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2. Strong Adhesion of Electroless Plated Copper by Optimizing Lamination Temperature of Epoxy Composite Film for Advanced Chip Packaging Substrates.

Author

Luo, Suibin, Yu, Junyi, Ma, Peilin, Gao, Chunbo, Li, Peng, Zhu, Chuanxi, Yang, Yiquan, Xu, Pengpeng, Yang, Jie, Sun, Rong, and Yu, Shuhui

Subjects
ELECTROLESS plating, SUBSTRATES (Materials science), SURFACE roughness, COPPER, INTEGRATED circuits
Abstract

Semi‐additive process (SAP) is a pivotal technique for fabricating integrated circuit (IC) packaging substrates, achieving fine line/space resolution below 20 μm. The adhesion strength between the epoxy composite dielectric layer and electroplated copper is critical for ensuring the long‐term service reliability of high‐performance substrates. Herein, an epoxy composite film suitable for SAP is deposited with copper layer via electroless plating followed by electroplating. The effects of lamination and pre‐curing temperatures in SAP on the butter layer thickness, desmear weight, surface roughness (Ra), and adhesion strength of the plated copper are systematically investigated. The desmear weight decreases with the rising of lamination temperature attributed to the increased butter layer thickness. The lamination temperature is demonstrated to be one of the most influential factors in determining the adhesion strength between the plated copper and the epoxy composite. A high and stable peel strength exceeding 6.0 N cm−1 is achieved under the circumstance of a low Ra of merely 0.95 μm, indicating significant potential for these epoxy composite films in the fabrication of fine‐line and high‐density packaging substrates. [ABSTRACT FROM AUTHOR]

Published
2024
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6. Supplementary Table 1 from Patient-Driven Discovery, Therapeutic Targeting, and Post-Clinical Validation of a Novel AKT1 Fusion–Driven Cancer

Author

Slotkin, Emily K., primary, Diolaiti, Daniel, primary, Shukla, Neerav N., primary, Dela Cruz, Filemon S., primary, Clark, Jennifer J., primary, Gundem, Gunes, primary, Yellapantula, Venkata D., primary, Levine, Max F., primary, You, Daoqi, primary, Ma, Peilin, primary, Pachhal, Sagarika, primary, Ibanez Sanchez, Glorymar, primary, Benayed, Ryma, primary, Jungbluth, Achim A., primary, Smyth, Lillian M., primary, Mauguen, Audrey, primary, Gushterova, Irena, primary, Ding, Hongxu, primary, Spraggon, Lee, primary, Darnell, Robert, primary, Califano, Andrea, primary, Ladanyi, Marc, primary, Papaemmanuil, Elli, primary, Kung, Andrew L., primary, Hyman, David M., primary, and Roberts, Stephen S., primary

Published
2023
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7. Supplementary Data from Patient-Driven Discovery, Therapeutic Targeting, and Post-Clinical Validation of a Novel AKT1 Fusion–Driven Cancer

Author

Slotkin, Emily K., primary, Diolaiti, Daniel, primary, Shukla, Neerav N., primary, Dela Cruz, Filemon S., primary, Clark, Jennifer J., primary, Gundem, Gunes, primary, Yellapantula, Venkata D., primary, Levine, Max F., primary, You, Daoqi, primary, Ma, Peilin, primary, Pachhal, Sagarika, primary, Ibanez Sanchez, Glorymar, primary, Benayed, Ryma, primary, Jungbluth, Achim A., primary, Smyth, Lillian M., primary, Mauguen, Audrey, primary, Gushterova, Irena, primary, Ding, Hongxu, primary, Spraggon, Lee, primary, Darnell, Robert, primary, Califano, Andrea, primary, Ladanyi, Marc, primary, Papaemmanuil, Elli, primary, Kung, Andrew L., primary, Hyman, David M., primary, and Roberts, Stephen S., primary

Published
2023
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8. Supplementary Table 2 from Patient-Driven Discovery, Therapeutic Targeting, and Post-Clinical Validation of a Novel AKT1 Fusion–Driven Cancer

