S
Saad S. Kenderian
Researcher at Mayo Clinic
Publications - 176
Citations - 4704
Saad S. Kenderian is an academic researcher from Mayo Clinic. The author has contributed to research in topics: Chimeric antigen receptor & Medicine. The author has an hindex of 25, co-authored 128 publications receiving 2976 citations. Previous affiliations of Saad S. Kenderian include Murphy Oil & University of Pennsylvania.
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Journal ArticleDOI
Human chimeric antigen receptor macrophages for cancer immunotherapy.
Michael Klichinsky,Marco Ruella,Olga Shestova,Xueqing Maggie Lu,Andrew Best,Martha Zeeman,Maggie Schmierer,Konrad Gabrusiewicz,Nicholas R. Anderson,Nicholas E. Petty,Katherine D. Cummins,Feng Shen,Xinhe Shan,Kimberly Veliz,Kristin Blouch,Yumi Yashiro-Ohtani,Saad S. Kenderian,Saad S. Kenderian,Miriam Y. Kim,Miriam Y. Kim,Roddy S. O’Connor,Stephen R. Wallace,Miroslaw Kozlowski,Dylan M. Marchione,Maksim Shestov,Benjamin A. Garcia,Carl H. June,Saar Gill +27 more
TL;DR: It is found that a chimeric adenoviral vector overcame the inherent resistance of primary human macrophages to genetic manipulation and imparted a sustained pro-inflammatory (M1) phenotype in humanized mice.
Journal ArticleDOI
Dual CD19 and CD123 targeting prevents antigen-loss relapses after CD19-directed immunotherapies
Marco Ruella,David M. Barrett,Saad S. Kenderian,Olga Shestova,Ted J. Hofmann,Jessica Perazzelli,Michael Klichinsky,Vania Aikawa,Farzana Nazimuddin,Miroslaw Kozlowski,John Scholler,Simon F. Lacey,J. Joseph Melenhorst,Jennifer J.D. Morrissette,David A. Christian,Christopher A. Hunter,Michael Kalos,Michael Kalos,David L. Porter,Carl H. June,Stephan A. Grupp,Saar Gill +21 more
TL;DR: It is found that in primary patient samples, the IL-3 receptor α chain CD123 was highly expressed on leukemia-initiating cells and CD19-negative blasts in bulk B-ALL at baseline and at relapse after CART19 administration, indicating that targeting CD19 and CD123 on leukemic blasts represents an effective strategy for treating and preventing antigen-loss relapses occurring after CD19
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GM-CSF inhibition reduces cytokine release syndrome and neuroinflammation but enhances CAR-T cell function in xenografts
Rosalie M. Sterner,Reona Sakemura,Michelle J. Cox,Nan Yang,Roman H. Khadka,Cynthia L. Forsman,Michael J. Hansen,Fang Jin,Katayoun Ayasoufi,Mehrdad Hefazi,Kendall J. Schick,Denise K. Walters,Omar H. Ahmed,Dale Chappell,Tarek Sahmoud,Cameron Durrant,Wendy K. Nevala,Mrinal M. Patnaik,Larry R. Pease,Karen E. Hedin,Neil E. Kay,Aaron J. Johnson,Saad S. Kenderian +22 more
TL;DR: It is shown that GM-CSF neutralization with lenzilumab does not inhibit CART19 cell function in vitro or in vivo, and a novel approach to abrogate NI and CRS through GM- CSF neutralized, which may potentially enhance CAR-T cell function.
Journal ArticleDOI
CD33-specific chimeric antigen receptor T cells exhibit potent preclinical activity against human acute myeloid leukemia
Saad S. Kenderian,Marco Ruella,Olga Shestova,Michael Klichinsky,Vania Aikawa,Jennifer J.D. Morrissette,John Scholler,De-Gang Song,David L. Porter,Michael C Carroll,Carl H. June,Sheila R Gill +11 more
TL;DR: Preclinical studies show potent activity of CART33 and indicate that transient expression of anti-CD33 CAR by RNA modification could be used in patients to avoid long-term myelosuppression.
Journal ArticleDOI
Genetic Inactivation of CD33 in Hematopoietic Stem Cells to Enable CAR T Cell Immunotherapy for Acute Myeloid Leukemia
Miriam Y. Kim,Kyung-Rok Yu,Saad S. Kenderian,Marco Ruella,Shirley Chen,Tae Hoon Shin,Aisha A. AlJanahi,Aisha A. AlJanahi,Daniel M. Schreeder,Michael Klichinsky,Olga Shestova,Miroslaw Kozlowski,Katherine D. Cummins,Xinhe Shan,Maksim Shestov,Adam Bagg,Jennifer J.D. Morrissette,Palak Sekhri,Cicera R. Lazzarotto,Katherine R. Calvo,Douglas B. Kuhns,Robert E. Donahue,Gregory K. Behbehani,Shengdar Q. Tsai,Cynthia E. Dunbar,Saar Gill +25 more
TL;DR: CD33-deficient cells were impervious to CD33-targeting CAR T cells, allowing for efficient elimination of leukemia without myelotoxicity, and illuminate a novel approach to antigen-specific immunotherapy by genetically engineering the host to avoid on-target, off-tumor toxicity.