Distinct invitro sensitivity of p53-mutated and ATM-mutated chronic lymphocytic leukemia cells to ofatumumab and rituximab

Experimental Hematology

Volumn 42, Issue 10, 2014, Pages 867-874.e1

  Sebejova, Ludmila ^a,b   Borsky, Marek ^b   Jaskova, Zuzana ^a,b   Potesil, David ^a   Navrkalova, Veronika ^a,b   Malcikova, Jitka ^a,b   Sramek, Martin ^b   Doubek, Michael ^a,b   Loja, Tomas ^b   Pospisilova, Sarka ^a,b   Mayer, Jiri ^a,b   Trbusek, Martin ^a,b  

^a MASARYK UNIVERSITY   (Czech Republic)

^b UNIVERSITY HOSPITAL BRNO   (Czech Republic)

Author keywords

[No Author keywords available]

Indexed keywords

ATM PROTEIN; CD20 ANTIBODY; CD59 ANTIGEN; DECAY ACCELERATING FACTOR; MONOCLONAL ANTIBODY; OFATUMUMAB; PROTEIN P53; RITUXIMAB; ATM PROTEIN, HUMAN; CD20 ANTIGEN; CD59 PROTEIN, HUMAN; COMPLEMENT; CULTURE MEDIUM; TP53 PROTEIN, HUMAN; TUMOR ANTIGEN; TUMOR PROTEIN;

ADULT; AGED; ANTIBODY RESPONSE; ANTINEOPLASTIC ACTIVITY; ARTICLE; ATM GENE; CANCER CELL DESTRUCTION; CHRONIC LYMPHATIC LEUKEMIA; COMPLEMENT SYSTEM; CONCENTRATION RESPONSE; CONTROLLED STUDY; DRUG CYTOTOXICITY; DRUG MECHANISM; DRUG SENSITIVITY; FEMALE; GENE INACTIVATION; GENE MUTATION; GENETIC DISORDER; HUMAN; HUMAN CELL; IN VITRO STUDY; LEUKEMIA CELL; MAJOR CLINICAL STUDY; MALE; TUMOR SUPPRESSOR GENE; WILD TYPE; COMPARATIVE STUDY; CULTURE MEDIUM; DEFICIENCY; DNA REPAIR; DRUG EFFECTS; DRUG RESISTANCE; DRUG SCREENING; GENETICS; IMMUNOLOGY; MIDDLE AGED; PATHOLOGY; PHYSIOLOGY; SERUM; TUMOR CELL CULTURE; VERY ELDERLY;

ADULT; AGED; AGED, 80 AND OVER; ANTIBODIES, MONOCLONAL; ANTIBODIES, MONOCLONAL, MURINE-DERIVED; ANTIGENS, CD20; ANTIGENS, CD55; ANTIGENS, CD59; ANTIGENS, NEOPLASM; ATAXIA TELANGIECTASIA MUTATED PROTEINS; COMPLEMENT SYSTEM PROTEINS; CULTURE MEDIA; DNA REPAIR; DRUG RESISTANCE, NEOPLASM; DRUG SCREENING ASSAYS, ANTITUMOR; FEMALE; GENES, P53; HUMANS; LEUKEMIA, LYMPHOCYTIC, CHRONIC, B-CELL; MALE; MIDDLE AGED; NEOPLASM PROTEINS; SERUM; TUMOR CELLS, CULTURED; TUMOR SUPPRESSOR PROTEIN P53;

EID: 84908375023     PISSN: 0301472X     EISSN: 18732399     Source Type: Journal    
DOI: 10.1016/j.exphem.2014.06.003     Document Type: Article

References (37)