Author

Slotkin, Emily K., primary, Diolaiti, Daniel, primary, Shukla, Neerav N., primary, Dela Cruz, Filemon S., primary, Clark, Jennifer J., primary, Gundem, Gunes, primary, Yellapantula, Venkata D., primary, Levine, Max F., primary, You, Daoqi, primary, Ma, Peilin, primary, Pachhal, Sagarika, primary, Ibanez Sanchez, Glorymar, primary, Benayed, Ryma, primary, Jungbluth, Achim A., primary, Smyth, Lillian M., primary, Mauguen, Audrey, primary, Gushterova, Irena, primary, Ding, Hongxu, primary, Spraggon, Lee, primary, Darnell, Robert, primary, Califano, Andrea, primary, Ladanyi, Marc, primary, Papaemmanuil, Elli, primary, Kung, Andrew L., primary, Hyman, David M., primary, and Roberts, Stephen S., primary

Published
2023
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9. Data from Patient-Driven Discovery, Therapeutic Targeting, and Post-Clinical Validation of a Novel AKT1 Fusion–Driven Cancer

Author

Slotkin, Emily K., primary, Diolaiti, Daniel, primary, Shukla, Neerav N., primary, Dela Cruz, Filemon S., primary, Clark, Jennifer J., primary, Gundem, Gunes, primary, Yellapantula, Venkata D., primary, Levine, Max F., primary, You, Daoqi, primary, Ma, Peilin, primary, Pachhal, Sagarika, primary, Ibanez Sanchez, Glorymar, primary, Benayed, Ryma, primary, Jungbluth, Achim A., primary, Smyth, Lillian M., primary, Mauguen, Audrey, primary, Gushterova, Irena, primary, Ding, Hongxu, primary, Spraggon, Lee, primary, Darnell, Robert, primary, Califano, Andrea, primary, Ladanyi, Marc, primary, Papaemmanuil, Elli, primary, Kung, Andrew L., primary, Hyman, David M., primary, and Roberts, Stephen S., primary

Published
2023
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10. Supplementary Methods from Patient-Driven Discovery, Therapeutic Targeting, and Post-Clinical Validation of a Novel AKT1 Fusion–Driven Cancer

Author

Slotkin, Emily K., primary, Diolaiti, Daniel, primary, Shukla, Neerav N., primary, Dela Cruz, Filemon S., primary, Clark, Jennifer J., primary, Gundem, Gunes, primary, Yellapantula, Venkata D., primary, Levine, Max F., primary, You, Daoqi, primary, Ma, Peilin, primary, Pachhal, Sagarika, primary, Ibanez Sanchez, Glorymar, primary, Benayed, Ryma, primary, Jungbluth, Achim A., primary, Smyth, Lillian M., primary, Mauguen, Audrey, primary, Gushterova, Irena, primary, Ding, Hongxu, primary, Spraggon, Lee, primary, Darnell, Robert, primary, Califano, Andrea, primary, Ladanyi, Marc, primary, Papaemmanuil, Elli, primary, Kung, Andrew L., primary, Hyman, David M., primary, and Roberts, Stephen S., primary

Published
2023
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11. Supplementary Table 4 from Patient-Driven Discovery, Therapeutic Targeting, and Post-Clinical Validation of a Novel AKT1 Fusion–Driven Cancer

Author

Slotkin, Emily K., primary, Diolaiti, Daniel, primary, Shukla, Neerav N., primary, Dela Cruz, Filemon S., primary, Clark, Jennifer J., primary, Gundem, Gunes, primary, Yellapantula, Venkata D., primary, Levine, Max F., primary, You, Daoqi, primary, Ma, Peilin, primary, Pachhal, Sagarika, primary, Ibanez Sanchez, Glorymar, primary, Benayed, Ryma, primary, Jungbluth, Achim A., primary, Smyth, Lillian M., primary, Mauguen, Audrey, primary, Gushterova, Irena, primary, Ding, Hongxu, primary, Spraggon, Lee, primary, Darnell, Robert, primary, Califano, Andrea, primary, Ladanyi, Marc, primary, Papaemmanuil, Elli, primary, Kung, Andrew L., primary, Hyman, David M., primary, and Roberts, Stephen S., primary

