Leukaemia and Blood Cancer Research

Leukaemia & Blood Cancer Research Unit at the University of Auckland

Principle Investigator

Professor Stefan K. Bohlander

Professor Bohlander is the holder of the Marijanna Kumerich Chair in Leukaemia and Lymphoma Research and heads the Leukaemia & Blood Cancer Research Unit at the University of Auckland’s Department of Molecular Medicine in the School of Medical Sciences.


Dr. Martin Chopra
Dr. Purvi Kakadiya


Sarvenaz Taghavi
Rhea Desai


Marijanna Kumerich Donation
Leukaemia & Blood Cancer New Zealand



Blood cancer - encompassing leukemia, lymphoma, and myeloma - arises from the disrupted development of white blood cells and can affect people of any age. Many different types of genetic alterations in blood cells cause a great variety of blood cancers and it is estimated that over 10,000 people in New Zealand are living with such diseases.

The mission of our research unit is to identify and understand genetic changes in the patient’s blood cells that are responsible for the cancer. Several new technologies, including next-generation DNA sequencing (NGS), have only become available to us in the last couple of years. With the help of these innovative techniques, we are able to precisely identify the genetic changes in the patient’s blood cancer cells. These genetic changes can then be introduced into cells in culture and small laboratory animals to help us understand how these genetic alteration cause malignant transformation and blood cancer. Based on the insights we gain from studying the genetic changes, we hope to develop innovative treatment strategies and ultimately improve the quality of life for blood cancer patients.

One very important insight that has already emerged in the last few years is that even though the blood cancer cells from two different patients might look alike under the microscope, they are most of the time quite different at the genetic level. With other words, just as all human beings look different and are distinct individuals all the blood cancers are “individuals” as well. It will be a great challenge and also a great opportunity to identify the individual genetic changes of the blood cancers of every patient and then to use the best treatment strategies for every individual patient. It is also very important to bear in mind that we now know that not only one but several genetic changes (we estimate about 3 to 8 in acute myeloid leukaemia) are required to work together to convert a normal cell into a cancer cell.

Understanding Individual Leukaemias in Patients

We will use NGS approaches (whole exome, transcriptome, gene panel and whole genome sequencing) to identify all the genetic changes (if possible) in the leukaemia cells from patients at the Auckland City Hospital. This information will not only help us to better understand the individual leukaemia but also to develop so-called Minimal Residual Disease (MRD) assays specific for the patient’s leukaemia. The MRD assay will enable us to track the number of cancer cells in the patient during and after treatment and thus allow us to monitor the effectiveness of the treatment and maybe sound an early warning bell when the cancer is about to come back. We will join forces with the physicians at Auckland City Hospital to provide a more effective and personalized anti-cancer treatment for our patients.

Mouse and Zebrafish Models to Understand Human Leukaemia

We have developed several mouse models that develop leukaemia because they have genetic alterations that were found in human leukemias. These mice are very important because they allow us to study blood cancer development starting from the introduction of the very first genetic event untill the outbreak of the leukaemia. Identifying pre-malignant changes in the blood cells of these animals helps us understand what exactly is happening in the course of disease development. By knowing what has gone wrong, we can identify possible molecular structures that can be used as anti-cancer drug targets. We will follow this strategy with newly identified genetic changes in the future, learning more about the huge number of genetic alterations that cause blood cancer and related diseases in humans.

Our department has the largest zebrafish facilities for biomedical research in New Zealand. The comprehensive knowledge acquired over many years of genetically engineering zebrafish helps us to model blood cancer in these animals. While mice are more closely related to humans than zebrafish, the rapid life cycle and comparably easy handling of large numbers of zebrafish allow for the screening of large numbers of candidate drugs.

Identifying new anti-leukemic drugs

The University of Auckland and especially the Auckland Cancer Society Research Centre have a long-standing history in medicinal chemistry having developed a number of anti-cancer drug candidates. We plan to screen newly developed drugs for their anti-cancer properties in our leukaemia models. This might help us to identify completely novel therapeutic strategies for the treatment of blood cancer. Furthermore, by screening drugs that are in use for humans for different indications, we can identify drugs with anti-leukaemic properties that are already approved for clinical use.

