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Three days later that mf dead1/7/2024 Romee R, Cooley S, Berrien-Elliott MM, Westervelt P, Verneris MR, Wagner JE, et al. Successful adoptive transfer and in vivo expansion of human haploidentical NK cells in patients with cancer. Miller JS, Soignier Y, Panoskaltsis-mortari A, Mcnearney SA, Yun GH, Fautsch SK, et al. Perforin-mediated target-cell death and immune homeostasis. Vivier E, Tomasello E, Baratin M, Walzer T, Ugolini S. Development of a chimeric antigen receptor targeting c-type lectin-like molecule-1 for human acute myeloid leukemia. Laborda E, Mazagova M, Shao S, Wang X, Quirino H, Woods AK, et al. CLT030, a leukemic stem cell-targeting CLL1 antibody-drug conjugate for treatment of acute myeloid leukemia. Jiang YP, Liu BY, Zheng Q, Panuganti S, Chen R, Zhu J, et al. MCLA-117, a CLEC12AxCD3 bispecific antibody targeting a leukaemic stem cell antigen, induces T cell-mediated AML blast lysis. Van Loo PF, Hangalapura BN, Thordardottir S, Gibbins JD, Veninga H, Hendriks LJA, et al. Prognostic and therapeutic role of CLEC12A in acute myeloid leukemia. Expression of the hMICL in acute myeloid leukemia-a highly reliable disease marker at diagnosis and during follow-up. Larsen HØ, Roug AS, Just T, Brown GD, Hokland P. The novel AML stem cell-associated antigen CLL-1 aids in discrimination between normal and leukemic stem cells. Van Rhenen A, Van Dongen GAMS, Rombouts EJ, Feller N, Moshaver B, Walsum MS, et al. Phase I studies of AVE9633, an anti-CD33 antibody-maytansinoid conjugate, in adult patients with relapsed/refractory acute myeloid leukemia. Lapusan S, Vidriales MB, Thomas X, de Botton S, Vekhoff A, Tang R, et al. Phase III randomized multicenter study of a humanized anti-CD33 monoclonal antibody, lintuzumab, in combination with chemotherapy, versus chemotherapy alone in patients with refractory or first-relapsed acute myeloid leukemia. 2011 17:6417–27.įeldman EJ, Brandwein J, Stone R, Kalaycio M, Moore J, O’Connor J, et al. Antibody-drug conjugates of calicheamicin derivative: gemtuzumab ozogamicin and inotuzumab ozogamicin. Addition of gemtuzumab ozogamicin to induction chemotherapy in adult patients with acute myeloid leukaemia: a meta-analysis of individual patient data from randomised controlled trials. Hills RK, Castaigne S, Appelbaum FR, Delaunay J, Petersdorf S, Othus M, et al. A phase 1 trial of vadastuximab talirine as monotherapy in patients with CD33-positive acute myeloid leukemia. Stein EM, Walter RB, Erba HP, Fathi AT, Advani AS, Lancet JE, et al. Gemtuzumab ozogamicin in combination with vorinostat and azacitidine in older patients with relapsed or refractory acute myeloid leukemia: a phase I/II study. Walter RB, Medeiros BC, Gardner KM, Orlowski KF, Gallegos L, Scott BL, et al. Current Advances in Immunotherapy for Acute Leukemia: An Overview of Antibody, Chimeric Antigen Receptor, Immune Checkpoint, and Natural Killer. Targeting acute myeloid leukemia stem cells: a review and principles for the development of clinical trials. Pollyea DA, Gutman JA, Gore L, Smith CA, Jordan CT. A niche-like culture system allowing the maintenance of primary human acute myeloid leukemia-initiating cells: a new tool to decipher their chemoresistance and self-renewal mechanisms. Griessinger E, Anjos-Afonso F, Pizzitola I, Rouault-Pierre K, Vargaftig J, Taussig D, et al. Recent drug approvals for acute myeloid leukemia. Emerging therapies for acute myeloid leukemia. Frontline treatment of acute myeloid leukemia in adults. Tamamyan G, Kadia T, Ravandi F, Borthakur G, Cortes J, Jabbour E, et al. These findings highlight the clinical potential of the CLEC12A TriKE for the effective treatment of AML. Additionally, the CLEC12A TriKE was able to reduce tumor burden in preclinical mouse models. The CLEC12A TriKE induced robust NK-cell specific proliferation, enhanced NK-cell activation, and killing of both AML cell lines and primary patient-derived AML blasts in vitro while sparing healthy HSCs. CLEC12A is a myeloid lineage antigen that is highly expressed by AML cells and LSCs, but not expressed by normal hematopoietic stem cells (HSCs), thus minimizing off-target toxicity. To target AML blasts and LSCs using natural killer (NK) cells, we have developed a trispecific killer engager (TriKE TM) molecule containing a humanized anti-CD16 heavy chain camelid single-domain antibody (sdAb) that activates NK cells, an IL-15 molecule that drives NK-cell priming, expansion and survival, and a single-chain variable fragment (scFv) against human CLEC12A (CLEC12A TriKE). Disease relapse is facilitated by leukemic stem cells (LSCs) that are resistant to standard chemotherapy and promote tumor growth. The low 5-year survival rate for patients with acute myeloid leukemia (AML), primarily caused due to disease relapse, emphasizes the need for better therapeutic strategies.
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