How To Donate

Join The Fight Against Blood Cancers!

Donate to the Blood Cancer Research Fund

The BCRF continues to make numerous contributions to blood cancer research and cancer in general:

    • Discovery of the how Zap-70, an intracellular protein, that can be used as a useful prognostic factor in determining the aggressiveness of CLL.
    • The first laboratory to understand the microenvironment of leukemic cells and how the “nurse-like” cells support them.
    • Leadership of the national consortium of 7 prestigious universities studying the causes and treatment of CLL. Member scientists are among the most prominent investigators in the field.
    • Conducted the first-in-human gene therapy trials
    • Intra-Nodal Gene therapy trials (expanding to multi-site injections)
    • Key member of the researchers involved in familial cancer research
    • Principal investigators of a new breakthrough research effort using nanotechnology in the early diagnosis and treatment of early stage cancers.

Donations to Blood Cancer Research Fund:

There are three options for donating to the Blood Cancer Research Fund:

  1. Make a secure on-line donation by clicking here
  2. For using regular mail you can download and print the the Download the BCRF Brochure
  3. Request a brochure by contacting the BCRF administrator
  4. Gifts should be mailed to:

UC San Diego,  Moores Cancer Center
Office of Philanthropy
ATTN: Blood Cancer Research Fund (F-3133)
9500 Gilman Drive, MC 0853
La Jolla, CA 92093-0853

Please make check payable to UC San Diego Foundation, designated for Blood Cancer Research Fund (F-3133) for Dr. Thomas Kipps.  UC San Diego Foundation Tax ID is 95-2872494

Recent Posts

Wnt5a induces ROR1 to associate with 14-3-3ζ for enhanced chemotaxis and proliferation of chronic lymphocytic leukemia cells.


Wnt5a can activate Rho GTPases in chronic lymphocytic leukemia cells by inducing the recruitment of ARHGEF2 to ROR1. Mass spectrometry on immune-precipitates of Wnt5a-activated ROR1 identified 14-3-3ζ, which was confirmed by co-immunoprecipitation. The capacity of Wnt5a to induce ROR1 to complex with 14-3-3ζ could be blocked in CLL cells treated with cirmtuzumab, a humanized mAb targeting ROR1. Silencing 14-3-3ζ via siRNA impaired the capacity of Wnt5a to: (1) induce recruitment of ARHGEF2 to ROR1, (2) enhance in vitro exchange activity of ARHGEF2, and (3) induce activation of RhoA and Rac1 in CLL cells. Furthermore, CRISPR/Cas9 deletion of 14-3-3ζ in ROR1-negative CLL cell-line MEC1, and in MEC1 cells transfected to express ROR1 (MEC1-ROR1), demonstrated that 14-3-3ζ was necessary for the growth/engraftment advantage of MEC1-ROR1 over MEC1 cells. We identified a binding motif (RSPS857SAS) for 14-3-3ζ on ROR1. Site-directed mutagenesis of ROR1 demonstrated that serine-857 was required for the recruitment of 14-3-3ζ and ARHGEF2 to ROR1, and activation of RhoA and Rac1. Collectively, this study reveals that 14-3-3ζ plays a critical role in Wnt5a/ROR1 signaling leading to enhanced CLL migration and proliferation.Leukemia accepted article preview online, 03 May 2017. doi:10.1038/leu.2017.132.

  1. Wnt5a induces ROR1 to complex with HS1 to enhance migration of chronic lymphocytic leukemia cells. Leave a reply
  2. The long noncoding RNA, treRNA, decreases DNA damage and is associated with poor response to chemotherapy in chronic lymphocytic leukemia. Leave a reply
  3. Use of anticoagulants and antiplatelet in patients with chronic lymphocytic leukaemia treated with single-agent ibrutinib. Leave a reply
  4. Venetoclax and obinutuzumab in chronic lymphocytic leukemia. Leave a reply
  5. Chronic lymphocytic leukaemia. Leave a reply
  6. Leukemia-cell proliferation and disease progression in patients with early stage chronic lymphocytic leukemia. Leave a reply
  7. Chronic lymphocytic leukaemia. Leave a reply
  8. Phase I First-in-Human Study of Venetoclax in Patients With Relapsed or Refractory Non-Hodgkin Lymphoma. Leave a reply
  9. Venetoclax plus rituximab in relapsed or refractory chronic lymphocytic leukaemia: a phase 1b study. Leave a reply