Deutsch | English | по-русски | Türkçe 

Tumor Immunology Group (TIG)

Contact/Address of the research group:

Tumor-Immunology-Group (TIG)

Department of Internal Medicine III

University Hospital Ulm

Albert-Einstein-Allee 23

89081 Ulm

Germany

Phone (Lab): 0049-731-150-6754

Fax (Lab): 0049-731-150-6477

 

Head of the research group

Prof. Dr. med. Jochen Greiner

Medical director

Hematology and oncology

Diakonie-Klinikum Stuttgart

Rosenbergstrasse 38

70176 Stuttgart

Tel.: 0711-991-3501

Direct call: 0711-991-3504

Fax: 0711-991-3591

Email: greiner[at]diak-stuttgart.de

                 

Head of Tumor-Immunology-Group (TIG)

Department of Internal Medicine III

University Hospital Ulm

Albert-Einstein-Allee 23

89081 Ulm

Germany

Phone (Lab): 0049-731-150-6754

Fax (Lab): 0049-731-150-6477

jochen.greiner@uniklinik-ulm.de

 

Local Leader

Dr. med. Susanne Hofmann

Department of Internal Medicine III

University Hospital Ulm

Albert-Einstein-Allee 23

89081 Ulm

Germany

Phone (Lab): 0049-731-150-6754

Phone (Clinic): 0049-731-500-45715

susanne.hofmann@uniklinik-ulm.de

 

Project Leaders

Dr. med. Anna Babiak

 

Laboratory Technicians

Marlies Götz

Anita Szmaragowska

Alexandro Landshammer

 

Medical students

Daniel Scherbaum

Lisa Müller

Adrian Hack

Melanie Munz

Simon Mannes

Maximilian Steinhauser

Daria Ushmorova

Myrjam Weisschuh

Anne-Katrin Wolf

Research Fields

Our research focuses on the definition of new targets for immunotherapy and on the development of vaccines for the clinical treatment of leukemia, multiple myeloma, lung cancer, renal cell carcinoma, prostate cancer and other solid tumors. Our activities include in vitro T cell assays, preclinical studies and clinical trials.

Figure 1: Overview over the research activities of the Tumorimmunology Group in Ulm

Identification and characterization of immunogenic targets in leukemia and solid tumors

Tumor cells can be efficiently eliminated by specific T cells of the immune system. Targeted immunotherapies require the identification and characterization of appropriate antigen structures. To date, a huge number of tumor-associated antigens (TAAs) has been identified. Several strategies to target these antigens to reduce tumor load or to prevent relapse in solid tumors like lung cancer, prostate cancer or renal cell carcinoma are under investigation. Several promising immunological and even clinical responses have prompted to implement vaccination strategies to hematological malignancies like acute or chronic myeloid leukemia (AML/CML), myelodysplastic syndrome (MDS), multiple myeloma (MM) and also lymphoma. Several immunogenic antigens associated with leukemias (LAAs) have been identified in the last years in patients with hematological malignancies like BAGE, BCR-ABL, BCL-2, OFA-iLRP, FLT3-ITD, G250, hTERT, PRAME, proteinase 3, RHAMM, surviving, WT-1 and recently also NPM1 (see next section). Cellular as well as humoral immune responses against these LAAs were characterized and clinical trials targeting these antigens were performed.

Figure 2: Leukemia-associated antigens have been used in clinical trials for myeloid diseases (Hofmann/Greiner, Current Cancer Drug Targets 2011).

Immune responses against mutation-specific (tumor-specific) antigens as candidates for specific immunotherapy

In AML, NPM1 mutations are one of the most frequent molecular alterations thereby constituting an important prognostic marker. The mutations cause an abnormal shift of the NPM1 protein from the nucleus to the cytoplasm, a mechanism first described by Falini et al. AML patients with NPM1mut but without FLT3 internal tandem duplication (ITD) mutation show improved overall survival. In first-line treatment, patients with NPM1mut do not seem to benefit from allogeneic stem cell transplantation. The functional role of NPM1mut for the improved clinical outcome is still under evaluation. Immune responses to NPM1mut may contribute to the favourable prognosis of this AML entitiy.

Recently, we described specific CD4+ and CD8+ T cell responses against epitopes derived from mutated regions of NPM1 (Greiner et al., Blood 2012). Two NPM1mut-derived peptides, called #1 and #3, induced specific T cell responses in patients with NPM1mut (33 % versus 44%). NPM1mut AML patients showed a significantly higher frequency of CTL responses against peptide #3 compared to healthy volunteers (p=0.046) (Greiner et al., Blood 2012).