1. Döhner H., Stilgenbauer S., Benner A., et al. Genomic aberrations and survival in chronic lymphocytic leukemia. N Engl J Med 2000, 343:1910-1916.
2. Zenz T., Häbe S., Denzel T., et al. Detailed analysis of p53 pathway defects in fludarabine-refractory chronic lymphocytic leukemia (CLL): dissecting the contribution of 17p deletion, TP53 mutation, p53-p21 dysfunction, and miR34a in a prospective clinical trial. Blood 2009, 114:2589-2597.
3. Pettitt A., Sherrington P., Stewart G., Cawley J., Taylor A., Stankovic T. p53 dysfunction in B-cell chronic lymphocytic leukemia: inactivation of ATM as an alternative to TP53 mutation. Blood 2001, 98:814-822.
4. Gonzalez D., Martinez P., Wade R., et al. Mutational status of the TP53 gene as a predictor of response and survival in patients with chronic lymphocytic leukemia: results from the LRF CLL4 trial. J Clin Oncol 2011, 29:2223-2229.
5. Byrd J., Gribben J., Peterson B., et al. Select high-risk genetic features predict earlier progression following chemoimmunotherapy with fludarabine and rituximab in chronic lymphocytic leukemia: justification for risk-adapted therapy. J Clin Oncol 2006, 24:437-443.
6. Badoux X.C., Keating M.J., Wang X., et al. Fludarabine, cyclophosphamide, and rituximab chemoimmunotherapy is highly effective treatment for relapsed patients with CLL. Blood 2011, 117:3016-3024.
7. Döhner H., Stilgenbauer S., James M.R., et al. 11q deletions identify a new subset of B-cell chronic lymphocytic leukemia characterized by extensive nodal involvement and inferior prognosis. Blood 1997, 89:2516-2522.
8. Guarini A., Marinelli M., Tavolaro S., et al. ATM gene alterations in chronic lymphocytic leukemia patients induce a distinct gene expression profile and predict disease progression. Haematologica 2012, 97:47-55.
9. Hallek M., Fischer K., Fingerle-Rowson G., et al. Addition of rituximab to fludarabine and cyclophosphamide in patients with chronic lymphocytic leukaemia: a randomised, open-label, phase 3 trial. Lancet 2010, 376:1164-1174.
10. Tsimberidou A.M., Tam C., Abruzzo L.V., et al. Chemoimmunotherapy may overcome the adverse prognostic significance of 11q deletion in previously untreated patients with chronic lymphocytic leukemia. Cancer 2009, 115:373-380.
11. Austen B., Skowronska A., Baker C., et al. Mutation status of the residual ATM allele is an important determinant of the cellular response to chemotherapy and survival in patients with chronic lymphocytic leukemia containing an 11q deletion. J Clin Oncol 2007, 25:5448-5457.
12. Navrkalova V., Sebejova L., Zemanova J., et al. ATM mutations uniformly lead to ATM dysfunction in chronic lymphocytic leukemia: application of functional test using doxorubicin. Haematologica 2013, 98:1124-1131.
13. Hupp T.R., Lane D.P., Ball K.L. Strategies for manipulating the p53 pathway in the treatment of human cancer. Biochem J 2000, 1(352 Pt):1-17.
14. Jain P., O'Brien S. Anti-CD20 monoclonal antibodies in chronic lymphocytic leukemia. Expert Opin Biol Ther 2013, 13:169-182.
15. Boross P., Leusen J.H. Mechanisms of action of CD20 antibodies. Am J Cancer Res 2012, 2:676-690.
16. Reff M.E., Carner K., Chambers K.S., et al. Depletion of B cells invivo by a chimeric mouse human monoclonal antibody to CD20. Blood 1994, 83:435-445.
17. Teeling J.L., Mackus W.J., Wiegman L.J., et al. The biological activity of human CD20 monoclonal antibodies is linked to unique epitopes on CD20. J Immunol 2006, 177:362-371.
18. Teeling J.L., French R.R., Cragg M.S., et al. Characterization of new human CD20 monoclonal antibodies with potent cytolytic activity against non-Hodgkin lymphomas. Blood 2004, 104:1793-1800.