Published
2023
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12. Supplementary Table 5 from Patient-Driven Discovery, Therapeutic Targeting, and Post-Clinical Validation of a Novel AKT1 Fusion–Driven Cancer

Author

Slotkin, Emily K., primary, Diolaiti, Daniel, primary, Shukla, Neerav N., primary, Dela Cruz, Filemon S., primary, Clark, Jennifer J., primary, Gundem, Gunes, primary, Yellapantula, Venkata D., primary, Levine, Max F., primary, You, Daoqi, primary, Ma, Peilin, primary, Pachhal, Sagarika, primary, Ibanez Sanchez, Glorymar, primary, Benayed, Ryma, primary, Jungbluth, Achim A., primary, Smyth, Lillian M., primary, Mauguen, Audrey, primary, Gushterova, Irena, primary, Ding, Hongxu, primary, Spraggon, Lee, primary, Darnell, Robert, primary, Califano, Andrea, primary, Ladanyi, Marc, primary, Papaemmanuil, Elli, primary, Kung, Andrew L., primary, Hyman, David M., primary, and Roberts, Stephen S., primary

Published
2023
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13. Supplementary Table 3 from Patient-Driven Discovery, Therapeutic Targeting, and Post-Clinical Validation of a Novel AKT1 Fusion–Driven Cancer

Author

Slotkin, Emily K., primary, Diolaiti, Daniel, primary, Shukla, Neerav N., primary, Dela Cruz, Filemon S., primary, Clark, Jennifer J., primary, Gundem, Gunes, primary, Yellapantula, Venkata D., primary, Levine, Max F., primary, You, Daoqi, primary, Ma, Peilin, primary, Pachhal, Sagarika, primary, Ibanez Sanchez, Glorymar, primary, Benayed, Ryma, primary, Jungbluth, Achim A., primary, Smyth, Lillian M., primary, Mauguen, Audrey, primary, Gushterova, Irena, primary, Ding, Hongxu, primary, Spraggon, Lee, primary, Darnell, Robert, primary, Califano, Andrea, primary, Ladanyi, Marc, primary, Papaemmanuil, Elli, primary, Kung, Andrew L., primary, Hyman, David M., primary, and Roberts, Stephen S., primary

Published
2023
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15. S6K1 regulates hematopoietic stem cell self-renewal and leukemia maintenance

Author

Ghosh, Joydeep, Kobayashi, Michihiro, Ramdas, Baskar, Chatterjee, Anindya, Ma, Peilin, Mali, Raghuveer Singh, Carlesso, Nadia, Liu, Yan, Plas, David R., Chan, Rebecca J., and Kapur, Reuben

Subjects
Leukemia -- Care and treatment -- Research, Hematopoietic stem cells -- Physiological aspects -- Research, Stem cells -- Transplantation, Health care industry
Abstract

Hyperactivation of the mTOR pathway impairs hematopoietic stem cell (HSC) functions and promotes leukemogenesis. mTORC1 and mTORC2 differentially control normal and leukemic stem cell functions. mTORC1 regulates p70 ribosomal protein S6 kinase 1 (S6K1) and eukaryotic initiation factor 4E-binding (eIF4E-binding) protein 1 (4E-BP1), and mTORC2 modulates AKT activation. Given the extensive crosstalk that occurs between mTORC1 and mTORC2 signaling pathways, we assessed the role of the mTORC1 substrate S6K1 in the regulation of both normal HSC functions and in leukemogenesis driven by the mixed lineage leukemia (MLL) fusion oncogene MLL-AF9. We demonstrated that S6K1 deficiency impairs self-renewal of murine HSCs by reducing p21 expression. Loss of S6K1 also improved survival in mice transplanted with MLL-AF9- positive leukemic stem cells by modulating AKT and 4E-BP1 phosphorylation. Taken together, these results suggest that S6K1 acts through multiple targets of the mTOR pathway to promote self-renewal and leukemia progression. Given the recent interest in S6K1 as a potential therapeutic target in cancer, our results further support targeting this molecule as a potential strategy for treatment of myeloid malignancies., Introduction Aberrant regulation of the intracellular signaling pathways that underlie normal hematopoietic stem cell (HSC) renewal and differentiation is one of the pathogenic hallmarks of human leukemia. mTOR plays an [...]

