee (G-BA), the SCID screening was implemented into newborn screening in Germany in 2019. The first results of the screening (dry blood spot cards from around 2 million newborns between August 2019 and February 2022) were recently published. As expected, in addition to classic SCID diseases (incidence 1:54,000), infants with syndromic disorders and T cell lymphopenia were also identified. All patients with classic SCID were scheduled for curative treatment. Of the 25 patients with classic SCID, 21 were already transplanted at the time of data analysis. Only one of 21 transplanted patients died due to pre-existing infections. A comparison of the recent screening data with historical data suggests that SCID newborn screening has been successfully implemented in Germany. Patients with SCID are routinely identified very early and scheduled for curative therapy.
MeSH term(s)	Infant ; Infant, Newborn ; Humans ; United States ; Severe Combined Immunodeficiency/diagnosis ; Severe Combined Immunodeficiency/therapy ; Severe Combined Immunodeficiency/epidemiology ; Lymphopenia/diagnosis ; Neonatal Screening/methods ; Germany ; T-Lymphocytes ; Receptors, Antigen, T-Cell/genetics
Chemical Substances	Receptors, Antigen, T-Cell
Language	German
Publishing date	2023-09-19
Publishing country	Germany
Document type	English Abstract ; Journal Article ; Review
ZDB-ID	1461973-8
ISSN	1437-1588 ; 1436-9990
ISSN (online)	1437-1588
ISSN	1436-9990
DOI	10.1007/s00103-023-03773-6
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Article ; Online: K-Ras(V12) differentially affects the three Akt isoforms in lung and pancreatic carcinoma cells and upregulates E-cadherin and NCAM via Akt3.

Geißert, Rebekka / Lammert, Angela / Wirth, Stefanie / Hönig, Rabea / Lohfink, Dirk / Unger, Monika / Pek, Denis / Schlüter, Konstantin / Scheftschik, Theresa / Smit, Daniel J / Jücker, Manfred / Menke, Andre / Giehl, Klaudia

Cell communication and signaling : CCS

2024 Volume 22, Issue 1, Page(s) 85

Abstract: K-Ras is the most frequently mutated Ras variant in pancreatic, colon and non-small cell lung adenocarcinoma. Activating mutations in K-Ras result in increased amounts of active Ras-GTP and subsequently a hyperactivation of effector proteins and ... ...

Abstract	K-Ras is the most frequently mutated Ras variant in pancreatic, colon and non-small cell lung adenocarcinoma. Activating mutations in K-Ras result in increased amounts of active Ras-GTP and subsequently a hyperactivation of effector proteins and downstream signaling pathways. Here, we demonstrate that oncogenic K-Ras(V12) regulates tumor cell migration by activating the phosphatidylinositol 3-kinases (PI3-K)/Akt pathway and induces the expression of E-cadherin and neural cell adhesion molecule (NCAM) by upregulation of Akt3. In vitro interaction and co-precipitation assays identified PI3-Kα as a bona fide effector of active K-Ras4B but not of H-Ras or N-Ras, resulting in enhanced Akt phosphorylation. Moreover, K-Ras(V12)-induced PI3-K/Akt activation enhanced migration in all analyzed cell lines. Interestingly, Western blot analyses with Akt isoform-specific antibodies as well as qPCR studies revealed, that the amount and the activity of Akt3 was markedly increased whereas the amount of Akt1 and Akt2 was downregulated in EGFP-K-Ras(V12)-expressing cell clones. To investigate the functional role of each Akt isoform and a possible crosstalk of the isoforms in more detail, each isoform was stably depleted in PANC-1 pancreatic and H23 lung carcinoma cells. Akt3, the least expressed Akt isoform in most cell lines, is especially upregulated and active in Akt2-depleted cells. Since expression of EGFP-K-Ras(V12) reduced E-cadherin-mediated cell-cell adhesion by induction of polysialylated NCAM, Akt3 was analyzed as regulator of E-cadherin and NCAM. Western blot analyses revealed pronounced reduction of E-cadherin and NCAM in the Akt3-kd cells, whereas Akt1 and Akt2 depletion upregulated E-cadherin, especially in H23 lung carcinoma cells. In summary, we identified oncogenic K-Ras4B as a key regulator of PI3-Kα-Akt signaling and Akt3 as a crucial regulator of K-Ras4B-induced modulation of E-cadherin and NCAM expression and localization.
MeSH term(s)	Humans ; Proto-Oncogene Proteins c-akt/metabolism ; Neural Cell Adhesion Molecules ; Cadherins ; Lung Neoplasms/genetics ; Adenocarcinoma ; Protein Isoforms ; Phosphatidylinositol 3-Kinases/metabolism ; Lung/metabolism ; Pancreatic Neoplasms/pathology
Chemical Substances	Proto-Oncogene Proteins c-akt (EC 2.7.11.1) ; Neural Cell Adhesion Molecules ; Cadherins ; Protein Isoforms ; Phosphatidylinositol 3-Kinases (EC 2.7.1.-)
Language	English
Publishing date	2024-01-30
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2126315-2
ISSN	1478-811X ; 1478-811X
ISSN (online)	1478-811X
ISSN	1478-811X
DOI	10.1186/s12964-024-01484-2
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Article ; Online: BCG Disease in SCID: Three Decades of Experience in a Pediatric Transplant Center.