Figure 3: ELISpot analysis for IFN- (a) and Granzyme B (b) of several NPM1-derived peptides in an NPM1mut AML patient. ELISpot assays for the release of interferon gamma (panel a) and granzyme B (panel b) were performed after stimulation with several NPM1 derived peptides. Stimulation with an influenza matrix protein (IMP) derived peptide served as a positive control, no peptide stimulation as a negative control. Peptide specific T cell activity was measured by interferon release, whereas granzyme B secretion indicated the lytic potential of the T cells. This patient showed a significant increase in frequency for the epitopes #1 and #3 derived from the mutational region NPM1.
Figure 4: Frequency of specific T-cell responses against the two most interesting epitopes derived from the NPM1 mutation. NPM1mut AML patients showed a significantly higher frequency of T cell responses against peptide #3 in contrast to HVs (p=0.046) (Greiner et al., Blood 2012).

Ten peptides derived from NPM1wt and NPM1mut were subjected to ELISpot analysis in 33 healthy volunteers and 27 AML patients. Tetramer assays against most interesting epitopes were performed and chromium release assays were used to show the cytotoxicity of peptide-specific T cells. Moreover, HLA-DR-binding epitopes were used to test the role of CD4+ T cells in NPM1 immunogenicity. Specific lysis of leukemic blasts was detected. NPM1mut induces specific T cell responses of CD4+ and CD8+ T cells and thus presents a promising target for specific immunotherapies in AML.

Immune responses against NPM1 and other antigens before and after donor lymphocyte infusion and allogeneic stem cell transplantation

The GvL-effect observed after HSCT and DLI is based on CTL mediated immunity which is reactive against minor histocompatibility antigens (mHAg) restricted to hematopoietic cells. Unselected DLI still holds the potential risk for GvHD. Therefore, several efforts are being made to enhance the GvL-effect without causing GvHD. Our main focus is to elucidate the role of LAAs in the mechanisms of GvL to possibly booster DLI and induce a long-lasting remission in case of molecular relapse in AML. These LAAs can be recognized by specific CTLs and for some antigens also humoral immune responses have been demonstrated. LAAs might enable the immune system to more easily eliminate MRD after initial chemotherapy and therefore LAA expression might also influence clinical outcomes.

Here (Figure 5), we could demonstrate for the first time to our knowledge polyspecific CTL-responses against several known LAAs in a patient with AML with NPM1mut after preemptive DLI in molecular relapse. Interestingly, the immune responses against LAAs were associated with MRD negativity. Whether specific CTL-responses against epitopes derived from the NPM1mut peptide or the polyspecificity of the CTLs against several LAAs are decisive in the elimination of the myeloid blasts with NPM1mut remains to be determined in a larger cohort of patients.

Figure 5: T cell responses against different LAAs before and after donor lymphocyte infusion. We detected polyspecific CTL-responses against several known LAAs in a patient with AML with NPM1mut after preemptive DLI in molecular relapse (Hofmann et al, DGHO 2012).

Analysis of further patients is ongoing.


Functional role of leukemia-associated antigens (LAAs) and correlation with overall survival

LAAs might enable the immune system to more easily eliminate MRD following chemotherapy and therefore LAA expression might also influence clinical outcomes. The expression of at least one of the three LAAs RHAMM, PRAME or G250 proved to be favorable for the prognosis of AML. Similar results were demonstrated for the co-expression of other specific LAAs (Figure 6a+b). Co-expression of Leukemia-associated antigens might be associated with a better clinical outcome in AML patients (Figure 6a+b).

Figure 6a: Co-expression in 116 AML patients of RHAMM, PRAME and G250 provided a favorable prognostic effect on the overall survival in AML maybe due to immune reactions (Greiner et al., Blood 2006).
Figure 6b: Overall survival compared to mRNA expression of TAA (RHAMM, SSX2IP, Survivin). Patients with co-expression of these LAAs showed a better OS than patients without expression of these antigens (Guinn, Greiner et al., Blood 2009).

Recently, we demonstrated that T cell responses against NPM1 might be involved in the favorable outcome of this AML subtype (Figure 7, Greiner/Hofmann, Blood 2013)

 

Figure 7: Survival analysis of NPM1mut patients (A) Kaplan Meier plot with the survival analysis of 25 NPM1mut patients. (B) Overall survival of patients with specific CTL responses against peptide #1 or #3. Blue - patients with an immune response; green - patients without any specific CTL response. (C) Overall survival in dependence of the specific epitope. Blue -peptide #1; green - peptide #3; yellow - peptide #1 and 3; purple - no peptide.(Greiner/Hofmann, Blood 2013)

The LAA PRAME seems to play a key role in the survival of AML patients.