Published
2016
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17. Role of SHP2 phosphatase in KIT-induced transformation: identification of SHP2 as a druggable target in diseases involving oncogenic KIT

Author

Mali, Raghuveer Singh, Ma, Peilin, Zeng, Li-Fan, Martin, Holly, Ramdas, Baskar, He, Yantao, Sims, Emily, Nabinger, Sarah, Ghosh, Joydeep, Sharma, Namit, Munugalavadla, Veerendra, Chatterjee, Anindya, Li, Shuo, Sandusky, George, Craig, Andrew W., Bunting, Kevin D., Feng, Gen-Sheng, Chan, Rebecca J., Zhang, Zhong-Yin, and Kapur, Reuben

Published
2012
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19. Rho Kinase Regulates the Survival and Transformation of Cells Bearing Oncogenic Forms of KIT, FLT3, and BCR-ABL

Author

Mali, Raghuveer Singh, Ramdas, Baskar, Ma, Peilin, Shi, Jianjian, Munugalavadla, Veerendra, Sims, Emily, Wei, Lei, Vemula, Sasidhar, Nabinger, Sarah C., Goodwin, Charles B., Chan, Rebecca J., Traina, Fabiola, Visconte, Valeria, Tiu, Ramon V., Lewis, Timothy A., Stern, Andrew M., Wen, Qiang, Crispino, John D., Boswell, H. Scott, and Kapur, Reuben

Published
2011
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21. Pak and Rac GTPases promote oncogenic KIT--induced neoplasms

Author

Martin, Holly, Mali, Raghuveer Singh, Ma, Peilin, Chatterjee, Anindya, Ramdas, Baskar, Sims, Emily, Munugalavadla, Veerendra, Ghosh, Joydeep, Mattingly, Ray R., Visconte, Valeria, Tiu, Ramon V., Vlaar, Cornelis P., Dharmawardhane, Suranganie, and Kapur, Reuben

Subjects
Gene mutations -- Observations, Hydrolases -- Properties, Drug targeting -- Research, Cancer -- Care and treatment, Enzymes -- Properties, Health care industry
Abstract

An acquired somatic mutation at codon 816 in the KIT receptor tyrosine kinase is associated with poor prognosis in patients with systemic mastocytosis and acute myeloid leukemia (AML). Treatment of [...]

Published
2013
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22. Preclinical and Translational Data Support Development of Iberdomide in Combination with CD38- and SLAMF7-Directed Monoclonal Antibodies: Evidence for Rational Combinations

Author

Amatangelo, Michael, primary, Bjorklund, Chad, additional, Ma, Peilin, additional, Wollerman, Krista, additional, Pierceall, William, additional, Lonial, Sagar, additional, van de Donk, Niels W.C.J., additional, Popat, Rakesh, additional, Jagannath, Sundar, additional, Zonder, Jeffrey, additional, Minnema, Monique C., additional, Oriol, Albert, additional, Larsen, Jeremy, additional, Badros, Ashraf Z., additional, Rodriguez-Otero, Paula, additional, Sonneveld, Pieter, additional, Nguyen, Tuong Vi, additional, Hong, Kevin, additional, Sorrell, April, additional, and Thakurta, Anjan, additional

Published
2020
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25. Patient-Driven Discovery, Therapeutic Targeting, and Post-Clinical Validation of a Novel AKT1 Fusion–Driven Cancer

Author

Slotkin, Emily K., primary, Diolaiti, Daniel, additional, Shukla, Neerav N., additional, Dela Cruz, Filemon S., additional, Clark, Jennifer J., additional, Gundem, Gunes, additional, Yellapantula, Venkata D., additional, Levine, Max F., additional, You, Daoqi, additional, Ma, Peilin, additional, Pachhal, Sagarika, additional, Ibanez Sanchez, Glorymar, additional, Benayed, Ryma, additional, Jungbluth, Achim A., additional, Smyth, Lillian M., additional, Mauguen, Audrey, additional, Gushterova, Irena, additional, Ding, Hongxu, additional, Spraggon, Lee, additional, Darnell, Robert, additional, Califano, Andrea, additional, Ladanyi, Marc, additional, Papaemmanuil, Elli, additional, Kung, Andrew L., additional, Hyman, David M., additional, and Roberts, Stephen S., additional

