Search

Your search keyword '"Hattori, Takamitsu"' showing total 19 results
Start Over Author "Hattori, Takamitsu" Publication Year Range Last 3 years
19 results on '"Hattori, Takamitsu"'

2. The expression profile and tumorigenic mechanisms of CD97 (ADGRE5) in glioblastoma render it a targetable vulnerability

Author

Ravn-Boess, Niklas, Roy, Nainita, Hattori, Takamitsu, Bready, Devin, Donaldson, Hayley, Lawson, Christopher, Lapierre, Cathryn, Korman, Aryeh, Rodrick, Tori, Liu, Enze, Frenster, Joshua D., Stephan, Gabriele, Wilcox, Jordan, Corrado, Alexis D., Cai, Julia, Ronnen, Rebecca, Wang, Shuai, Haddock, Sara, Sabio Ortiz, Jonathan, Mishkit, Orin, Khodadadi-Jamayran, Alireza, Tsirigos, Aris, Fenyö, David, Zagzag, David, Drube, Julia, Hoffmann, Carsten, Perna, Fabiana, Jones, Drew R., Possemato, Richard, Koide, Akiko, Koide, Shohei, Park, Christopher Y., and Placantonakis, Dimitris G.

Published
2023
Full Text
View/download PDF

4. Antibody isotype diversity against SARS-CoV-2 is associated with differential serum neutralization capacities

Author

Noval, Maria G., Kaczmarek, Maria E., Koide, Akiko, Rodriguez-Rodriguez, Bruno A., Louie, Ping, Tada, Takuya, Hattori, Takamitsu, Panchenko, Tatyana, Romero, Larizbeth A., Teng, Kai Wen, Bazley, Andrew, de Vries, Maren, Samanovic, Marie I., Weiser, Jeffrey N., Aifantis, Ioannis, Cangiarella, Joan, Mulligan, Mark J., Desvignes, Ludovic, Dittmann, Meike, Landau, Nathaniel R., Aguero-Rosenfeld, Maria, Koide, Shohei, and Stapleford, Kenneth A.

Published
2021
Full Text
View/download PDF

6. The expression profile and tumorigenic mechanisms of CD97 (ADGRE5) in glioblastoma render it a targetable vulnerability

Author

Ravn-Boess, Niklas, primary, Roy, Nainita, additional, Hattori, Takamitsu, additional, Bready, Devin, additional, Donaldson, Hayley, additional, Lawson, Christopher, additional, Lapierre, Cathryn, additional, Korman, Aryeh, additional, Rodrick, Tori, additional, Liu, Enze, additional, Frenster, Joshua D., additional, Stephan, Gabriele, additional, Wilcox, Jordan, additional, Corrado, Alexis D., additional, Cai, Julia, additional, Ronnen, Rebecca, additional, Wang, Shuai, additional, Haddock, Sara, additional, Sabio Ortiz, Jonathan, additional, Mishkit, Orin, additional, Khodadadi-Jamayran, Alireza, additional, Tsirigos, Aris, additional, Fenyo, David, additional, Zagzag, David, additional, Perna, Fabiana, additional, Jones, Drew R., additional, Possemato, Richard, additional, Koide, Akiko, additional, Koide, Shohei, additional, Park, Christopher Y., additional, and Placantonakis, Dimitris G., additional

Published
2023
Full Text
View/download PDF

7. Exploring switch II pocket conformation of KRAS(G12D) with mutant-selective monobody inhibitors

Author

Akkapeddi, Padma, primary, Hattori, Takamitsu, additional, Khan, Imran, additional, Glasser, Eliezra, additional, Koide, Akiko, additional, Ketavarapu, Gayatri, additional, Whaby, Michael, additional, Zuberi, Mariyam, additional, Teng, Kai Wen, additional, Lefler, Julia, additional, Maso, Lorenzo, additional, Bang, Injin, additional, Ostrowski, Michael C., additional, O’Bryan, John P., additional, and Koide, Shohei, additional

Published
2023
Full Text
View/download PDF

9. Abstract B013: Exploring the switch II pocket of KRAS(G12D) with mutant-selective monobody inhibitors

Author

Hattori, Takamitsu, primary, Akkapeddi, Padma, additional, Khan, Imran, additional, Koide, Akiko, additional, Glasser, Eliezra, additional, Ketavarapu, Gayatri, additional, Whaby, Michael, additional, Zuberi, Mariyam, additional, Teng, Kai Wen, additional, Lefler, Julia, additional, Maso, Lorenzo, additional, Bang, Injin, additional, Ostrowski, Michael C., additional, O’Bryan, John P., additional, and Koide, Shohei, additional

