The Cambridge Blood and Stem Cell Biobank (CBSB) is a tissue bank for samples from patients with haematological malignancies and normal individuals, including cord blood. We are also the repository for the UK Myeloproliferative Disorders (MPD) sample bank, and several clinical trials for this group of disorders. Since our foundation in 2009, most of our work has involved recruiting and collecting samples from patients both locally and nationally, in close collaboration with clinical and research staff. Our team consists of a core sample processing and quality monitoring laboratory, and research midwives and nurses liaising with clinical teams locally to actively recruit new and actively follow up existing patients on the study.
The bank has collected over 15,000 blood and bone marrow-derived samples to date from patients with haematological malignancies and approximately 2600 normal individuals, all curated in a bespoke database designed to facilitate research activities. Existing samples and prospective collections are available to researchers working on ethically approved studies in malignant blood disorders and normal blood development, and 4800 samples have been transferred to researchers both in the UK and internationally. The laboratory and clinical teams are supported by the Cambridge NIHR Biomedical Research Centre, the Cambridge Experimental Cancer Medicine Centre, Wellcome Trust-MRC Stem Cell Institute and Bloodwise.
The CBSB is based in the NHS Blood and Transplant Cambridge Centre on the Cambridge Biomedical Campus.
For further information contact the biobank’s lead scientist and study coordinator: Dr Joanna Baxter
Cambridge Blood and Stem Cell Biobank
NHSBT Cambridge Centre
Tel: 01223 588048
Follow our Twitter feed: https://twitter.com/CBSB_Cambridge.
Selected publications supported by the CBSB:
Wagner M, et al. Integration of innate into adaptive immune responses in ZAP-70-positive chronic lymphocytic leukemia. Blood 2016; 127(4), 436-448. PMID: 26508782 (2016).
McKerrell T, et al. Development and validation of a comprehensive genomic diagnostic tool for myeloid malignancies. Blood 2016; 128(1):e1-9. PMID: 27121471 (2016).
McKerrell T, et al. Leukemia-associated somatic mutations drive distinct patterns of age-related clonal hemopoiesis. Cell Reports 2015; 10;8;1239-45. PMID: 25732814 (2015).
Ortmann CA et al. Effect of mutation order on myeloproliferative neoplasms. The New England Journal of Medicine 2015; 372;7;601-12. PMID: 25671252 (2015).
Nangalia J, et al. DNMT3A mutations occur early or late in patients with myeloproliferative neoplasms and mutation order influences phenotype. Haematologica 2015 Nov; 100(11):e438-42 (2015).
Tapper W, et al. Genetic variation at MECOM, TERT, JAK2 and HBS1L-MYB predisposes to myeloproliferative neoplasms. Nat Commun 2015 Apr 7;6:6691. PMID: 25849990 (2015).
Girardot M, et al. Persistent STAT5 activation in myeloid neoplasms recruits p53 into gene regulation. Oncogene 2015 Mar 5;34(10):1323-32. PMID:24681953 (2015).
Godfrey AL, et al. Nongenetic stochastic expansion of JAK2V617F-homozygous subclones in polycythemia vera? Blood 2014 Nov 20;124(22):3332-4. PMID:25414437 (2014).
Nangalia J, et al. Somatic CALR Mutations in Myeloproliferative Neoplasms with Nonmutated JAK2. The New England Journal of Medicine 2013; 369:2391-2405 doi:10.1056/NEJMoa1312542 (2013).
Papaemmanuil E, et al. Clinical and biological implications of driver mutations in myelodysplastic syndromes. Blood 122, 3616-3627, doi:10.1182/blood-2013-08-518886 (2013).
Bashford-Rogers RJ, et al. Network properties derived from deep sequencing of human B-cell receptor repertoires delineate B-cell populations. Genome Research 23, 1874-1884, doi:10.1101/gr.154815.113 (2013).
Conte N, et al. Detailed molecular characterisation of acute myeloid leukaemia with a normal karyotype using targeted DNA capture. Leukemia 27, 1820-1825, doi:10.1038/leu.2013.117 (2013).
Aziz A, et al. Cooperativity of imprinted genes inactivated by acquired chromosome 20q deletions. The Journal of Clinical Investigation 123, 2169-2182, doi:10.1172/JCI66113 (2013).
Godfrey AL, et al. JAK2V617F homozygosity arises commonly and recurrently in PV and ET, but PV is characterized by expansion of a dominant homozygous subclone. Blood 120, 2704-2707, doi:10.1182/blood-2012-05-431791 (2012).
Papaemmanuil E, et al. Somatic SF3B1 mutation in myelodysplasia with ring sideroblasts. The New England Journal of Medicine 365, 1384-1395, doi:10.1056/NEJMoa1103283 (2011).
Anand S, et al. Effects of the JAK2 mutation on the hematopoietic stem and progenitor compartment in human myeloproliferative neoplasms. Blood 118, 177-181, doi:10.1182/blood-2010-12-327593 (2011).
Anand S, et al. Increased basal intracellular signaling patterns do not correlate with JAK2 genotype in human myeloproliferative neoplasms. Blood 118, 1610-1621, doi:10.1182/blood-2011-02-335042 (2011).
Chen E, et al. Distinct clinical phenotypes associated with JAK2V617F reflect differential STAT1 signaling. Cancer Cell 18, 524-535, doi:10.1016/j.ccr.2010.10.013 (2010).