Published
2019
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26. The protective role of DOT1L in UV-induced melanomagenesis

Author

Zhu, Bo, primary, Chen, Shuyang, additional, Wang, Hongshen, additional, Yin, Chengqian, additional, Han, Changpeng, additional, Peng, Cong, additional, Liu, Zhaoqian, additional, Wan, Lixin, additional, Zhang, Xiaoyang, additional, Zhang, Jie, additional, Lian, Christine G., additional, Ma, Peilin, additional, Xu, Zhi-xiang, additional, Prince, Sharon, additional, Wang, Tao, additional, Gao, Xiumei, additional, Shi, Yujiang, additional, Liu, Dali, additional, Liu, Min, additional, Wei, Wenyi, additional, Wei, Zhi, additional, Pan, Jingxuan, additional, Wang, Yongjun, additional, Xuan, Zhenyu, additional, Hess, Jay, additional, Hayward, Nicholas K., additional, Goding, Colin R., additional, Chen, Xiang, additional, Zhou, Jun, additional, and Cui, Rutao, additional

Published
2018
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27. PRDM16 suppresses MLL leukemia via intrinsic histone methyltransferase activity

Author

Zhou, Bo, Wang, Jingya, Lee, Shirley Y., Xiong, Jie, Bhanu, Natarajan, Guo, Qi, Ma, Peilin, Sun, Yuqing, Rao, Rajesh C., Garcia, Benjamin A., Hess, Jay L., and Dou, Yali

Subjects
Article
Abstract

PRDM16 is a transcription co-factor that plays critical roles in development of brown adipose tissue, as well as maintenance of adult hematopoietic and neural stem cells. Here we report that PRDM16 is a histone H3K4 methyltransferase on chromatin. Mutation in the N-terminal PR domain of PRDM16 abolishes the intrinsic enzymatic activity of PRDM16. We show that the methyltransferase activity of PRDM16 is required for specific suppression of MLL fusion protein-induced leukemogenesis both in vitro and in vivo. Mechanistic studies show that PRDM16 directly activates the SNAG family transcription factor Gfi1b, which in turn downregulates the HOXA gene cluster. Knockdown Gfi1b represses PRDM16-mediated tumor suppression, while Gfi1b overexpression mimics PRDM16 overexpression. In further support of the tumor suppressor function of PRDM16, silencing PRDM16 by DNA methylation is concomitant with MLL-AF9-induced leukemic transformation. Taken together, our study reveals a previously uncharacterized function of PRDM16 that depends on its PR domain activity.

Published
2016

30. Preclinical and Translational Biomarker Analyses to Inform Clinical Development of Mezigdomide (CC-92480) in Combination with Dexamethasone and Daratumumab in Multiple Myeloma

Author

Chow, Tracy T., Amatangelo, Michael, Ma, Peilin, Bjorklund, Chad C., Wollerman, Krista, Civardi, Tiziana, Koo, Phillip, Zhu, Yue, Maciag, Paulo, Katz, Jessica, Raval, Aparna, Oriol, Albert, Orlowski, Robert Z., White, Darrell, Richardson, Paul G., and Gandhi, Anita K.

Abstract

Introduction:Mezigdomide (MEZI) is a novel, oral cereblon (CRBN) E3 ligase modulator (CELMoD) that induces rapid and potent degradation of lkaros and Aiolos. Reduction of these transcription factors results in direct tumoricidal and immunomodulatory effects in multiple myeloma (MM). MEZI showed promising efficacy and safety in combination with dexamethasone in the phase 1/2 CC-92480-MM-001 trial (NCT03374085) in Relapsed/Refractory MM. MEZI is currently being investigated in combination with daratumumab and dexamethasone (MEZI + DARA + DEX or MEZI-Dd) in the phase 1/2 CC-92480-MM-002 trial (NCT03989414). In MEZI-Dd cohort, MEZI is administered at three different schedules (B1 for 21/28 days; B2 for 14/21 days; B3 for 7/14 days), and at two different doses (0.3mg; 0.6mg). Here we report preclinical data and pharmacodynamic (PD) biomarker analyses from blood and bone marrow samples collected in CC-92480-MM-002 to support dose and schedule optimization of MEZI-Dd.