19. Wierda W.G., Kipps T.J., Mayer J., et al. Ofatumumab as single-agent CD20 immunotherapy in fludarabine-refractory chronic lymphocytic leukemia. J Clin Oncol 2010, 28:1749-1755.
20. Shanafelt T., Lanasa M.C., Call T.G., et al. Ofatumumab-based chemoimmunotherapy is effective and well tolerated in patients with previously untreated chronic lymphocytic leukemia (CLL). Cancer 2013, 119:3788-3796.
21. Malcikova J., Smardova J., Rocnova L., et al. Monoallelic and biallelic inactivation of TP53 gene in chronic lymphocytic leukemia: selection, impact on survival, and response to DNA damage. Blood 2009, 114:5307-5314.
22. Bologna L., Gotti E., Da Roit F., et al. Ofatumumab is more efficient than rituximab in lysing B chronic lymphocytic leukemia cells in whole blood and in combination with chemotherapy. J Immunol 2013, 190:231-239.
23. Patz M., Isaeva P., Forcob N., et al. Comparison of the invitro effects of the anti-CD20 antibodies rituximab and GA101 on chronic lymphocytic leukaemia cells. Br J Haematol 2011, 152:295-306.
24. Golay J., Lazzari M., Facchinetti V., et al. CD20 levels determine the invitro susceptibility to rituximab and complement of B-cell chronic lymphocytic leukemia: further regulation by CD55 and CD59. Blood 2001, 98:3383-3389.
25. Baig N.A., Taylor R.P., Lindorfer M.A., et al. Induced resistance to ofatumumab-mediated cell clearance mechanisms, including complement-dependent cytotoxicity In: Chronic Lymphocytic Leukemia. J Immunol 2014, 192:1620-1629.
26. Kennedy A.D., Beum P.V., Solga M.D., et al. Rituximab infusion promotes rapid complement depletion and acute CD20 loss in chronic lymphocytic leukemia. J Immunol 2004, 172:3280-3288.
27. Zent C.S., Secreto C.R., LaPlant B.R., et al. Direct and complement dependent cytotoxicity in CLL cells from patients with high-risk early-intermediate stage chronic lymphocytic leukemia (CLL) treated with alemtuzumab and rituximab. Leuk Res 2008, 32:1849-1856.
28. Zenz T., Mertens D., Döhner H., Stilgenbauer S. Importance of genetics in chronic lymphocytic leukemia. Blood Rev 2011, 25:131-137.
29. Gazouli M., Kokotas S., Zoumpourlis V., et al. The complementinhibitor CD59 and the lymphocyte function-associated antigen-3(LFA-3, CD58) genes possess functional binding sites for the p53 tumor suppressor protein. Anticancer Res 2002, 22:4237-4241.
30. Sampaziotis F., Kokotas S., Gorgoulis V.G. P53 possibly upregulates the expression of CD58 (LFA-3) and CD59 (MIRL). Med Hypotheses 2002, 58:136-140.
31. Bartkova J., Horejsí Z., Koed K., et al. DNA damage response as a candidate anti-cancer barrier in early human tumorigenesis. Nature 2005, 434:864-870.
32. Tedder T.F., Engel P. CD20: a regulator of cell-cycle progression of B lymphocytes. Immunol Today 1994, 15:450-454.
33. Gupta D., Crosby M.E., Almasan A., Macklis R.M. Regulation of CD20 expression by radiation-induced changes in intracellular redox status. Free Radic Biol Med 2008, 44:614-623.
34. Gatei M., Shkedy D., Khanna K.K., et al. Ataxia-telangiectasia: chronic activation of damage-responsive functions is reduced by alpha-lipoic acid. Oncogene 2001, 20:289-294.
35. Taylor A., Shang F., Nowell T., Galanty Y., Shiloh Y. Ubiquitination capabilities in response to neocarzinostatin and H(2)O(2) stress in cell lines from patients with ataxia-telangiectasia. Oncogene 2002, 21:4363-4373.
36. Sablina A.A., Budanov A.V., Ilyinskaya G.V., Agapova L.S., Kravchenko J.E., Chumakov P.M. The antioxidant function of the p53 tumor suppressor. Nat Med 2005, 11:1306-1313.
37. Tam C.S., Otero-Palacios J., Abruzzo L.V., et al. Chronic lymphocytic leukaemia CD20 expression is dependent on the genetic subtype: a study of quantitative flow cytometry and fluorescent in-situ hybridization in 510 patients. Br J Haematol 2008, 141:36-40.