Figure 8: Kaplan Meier analyses based on PRAME expression and ATRA treatment in two randomized clinical trials (AML HD98B and AMLSG 07-04). (A) - (D) Kaplan Meier analyses based on PRAME expression defined grouping and ATRA treatment in AML HD98B, (A) and (B), and AMLSG 07-04 patients, (C) and (D), respectively (P-values are indicated; PRAME expression groups have been defined based on the median PRAME expression).

Vaccination trials performed by our group

a) Against hematological malignancies (AML, MDS, CLL, MM)

RHAMM is an immunogenic antigen which is strongly expressed in several hematological malignancies and induces humoral and cellular immune responses. We initiated a phase I/II RHAMM-R3 peptide vaccination for patients with AML, MDS, MM and CLL overexpressing RHAMM. In this clinical study, patients with RHAMM expression and a limited tumor load or a minimal residual disease were included. 26 patients were enrolled. The first 16 patients were vaccinated with 300 µg and further patients with 1000 µg R3 peptide.

We performed two RHAMM-R3 peptide vaccination trials using 300µg and 1000µg for AML, MDS and MM overexpressing RHAMM. In the 300µg cohort we detected specific immune responses in 7/10 patients and also positive clinical effects in 5/10 patients. In the second cohort of nine patients with AML, MDS and MM vaccinated with a higher peptide dose of 1000 µg RHAMM-R3 peptide we detected specific immune responses in a lower frequency (33%) in contrast to patients in the 300µg cohort. Similar mild toxicity of both cohorts was found, only mild drug-related adverse events were observed such as erythema and induration of the skin. Nevertheless, the patients in the 300µg cohort showed a higher frequency of positive immunological clinical effects. Higher doses of peptide application might induce immune tolerance (Schmitt/Greiner Blood 2008; Greiner et al., Haematologica 2010). Taken together, RHAMM-R3 peptide vaccination induced both immunological and clinical responses using lower and higher peptide doses. However, higher doses of peptide do not improve the frequency and intensity of immune responses in this clinical trial and might induce immune tolerance. Serological analysis and profiling is ongoing.

These mentioned trials are completed, a further trial is in preparation.

 

b) Against viral infections (CMV)

For patients after allogeneic stem cell transplantation we initiated a peptide vaccination trial against viral CMV infection. The trial is ongoing. The two most important inclusion criteria are:

•     Risk constellation donor CMV negative, recipient CMV positive

(preemptive use) or

•     Diagnosis of CMV infection/reactivation after allogeneic transplantation

Regulation and modulation of the immune system and immunogenicity of tumor and leukemic stem cells

This trial is still on going.

 

New targets in lung cancer

In solid tumors new therapeutic options like the use of T-cell activating antibodies  (e.g. CTLA-4 antibodies like ipilimumab, PD-1 antibodies like nivolumab or others) show the power of immune response to control cells from metastatic malignancies like melanoma, renal cell carcinoma or lung cancer.

These therapies might be more effective in combination of at least two antibodies (the results of the combination of ipilimumab and nivolumab are encouraging) or in a combination with target-specific procedures.

In lung cancer, encouraging results have been investigated including targeted immunotherapy, e.g. against MAGE-A3 and hTERT. Thus, tumor vaccination seems to be a promising strategy especially in situations of reduced tumor load, e.g. in maintenance therapy. In this work, we address the question, whether there are further interesting epitopes beside the antigens MAGE-A3 and hTERT inducing intensive immune reactions in a high frequency in lung cancer and are therefore eligible for immunotherapeutic approaches.