Published
2023
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35. Declined presentation

Author

Martin, Holly, primary, Mali, Raghuveer, additional, Ma, Peilin, additional, Chatterjee, Anindya, additional, Vlaar, Cornelis, additional, Ramdas, Baskar, additional, Dharmawardhane, Suraganie, additional, Visconte, Valeria, additional, Tiu, Ramon, additional, and Kapur, Reuben, additional

Published
2013
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36. Declined presentation

Author

Ghosh, Joydeep, primary, Ramdas, Baskar, additional, Chatterjee, Anindya, additional, Ma, Peilin, additional, Mali, Raghuveer, additional, and Kapur, Reuben, additional

Published
2013
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40. KIT Induced Myeloproliferative Disease Is Dependent on PI3Kinase and SHP2 Phosphatase: Identification of SHP2 As a Druggable Target for Treating MPD and AML

Author

Ma, Peilin, primary, Mali, Raghuveer, additional, Zeng, Li-Fan, additional, Martin, Holly, additional, Ramdas, Baskar, additional, He, Yantao, additional, Sims, Emily, additional, Ghosh, Joydeep, additional, Nabinger, Sarah C, additional, Li, Shuo, additional, Munugalavadla, Veerendra, additional, Chatterjee, Anindya, additional, Sandusky, George, additional, Craig, Andrew, additional, Bunting, Kevin D., additional, Feng, Gen-Sheng, additional, Chan, Rebecca J., additional, Zhang, Zhong-Yin, additional, and Kapur, Reuben, additional

Published
2011
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41. Balanced Interactions between Lyn, the p85α Regulatory Subunit of Class I A Phosphatidylinositol-3-Kinase, and SHIP Are Essential for Mast Cell Growth and Maturation

Author

Ma, Peilin, primary, Vemula, Sasidhar, additional, Munugalavadla, Veerendra, additional, Chen, Jinbiao, additional, Sims, Emily, additional, Borneo, Jovencio, additional, Kondo, Takako, additional, Ramdas, Baskar, additional, Mali, Raghuveer Singh, additional, Li, Shuo, additional, Hashino, Eri, additional, Takemoto, Clifford, additional, and Kapur, Reuben, additional

Published
2011
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42. The PI3K pathway drives the maturation of mast cells via microphthalmia transcription factor

Author

Ma, Peilin, primary, Mali, Raghuveer Singh, additional, Munugalavadla, Veerendra, additional, Krishnan, Subha, additional, Ramdas, Baskar, additional, Sims, Emily, additional, Martin, Holly, additional, Ghosh, Joydeep, additional, Li, Shuo, additional, Chan, Rebecca J., additional, Krystal, Gerald, additional, Craig, Andrew W., additional, Takemoto, Clifford, additional, and Kapur, Reuben, additional

Published
2011
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46. Rapid Preparation of Antifreezing Conductive Hydrogels for Flexible Strain Sensors and Supercapacitors

Author

Song, Yating, Niu, Li, Ma, Peilin, Li, Xu, Feng, Jacko, and Liu, Zhiming

Abstract

Conductive hydrogels have shown great promise in flexible electronics, but their practical applications may be impeded by the time-consuming and energy-consuming polymerization process. We proposed a sodium lignosulfonate–Fe (SLS–Fe) strategy to address this challenge and took advantage of carboxymethyl cellulose (CMC) and poly(acrylic acid) to prepare the CMC/PAA/Fe3+/LiCl interpenetrating conductive hydrogels with good self-healing properties, antifreezing properties, and a 6-fold increase in conductivity in this study. The hydrogel-based flexible strain sensors demonstrated a broad detection range (400%), high sensitivity (GF = 6.19 at 200–400%), and human motion detection capability. The hydrogel-based supercapacitor exhibited a single-electrode specific capacitance of 122.36 F g–1which successfully powered LEDs. Furthermore, the supercapacitor showed a single-electrode specific capacitance of 83.16 F g–1at −23 °C (68% of the one exhibited at 25 °C). Therefore, the multifunctional performance of the CMC/PAA/Fe3+/LiCl hydrogel is anticipated to play an exemplary role in a new generation of flexible electronics.