Published
2023
Full Text
View/download PDF

10. In vivo metabolomics identifies CD38 as an emergent vulnerability in LKB1-mutant lung cancer

Author

Deng, Jiehui, primary, Peng, David H, additional, Fenyo, David, additional, Hao, Yuan, additional, Lopez, Alfonso, additional, Levin, Daniel, additional, Meynardie, Mary, additional, Quinteros, Mari, additional, Ranieri, Michela, additional, Sahu, Soumyadip, additional, Lau, Sally, additional, Shum, Elaine, additional, Velcheti, Vamsidhar, additional, Punekar, Salman R, additional, Rekhtman, Natasha, additional, Dowling, Catriona M, additional, Weerasekara, Vajira, additional, Xue, Yun, additional, Ji, hongbin, additional, Siu, Yik, additional, Johns, Drew, additional, Hata, Aaron, additional, Shimamura, Takeshi, additional, Poirier, John, additional, Rudin, Charles M, additional, Hattori, Takamitsu, additional, Koide, Shohei, additional, Papagiannakopoulos, Thales, additional, Neel, Benjamin, additional, Bardeesy, Nabeel, additional, and Wong, Kwok-Kin, additional

Published
2023
Full Text
View/download PDF

18. In vivo metabolomics identifies CD38 as an emergent vulnerability in LKB1 -mutant lung cancer.

Author

Deng J, Peng DH, Fenyo D, Yuan H, Lopez A, Levin DS, Meynardie M, Quinteros M, Ranieri M, Sahu S, Lau SCM, Shum E, Velcheti V, Punekar SR, Rekhtman N, Dowling CM, Weerasekara V, Xue Y, Ji H, Siu Y, Jones D, Hata AN, Shimamura T, Poirier JT, Rudin CM, Hattori T, Koide S, Papagiannakopoulos T, Neel BG, Bardeesy N, and Wong KK

Abstract

LKB1/STK11 is a serine/threonine kinase that plays a major role in controlling cell metabolism, resulting in potential therapeutic vulnerabilities in LKB1-mutant cancers. Here, we identify the NAD + degrading ectoenzyme, CD38, as a new target in LKB1-mutant NSCLC. Metabolic profiling of genetically engineered mouse models (GEMMs) revealed that LKB1 mutant lung cancers have a striking increase in ADP-ribose, a breakdown product of the critical redox co-factor, NAD + . Surprisingly, compared with other genetic subsets, murine and human LKB1-mutant NSCLC show marked overexpression of the NAD+-catabolizing ectoenzyme, CD38 on the surface of tumor cells. Loss of LKB1 or inactivation of Salt-Inducible Kinases (SIKs)-key downstream effectors of LKB1- induces CD38 transcription induction via a CREB binding site in the CD38 promoter. Treatment with the FDA-approved anti-CD38 antibody, daratumumab, inhibited growth of LKB1-mutant NSCLC xenografts. Together, these results reveal CD38 as a promising therapeutic target in patients with LKB1 mutant lung cancer., Significance: Loss-of-function mutations in the LKB1 tumor suppressor of lung adenocarcinoma patients and are associated with resistance to current treatments. Our study identified CD38 as a potential therapeutic target that is highly overexpressed in this specific subtype of cancer, associated with a shift in NAD homeostasis.

Published
2023
Full Text
View/download PDF

19. Creating MHC-Restricted Neoantigens with Covalent Inhibitors That Can Be Targeted by Immune Therapy.

Author

Hattori T, Maso L, Araki KY, Koide A, Hayman J, Akkapeddi P, Bang I, Neel BG, and Koide S

Subjects
Humans, Histocompatibility Antigens Class I, Antigens, Neoplasm, Peptides pharmacology, Histocompatibility Antigens, Haptens, Major Histocompatibility Complex, Lung Neoplasms pathology
Abstract

Intracellular oncoproteins can be inhibited with targeted therapy, but responses are not durable. Immune therapies can be curative, but most oncogene-driven tumors are unresponsive to these agents. Fragments of intracellular oncoproteins can act as neoantigens presented by the major histocompatibility complex (MHC), but recognizing minimal differences between oncoproteins and their normal counterparts is challenging. We have established a platform technology that exploits hapten-peptide conjugates generated by covalent inhibitors to create distinct neoantigens that selectively mark cancer cells. Using the FDA-approved covalent inhibitors sotorasib and osimertinib, we developed "HapImmune" antibodies that bind to drug-peptide conjugate/MHC complexes but not to the free drugs. A HapImmune-based bispecific T-cell engager selectively and potently kills sotorasib-resistant lung cancer cells upon sotorasib treatment. Notably, it is effective against KRASG12C-mutant cells with different HLA supertypes, HLA-A*02 and A*03/11, suggesting loosening of MHC restriction. Our strategy creates targetable neoantigens by design, unifying targeted and immune therapies., Significance: Targeted therapies against oncoproteins often have dramatic initial efficacy but lack durability. Immunotherapies can be curative, yet most tumors fail to respond. We developed a generalizable technology platform that exploits hapten-peptides generated by covalent inhibitors as neoantigens presented on MHC to enable engineered antibodies to selectively kill drug-resistant cancer cells. See related commentary by Cox et al., p. 19. This article is highlighted in the In This Issue feature, p. 1., (©2022 The Authors; Published by the American Association for Cancer Research.)

Published
2023
Full Text
View/download PDF

Catalog

Books, media, physical & digital resources
See catalog results