Immune reactions of CD8+ T cells were measured in ELISPOT assays for interferon gamma and granzyme B. Moreover, tetramer assays and chromium release assays were performed. Epitopes were tested derived from the lung-cancer associated antigens MAGE-A3 and hTERT, but also from the antigens RHAMM, Survivin, WT-1, PRAME, HER2 and G250 known from other tumor entities and from novel antigen structures, like Aurorakinases A and B.Most frequent responses could be detected against PRAME (67%), hTERT (60%), G250 (60%) and RHAMM (40%). Lower frequency was measured for Survivin- (27%), WT-1- (27%), the two MAGE-A3- (27 and 20%) and Her2- (15%) derived peptides. Specific T cell responses could be also detected against Aurorakinases A and B. The novel peptides AuraA01 and AuraB01 showed specific T cell responses in 33% and 40% of patients respectively (Babiak/Greiner, submitted)

Immunogenicity of tumor/leukemic stem cells

Leukemic stem cells (LSC) might be the source for leukemic disease self-renewal and account for disease relapse after treatment. Therefore LSCs represent a critical target for further therapeutic options. Immunotherapeutic approaches might overcome the immune escape mechanisms of these cells and represent an alternative or a complementary option for inducing a long lasting remission of the leukemia by eradicating LSCs. Leukemia-associated antigens (LAAs) represent antigens that are recognized by cytotoxic T-cells and have been identified in several malignant myeloid disorders. Colony forming units, chromium release assays and murine experiments are ongoing.

Figure 9: Separation of CD34+CD38- leukemic stem cells

Techniques

     

    • SEREX
    • qRT-PCR techniques
    • DNA-cloning
    • DNA-sequencing
    • Western Blot
    • Immunocytology
    • Seven-color FACS analysis of surface and intracellular makers
    • ELISA
    • ELISPOT
    • T-cell cloning, Mixed lymphocyte peptide culture (MLPC)
    • 3-H proliferation assay
    • 5 1-Cr release assay
    • Affymetrix gene expression Arrays (in Cooperation)
    • Colony Forming Units (CFUs)
    • Stem cell assays

     

Grants/Funding

  • Bausteinförderung. Immunologische Charakterisierung von leukämischen Stamm- und Progenitorzellen bei der akuten myeloischen Leukämie (AML) mit NPM1-Mutation. Beginn ab 01/2013 2 Jahre, Antragsteller: Dr. med. S. Hofmann

  • Else Kröner-Fresenius-Stiftung "Untersuchung der Immunogenität von Leukämie-Stammzellen bei der akuten myeloischen Leukämie (AML)". Beginn ab 09/2011 für 3 Jahre. Antragsteller: Prof. Dr. J. Greiner, Vanessa Schneider.

  • Deutsche Forschungsgemeinschaft (DFG), “Immunogenität mutations-spezifischer Peptidsequenzen bei der akuten myeloischen Leukämie“ Beginn ab 02/2011, 3 Jahre, Antragsteller: Prof. Dr. J. Greiner, Dr. med. S. Hofmann

  • NOVARTIS-Stiftung, „Charakterisierung von immunogenen Leukämie-assoziierten Antigenen bei myeloischer Leukämien“. Laufzeit: 2001-2003. Antragsteller: Dr. J. Greiner, Dr. M. Schmitt.

  • Anschubfinanzierung ”Baustein-Förderung” der Universität Ulm. ”Nachweis einer spezifischen zellulären Immunantwort gegen die neu identifizierten tumor-assoziierten Antigene RHAMM, MAZ und MPP11 bei leukämischen Blasten”, Laufzeit 01/2002 bis 04/2004. Antragsteller: Dr. J. Greiner.

  • Deutsche José Carreras Leukämie-Stiftung e.V. "Charakterisierung von Antigenen bei der akuten myeloischen Leukämie". Zelluläre Assays für bereits definierte Leukämie-Antigene. Laufzeit bis einschl. 2003-2005. Antragsteller: Dr. M. Schmitt, Dr. J. Greiner, Dr. M. Wiesneth, Prof. Dr. H. Döhner.

  • Deutsche Forschungsgemeinschaft (DFG) „Rolle des Rezeptors für Hyaluronsäure-vermittelte Motilität (RHAMM/CD168) bei der Proliferation myeloischer Blasten“. Antragsteller: Dr. J. Greiner, PD Dr. M. Schmitt. Beginn der Förderung bis 2005-2007.

  • Deutsche José Carreras Leukämie-Stiftung e.V. „Entwicklung einer Polyvalenten Peptidvakzinierung für Patienten mit malignen hämatologischen Erkrankungen. Laufzeit 07/2007-06/2009. Antragsteller: PD Dr. J. Greiner, Prof. Dr. M. Schmitt, Dr. M. Wiesneth, Prof. Dr. H. Schrezenmeier.

  • Else Kröner-Fresenius-Stiftung „Peptid-Vakzinierung für Patienten mit Chronischer Lymphatischer Leukämie. Laufzeit 07/2007-06/2009. Antragsteller: Prof. Dr. M. Schmitt, PD Dr. J. Greiner, Dr. K. Giannopoulos.