Relevant Publications

1. Greif PA, Eck SH, Konstandin NP, Benet-Pagès A, Ksienzyk B, Dufour A, Vetter AT, Popp HD, Lorenz-Depiereux B, Meitinger T, Bohlander SK, Strom TM. Identification of recurring tumor-specific somatic mutations in acute myeloid leukemia by transcriptome sequencing. Leukemia. 2011;25:821-827.

2. Kakadia PM, Tizazu B, Mellert G, Harbott J, Röttgers S, Quentmeier H, Spiekermann K, Bohlander SK. A novel ABL1 fusion to the SH2 containing inositol phosphatase-1 (SHIP1) in acute lymphoblastic leukemia (ALL). Leukemia. 2011;25:1645-1649.

3. Greif PA, Dufour A, Konstandin NP, Ksienzyk B, Zellmeier E, Tizazu B, Sturm J, Benthaus T, Herold T, Yaghmaie M, Dörge P, Hopfner KP, Hauser A, Graf A, Krebs S, Blum H, Kakadia PM, Schneider S, Hoster E, Schneider F, Stanulla M, Braess J, Sauerland MC, Berdel WE, Büchner T, Woermann BJ, Hiddemann W, Spiekermann K*, Bohlander SK*. GATA2 zinc finger 1 mutations associated with biallelic CEBPA mutations define a unique genetic entity of acute myeloid leukemia. Blood. 2012;120:395-403.

4. Mulaw MA, Krause AJ, Deshpande AJ, Krause LF, Rouhi A, La Starza R, Borkhardt A, Buske C, Mecucci C, Ludwig WD, Lottaz C, Bohlander SK. CALM/AF10-positive leukemias show upregulation of genes involved in chromatin assembly and DNA repair processes and of genes adjacent to the breakpoint at 10p12. Leukemia. 2012;26:1012-1019.

5. Dufour A, Palermo G, Zellmeier E, Mellert G, Duchateau-Nguyen G, Schneider S, Benthaus T, Kakadia PM, Spiekermann K, Hiddemann W, Braess J, Truong S, Patten N, Wu L, Lohmann S, Dornan D, Guhathakurta D, Yeh RF, Salogub G, Solal-Celigny P, Dmoszynska A, Robak T, Montillo M, Catalano J, Geisler CH, Weisser M*, Bohlander SK*. Inactivation of TP53 correlates with disease progression and low miR-34a expression in previously treated chronic lymphocytic leukemia patients. Blood. 2013;121:3650-3657.

6. Opatz S, Polzer H, Herold T, Konstandin NP, Ksienzyk B, Zellmeier E, Vosberg S, Graf A, Krebs S, Blum H, Hopfner KP, Kakadia PM, Schneider S, Dufour A, Braess J, Sauerland MC, Berdel WE, Büchner T, Woermann BJ, Hiddemann W, Spiekermann K, Bohlander SK, Greif PA. Exome sequencing identifies recurring FLT3 N676K mutations in core-binding factor leukemia. Blood. 2013;122:1761-1769.

7. Bohlander SK. ABCs of genomics. Hematology Am Soc Hematol Educ Program. 2013;2013:316-323.

8. Li Z, Herold T, He C, Valk PJ, Chen P, Jurinovic V, Mansmann U, Radmacher MD, Maharry KS, Sun M, Yang X, Huang H, Jiang X, Sauerland MC, Büchner T, Hiddemann W, Elkahloun A, Neilly MB, Zhang Y, Larson RA, Le Beau MM, Caligiuri MA, Döhner K, Bullinger L, Liu PP, Delwel R, Marcucci G, Lowenberg B, Bloomfield CD, Rowley JD, Bohlander SK*, Chen J*. Identification of a 24-Gene Prognostic Signature That Improves the European LeukemiaNet Risk Classification of Acute Myeloid Leukemia: An International Collaborative Study. J Clin Oncol. 2013;31:1172-1181.

* denotes joint senior and corresponding authors.