Cocchi, Nicoletta / Jacobsen, Eva-Maria / Hoenig, Manfred / Schulz, Ansgar / Schuetz, Catharina

Journal of clinical immunology

2021 Volume 42, Issue 1, Page(s) 195–198

MeSH term(s)	BCG Vaccine ; Child ; Hematopoietic Stem Cell Transplantation ; Humans ; Infant ; Mycobacterium bovis ; Severe Combined Immunodeficiency/diagnosis ; Severe Combined Immunodeficiency/therapy
Chemical Substances	BCG Vaccine
Language	English
Publishing date	2021-10-07
Publishing country	Netherlands
Document type	Letter
ZDB-ID	779361-3
ISSN	1573-2592 ; 0271-9142
ISSN (online)	1573-2592
ISSN	0271-9142
DOI	10.1007/s10875-021-01143-y
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Article: Conditioning Perspectives for Primary Immunodeficiency Stem Cell Transplants.

Shaw, Peter / Shizuru, Judith / Hoenig, Manfred / Veys, Paul

Frontiers in pediatrics

2019 Volume 7, Page(s) 434

Abstract: The majority of children undergoing Hematopoietic Stem cell Transplantation (HSCT) require conditioning therapy to make space and prevent rejection of the donor stem cells. The exception is certain children with Severe Combined immune deficiency, who ... ...

Abstract	The majority of children undergoing Hematopoietic Stem cell Transplantation (HSCT) require conditioning therapy to make space and prevent rejection of the donor stem cells. The exception is certain children with Severe Combined immune deficiency, who have limited or no ability to reject the donor graft. Transplant conditioning is associated with significant morbidity and mortality from both direct toxic effects of chemotherapy as well as opportunistic infections associated with profound immunosuppression. The ultimate goal of transplant practice is to achieve sufficient engraftment of donor cells to correct the underlying disease with minimal short- and long-term toxicity to the recipient. Traditional combinations, such as busulfan and cyclophosphamide, achieve a high rate of full donor engraftment, but are associated with significant acute transplant-related-mortality and late effects such as infertility. Less "intensive" approaches, such as combinations of treosulfan or melphalan with fludarabine, are less toxic, but may be associated with rejection or low level chimerism requiring the need for re-transplantation. The major benefit of these novel approaches, however, which we hope will be realized in the decades to come, may be the preservation of fertility. Future approaches look to replace chemotherapy with non-toxic antibody conditioning. The lessons learnt in refining conditioning for HSCT are likely to be equally applicable to gene therapy protocols for the same diseases.
Language	English
Publishing date	2019-11-06
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2711999-3
ISSN	2296-2360
ISSN	2296-2360
DOI	10.3389/fped.2019.00434
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Book: Fundraising im Gesundheitswesen

Fischer, Martin / Bachmann, Alexandra / Böhle, Danielle / Fischer, Kai / Fleisch, Hans / Hönig, Hans-Josef / Kliment, Cornelia / Krause, Annette / Lautenschläger, Manfred / Reetz, Konstantin / Roy, Patrick / Ruzicka, Johannes / Schenke, Eckhard / Steiner, Oliver

Leitfaden für die professionelle Mittelbeschaffung

2012

Author's details	herausgegeben von Oliver Steiner und Martin Fischer. Mit Beiträgen von Alexandra Bachmann, Danielle Böhle, Kai Fischer, Martin Fischer, Hans Fleisch, Hans-Josef Hönig, Cornelia Kliment, Annette Krause, Manfred Lautenschläger, Konstantin Reetz, Patrick Roy, Johannes Ruzicka, Eckhard Schenke und Oliver Steiner
Keywords	Delivery of Health Care ; Financial Management ; Fund Raising ; Deutsches Sprachgebiet ; Gesundheitswesen ; Nonprofit-Organisation ; Spendensammlung
Subject	Geldsammlung ; Sammlung ; Fund Raising ; Fundraising ; Organisation ohne Erwerbscharakter ; Non-profit-Organisation ; NPO ; Gesundheitsdienst ; Gesundheitssystem ; Gesundheitswirtschaft ; Medizinalwesen ; Medizinalsystem
Language	German
Size	XVIII, 238 Seiten, Illustrationen, Diagramme, Karten
Publisher	Schattauer
Publishing place	Stuttgart
Publishing country	Germany
Document type	Book
HBZ-ID	HT016890637
ISBN	978-3-7945-2811-0 ; 3-7945-2811-5
Database	Catalogue ZB MED Medicine, Health

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Article ; Online: Finding a balance in reduced toxicity hematopoietic stem cell transplantation for thalassemia: role of infused CD3+ cell count and immunosuppression.