  • BMBF-Förderung des Antrages „Präventive und therapeutische Peptid-Vakzinierung gegen HCMV“ im Rahmen des Aufbaus einer Forschergruppe in der klinischen Infektiologie „Erkennung, Vermeidung und Behandlung von Infektionen des immunkompromittierten Patienten“. Laufzeit 2007-2010; Projektleiter: Prof. Dr. J. Greiner. Fördersumme: 474.300 Euro

  • Forschungsförderung „kooperative Reserach – Celgene“; „Evaluation des immunmodulatorischen Effektes von Lenalidomid/Revlimid®auf zytotoxische und regulatorische T-Zellen bei Patienten nach allogener Stammzelltransplantation. Antragsteller : PD Dr. J. Greiner; Laufzeit 2009-2010.

  • Deutsche José Carreras Leukämie-Stiftung e.V. „Einfluss Leukämie-assoziierter Antigene auf die Zellproliferation myeloischer Blasten und auf das Überleben von Patienten mit akuter myeloischer Leukämie“. Beginn ab 01/2009. Antragsteller: Prof. Dr. J. Greiner, PD Dr. L. Bullinger.

  • Deutsche José Carreras Leukämie-Stiftung e.V. „Vakzine-verstärkte Spenderlymphozyten“. Laufzeit 10/2010-09/2012. Antragsteller: Prof. Dr. J. Greiner, Prof. Dr. M. Schmitt, Dr. M. Wiesneth, Prof. Dr. H. Schrezenmeier.

  • Jose Carreras Career Award 2010 der Deutschen José Carreras Leukämie-Stiftung e.V. „Weiterentwicklung immunologischer Behandlungsansätze für eine zielgerichtete Immuntherapie von Leukämien“. Beginn ab 09/2010.

Gesamtfördersumme: 2.427.000 Euro

Representative Publications

1.    Greiner J, Schneider V, Schmitt M, Götz M, Döhner K, Wiesneth M, Döhner H, Hofmann S. Immune responses against the mutated region of cytoplasmatic nucleophosmin 1 (NPM1) might contribute to the favorable clinical outcome of AML patients with NPM1 mutations (NPM1mut). Blood, accepted. 2013
IF: 9,898
 
2.    Bullinger L, Schlenk RF, Götz M, Botzenhardt U, Hofmann S, Russ AC, Babiak A, Zhang L, Schneider V, Döhner K, Schmitt M, Döhner H, Greiner J. PRAME induced inhibition of retinoic acid receptor signaling-mediated differentiation – an explanation for ATRA response in AML without t(15;17). CCR 19:2562-71, 2013
IF: 7,742
 
3.    Schneider V, Egenrieder S, Götz M, Herbst C, Greiner J, Hofmann S. Specific immune responses against epitopes derived from Aurora kinase A and B in acute myeloid leukemia. Leukemia & Lymphoma, 54:1500-4, 2013
IF: 2,580
 
4.    Hofmann S, Götz M, Schneider V, Guillaume P, Bunjes D, Döhner H, Wiesneth M, Greiner J. Donor lymphocyte infusion induces polyspecific CD8+ T cell responses with concurrent molecular remission in AML with NPM1 mutation. JCO 31:e44-47,  2013
IF: 18,372
 
5.    Greiner J, Ono Y, Hofmann S, Schmitt A, Mehring E, Götz M, Guillaume P, Döhner K, Mytilineos J, Döhner H, Schmitt M. Mutated regions of nucleophosmin 1 (NPM1) elicit both CD4+ and CD8+ T cell responses in patients with acute myeloid leukemia (AML). Blood 120:1282-9, 2012
IF: 9,898
 
6.    Zhang L, Götz M, Hofmann S, Greiner J. Immunogenic targets for specific immunotherapy in multiple myeloma. Clin Dev Immunol 2012:820394, 2012
IF: 1,838

7.    Zhang L*, Hofmann S*, Guillaume P, Schneider V, Greiner J. Most favourable PRAME epitopes. e-Letter Blood November 16, 2011. Accessed April 19, 2012.
http://bloodjournal.hematologylibrary.org/content/117/12/3353/reply#bloodjournal_el_2260
IF: 9,898

8.    Hofmann S, Babiak A, Greiner J. Immunotherapy for Myeloproliferative Neoplasms (MPN). Curr Cancer Drug Targets 11: 72-84, 2011
IF: 5,129