Published
2023
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47. Class IA PI3Kinase Regulatory Subunit, p85α, Mediates Mast Cell Development through Regulation of Growth and Survival Related Genes.

Author

Krishnan, Subha, Mali, Raghuveer Singh, Koehler, Karl R., Vemula, Sasidhar, Chatterjee, Anindya, Ghosh, Joydeep, Ramdas, Baskar, Ma, Peilin, Hashino, Eri, and Kapur, Reuben

Subjects
MAST cells, CONNECTIVE tissue cells, REGULATION of cell growth, CELLULAR control mechanisms, BIOLOGICAL rhythms, CELL cycle, CELL adhesion
Abstract

Stem cell factor (SCF) mediated KIT receptor activation plays a pivotal role in mast cell growth, maturation and survival. However, the signaling events downstream from KIT are poorly understood. Mast cells express multiple regulatory subunits of class 1A PI3Kinase (PI3K) including p85α, p85β, p50α, and p55α. While it is known that PI3K plays an essential role in mast cells; the precise mechanism by which these regulatory subunits impact specific mast cell functions including growth, survival and cycling are not known. We show that loss of p85α impairs the growth, survival and cycling of mast cell progenitors (MCp). To delineate the molecular mechanism (s) by which p85α regulates mast cell growth, survival and cycling, we performed microarray analyses to compare the gene expression profile of MCps derived from WT and p85α-deficient mice in response to SCF stimulation. We identified 151 unique genes exhibiting altered expression in p85α-deficient cells in response to SCF stimulation compared to WT cells. Functional categorization based on DAVID bioinformatics tool and Ingenuity Pathway Analysis (IPA) software relates the altered genes due to lack of p85α to transcription, cell cycle, cell survival, cell adhesion, cell differentiation, and signal transduction. Our results suggest that p85α is involved in mast cell development through regulation of expression of growth, survival and cell cycle related genes. [ABSTRACT FROM AUTHOR]

Published
2012
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48. p85β regulatory subunit of class IAPI3 kinase negatively regulates mast cell growth, maturation, and leukemogenesis

Author

Krishnan, Subha, Mali, Raghuveer Singh, Ramdas, Baskar, Sims, Emily, Ma, Peilin, Ghosh, Joydeep, Munugalavadla, Veerendra, Hanneman, Philip, Beane, Joal D., and Kapur, Reuben

Abstract

We show that loss of p85α inhibits the growth and maturation of mast cells, whereas loss of p85β enhances this process. Whereas restoring the expression of p85α in P85α−/−cells restores these functions, overexpression of p85β has the opposite effect. Consistently, overexpression of p85β in WT mast cells represses KIT-induced proliferation and IL-3–mediated maturation by inhibiting the expression of Microphthalmia transcription factor. Because p85α and p85β differ in their N-terminal sequences, chimeric proteins consisting of amino or carboxy-terminal of p85α and/or p85β do not rescue the growth defects of p85α−/−cells, suggesting cooperation between these domains for normal mast cell function. Loss of p85β impaired ligand induced KIT receptor internalization and its overexpression enhanced this process, partly because of increased binding of c-Cbl to p85β relative to p85α. In vivo, loss of p85β resulted in increased mast cells, and bone marrow transplantation of cells overexpressing p85β resulted in significant reduction in some tissue mast cells. Overexpression of p85β suppressed the growth of oncogenic KIT-expressing cells in vitro and prolonged the survival of leukemic mice in vivo. Thus, p85α and p85β differentially regulate SCF and oncogenic KIT-induced signals in myeloid lineage-derived mast cells.

Published
2012
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49. A new target for differentiation therapy in AML

Author

Ma, Peilin, Song, Weihua, and Hess, Jay L

Abstract

Despite major advances in understanding the genetics and epigenetics of acute myelogenous leukemia, there is still a great need to develop more specific and effective therapies. High throughput approaches involving either genetic approaches or small molecule inhibitor screens are beginning to identify promising new therapeutic targets.

Published
2017
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