Bone marrow transplantation

2024

Abstract: We performed a retrospective analysis on 124 patients with transfusion-dependent thalassemia who were registered in the German pediatric registry for stem cell transplantation. All patients underwent first allogeneic hematopoietic stem cell ... ...

Abstract	We performed a retrospective analysis on 124 patients with transfusion-dependent thalassemia who were registered in the German pediatric registry for stem cell transplantation. All patients underwent first allogeneic hematopoietic stem cell transplantation (HSCT) between 2011 and 2020 and belonged mainly to Pesaro risk class 1-2. Four-year overall (OS) and thalassemia-free survival (TFS) were 94.5% ± 2.9% and 88.0% ± 3.4% after treosulfan-fludarabine-thiotepa- and 96.9% ± 3.1% (P = 0.763) and 96.9% ± 3.1% (P = 0.155) after busulfan-fludarabine-based conditioning. Mixed chimerism below 75% occurred predominantly in treosulfan-based regimens (27.5% versus 6.2%). OS and TFS did not differ significantly between matched sibling, other matched family and matched unrelated donor (UD) HSCTs (OS: 100.0%, 100.0%, 96.3% ± 3.6%; TFS: 96.5% ± 2.4%, 90.0% ± 9.5%, 88.9% ± 6.0%). However, mismatched UD-HSCTs performed less favorable (OS: 84.7% ± 7.3% (P = 0.029); TFS: 79.9% ± 7.4% (P = 0.082)). We generated a scoring system reflecting the risk to develop mixed chimerism in our cohort. The main risk-reducing factors were a high CD3+ cell count (≥6 × 10
Language	English
Publishing date	2024-02-07
Publishing country	England
Document type	Journal Article
ZDB-ID	632854-4
ISSN	1476-5365 ; 0268-3369 ; 0951-3078
ISSN (online)	1476-5365
ISSN	0268-3369 ; 0951-3078
DOI	10.1038/s41409-024-02219-0
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Article ; Online: Complement and platelets: prothrombotic cell activation requires membrane attack complex-induced release of danger signals.

Mannes, Marco / Pechtl, Veronika / Hafner, Susanne / Dopler, Arthur / Eriksson, Oskar / Manivel, Vivek Anand / Wohlgemuth, Lisa / Messerer, David Alexander Christian / Schrezenmeier, Hubert / Ekdahl, Kristina N / Nilsson, Bo / Jacobsen, Eva-Maria / Hoenig, Manfred / Huber-Lang, Markus / Braun, Christian K / Schmidt, Christoph Q

Blood advances

2023 Volume 7, Issue 20, Page(s) 6367–6380

Abstract: Complement activation in the diseases paroxysmal nocturnal hemoglobinuria (PNH) and atypical hemolytic uremic syndrome (aHUS) results in cytolysis and fatal thrombotic events, which are largely refractory to anticoagulation and/or antiplatelet therapy. ... ...

Abstract	Complement activation in the diseases paroxysmal nocturnal hemoglobinuria (PNH) and atypical hemolytic uremic syndrome (aHUS) results in cytolysis and fatal thrombotic events, which are largely refractory to anticoagulation and/or antiplatelet therapy. Anticomplement therapy, however, efficiently prevents thrombotic events in PNH and aHUS, but the underlying mechanisms remain unresolved. We show that complement-mediated hemolysis in whole blood induces platelet activation similarly to activation by adenosine 5'-diphosphate (ADP). Blockage of C3 or C5 abolished platelet activation. We found that human platelets failed to respond functionally to the anaphylatoxins C3a and C5a. Instead, complement activation did lead to prothrombotic cell activation in the whole blood when membrane attack complex (MAC)-mediated cytolysis occurred. Consequently, we demonstrate that ADP receptor antagonists efficiently inhibited platelet activation, although full complement activation, which causes hemolysis, occurred. By using an established model of mismatched erythrocyte transfusions in rats, we crossvalidated these findings in vivo using the complement inhibitor OmCI and cobra venom factor. Consumptive complement activation in this animal model only led to a thrombotic phenotype when MAC-mediated cytolysis occurred. In conclusion, complement activation only induces substantial prothrombotic cell activation if terminal pathway activation culminates in MAC-mediated release of intracellular ADP. These results explain why anticomplement therapy efficiently prevents thromboembolisms without interfering negatively with hemostasis.
MeSH term(s)	Humans ; Rats ; Animals ; Complement Membrane Attack Complex ; Hemolysis ; Erythrocytes/metabolism ; Complement Activation ; Blood Platelets/metabolism ; Hemoglobinuria, Paroxysmal/genetics ; Atypical Hemolytic Uremic Syndrome
Chemical Substances	Complement Membrane Attack Complex
Language	English
Publishing date	2023-07-10
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2915908-8
ISSN	2473-9537 ; 2473-9529
ISSN (online)	2473-9537
ISSN	2473-9529
DOI	10.1182/bloodadvances.2023010817
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