9.    Greiner J, Schmitt A, Giannopoulos K, Rojewski MT, Goetz M, Funk I, Ringhoffer M, Bunjes D, Hofmann S, Ritter G, Döhner H, Schmitt M. High dose RHAMM-R3 peptide vaccination for patients with acute myeloid leukemia (AML), myelodysplastic syndrome (MDS) and multiple myeloma (MM). Haematologica 95:1191-1197, 2010
IF: 5,516

10.   Guinn B*, Greiner J*, Schmitt M, and Mills K (*contributed equally). Elevated expression of the leukaemia associated antigen SSX2IP predicts good survival in acute myeloid leukaemia patients who lack detectable cytogenetic rearrangements. Blood 113: 1203-4, 2009
IF: 9,898

11.   Greiner J, Guinn B, Döhner H, Bullinger L, Schmitt M. Leukemia-associated antigens (LAAs) are critical for the proliferation of acute myeloid leukemia cells. Clin Cancer Res 14: 1-6, 2008
IF: 6,250

12.    Schmitt M, Schmitt A, Rojewski MT, Chen J, Giannopoulos K, Fei F, Yu Y, Götz M,Heyduk M, Ritter G, Speiser D, Gnjatic S, Guillaume P, Ringhoffer M, Schlenk RF, Liebisch P, Bunjes D, Shiku H, Döhner H, Greiner J. RHAMM-R3 peptide vaccination in patients with acute myeloid leukemia, myelodysplastic syndrome and multiple myeloma elicits immunological and clinical responses. Blood 111: 1357-1365, 2008
IF: 9,898
 
13.    Greiner J, Döhner H, Schmitt M. Cancer vaccines for patients with acute myeloid leukemia--definition of leukemia-associated antigens and current clinical protocols targeting these antigens. Haematologica 91: 1653-61, 2006
IF: 6,424

14.    Greiner J*, Schmitt M*, Li Li, Giannopoulos K, Bösch K, Schmitt A, Döhner K, Schlenk RF, Pollack JR, Döhner H, Bullinger L (*contributed equally). Expression of tumor-associated antigens in acute myeloid leukemia: implications for specific immunotherapeutic approaches. Blood 108: 4109-17, 2006
IF: 9,898
 
15.    Greiner J, Li L, Ringhoffer M, Barth T, Wiesneth M, Döhner H, Schmitt M. Identification and characterization of epitopes of the receptor for hyaluronic acid mediated motility (RHAMM/CD168) recognized by CD8 positive T cells of HLA-A2 positive patients with acute myeloid leukemia. Blood 106: 938-45, 2005
IF: 9,898

Collaborations

(in alphabetical order)

Thomas Barth, University of Ulm, Germany

Lars Bullinger, University of Ulm, Germany

Christian Buske, University of Ulm, Germany

Daniela Cilloni, University of Turino, Italy

Anna Dmoszynska, University of Lublin, Poland

Krzysztof Giannopoulos, University of Lublin, Poland

Barbara Guinn, University of Southampton, U.K.

Jacek Rolinski, University of Lublin, Poland

Reinhold Schirmbeck, University of Ulm, Germany

Michael Schmitt, University of Heidelberg, Germany

Hubert Schrezenmeier, University of Ulm, Germany

Hiroshi Shiku, Mie University, Tsu, Japan

Markus Wiesneth, University of Ulm, Germany

Dominik Wolf, University of Bonn, Germany

Am 26.11.2013, ab 18.30 Uhr findet unser diesjähriges Symposium Tumorimmunologie statt.

Forschungsbereiche

Molecular Genetics of Myeloid Leukemia
Prof. Dr. Konstanze Döhner / Prof. Dr. Lars Bullinger

Molecular Genetics of Myeloproliferative Disorders
Dr. Frank Stegelmann / Prof. Dr. Konstanze Döhner

Molecular Pathogenesis and Progression of Lymphoproliferative Disorders
Prof. Dr. Stephan Stilgenbauer

Mechanisms of Leukemogenesis
PD Dr. Daniel Mertens

Molecular Pathogenesis and Prognostic Markers in Monoclonal Gammopathies
PD Dr. Christian Langer

Tumor Immunology Group (TIG)
Prof. Dr. Jochen Greiner

Haemostaseology
PD Dr. Christian Langer
 

Molecular Hematopoiesis
PD Dr. Dr. Florian Kuchenbauer

 

Emmy Noether Research Group

Dr. Jan Krönke

gepunktete hellblaue Linie 176px breit
gepunktete blaue Linie 1000px breit