Jie Jiang

Rensselaer Polytechnic Institute

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i-10 index

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Co-Authors

Jianwei Che

Dana-Farber Cancer Institute

110

Pasi A. Jänne

Dana-Farber Cancer Institute

101

Magda Bahcall

Dana-Farber Cancer Institute

Danielle Haradon

Dana-Farber Cancer Institute

Simon Baldacci

Harvard University

Nishant Gandhi

Caris Life Sciences (United States)

C. Patrick

Penn State Milton S. Hershey Medical Center

Andrew Elliott

Caris Life Sciences (United States)

Stephen V. Liu

Georgetown University Medical Center

Vikas K. Goel

Bristol-Myers Squibb (United States)

Cooperative Institutions

Harvard University

138

Dana-Farber Cancer Institute

120

Chinese Academy of Medical Sciences & Peking Union Medical College

Chinese Academy of Sciences

King's College London

Brigham and Women's Hospital

King's College Hospital

Shanghai Jiao Tong University

Peking University

Sun Yat-sen University

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Intergenic variants of HBS1L-MYB are responsible for a major quantitative trait locus on chromosome 6q23 influencing fetal hemoglobin levels in adults

Proceedings of the National Academy of Sciences (2007)

Swee Lay Thein Stephan Menzel Peng Xu Steve Best Jie Jiang

Individual variation in fetal hemoglobin (HbF, alpha(2)gamma(2)) response underlies the remarkable diversity in phenotypic severity of sickle cell disease and beta thalassemia. HbF levels and HbF-associated quantitative traits (e.g., F cell levels) are highly heritable. We have previously mapped a major quantitative trait locus (QTL) controlling F cell levels in an extended Asian-Indian kindred with beta thalassemia to a 1.5-Mb interval on chromosome 6q23, but the causative gene(s) are not known. The QTL encompasses several genes including HBS1L, a member of the GTP-binding protein family that is expressed in erythroid progenitor cells. In this high-resolution association study, we have identified multiple genetic variants within and 5' to HBS1L at 6q23 that are strongly associated with F cell levels in families of Northern European ancestry (P = 10(-75)). The region accounts for 17.6% of the F cell variance in northern Europeans. Although mRNA levels of HBS1L and MYB in erythroid precursors grown in vitro are positively correlated, only HBS1L expression correlates with high F cell alleles. The results support a key role for the HBS1L-related genetic variants in HbF control and illustrate the biological complexity of the mechanism of 6q QTL as a modifier of fetal hemoglobin levels in the beta hemoglobinopathies.

MYB

10.1073/pnas.0611393104

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Citations (311)

Development of Highly Potent and Selective Pyrazolopyridine Inhibitor of CDK8/19

ACS Medicinal Chemistry Letters (2021)

John M. Hatcher Prasanna S. Vatsan Eric Wang Jie Jiang Nathanael S. Gray

CDK8 and its paralog CDK19 are cyclin-dependent kinases that are core components of the so-called Mediator complex that has essential roles as a positive and negative regulator of gene expression. Several efforts to develop inhibitors have yielded natural and synthetic ATP-competitive compounds including cortistatin A, Sel120, BCD-115, CCT251921 (1), and MSC2530818 (2). Here, we used a hybridization approach starting from CCT251921 and MSC2530818 to derive new inhibitors with the aim of developing highly potent and selective inhibitors of CDK8/19. Initial compounds suffered from rapid aldehyde oxidase-mediated metabolism. This liability was overcome by utilizing a pyrazolopyridine hinge binder with a chlorine at the C-3 position. These efforts resulted in JH-XVI-178 (compound 15), a highly potent and selective inhibitor of CDK8/19 that displays low clearance and moderate oral pharmacokinetic properties.

Cyclin-dependent kinase 8

10.1021/acsmedchemlett.1c00300

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Emulating Complex Synapses Using Interlinked Proton Conductors

arXiv (Cornell University) (2024)

Lifu Zhang Jian Li Yang Hu Jie Jiang Rongjie Lai

In terms of energy efficiency and computational speed, neuromorphic electronics based on non-volatile memory devices is expected to be one of most promising hardware candidates for future artificial intelligence (AI). However, catastrophic forgetting, networks rapidly overwriting previously learned weights when learning new tasks, remains as a pivotal hurdle in either digital or analog AI chips for unleashing the true power of brain-like computing. To address catastrophic forgetting in the context of online memory storage, a complex synapse model (the Benna-Fusi model) has been proposed recently[1], whose synaptic weight and internal variables evolve following a diffusion dynamics. In this work, by designing a proton transistor with a series of charge-diffusion-controlled storage components, we have experimentally realized the Benna-Fusi artificial complex synapse. The memory consolidation from coupled storage components is revealed by both numerical simulations and experimental observations. Different memory timescales for the complex synapse are engineered by the diffusion length of charge carriers, the capacity and number of coupled storage components. The advantage of the demonstrated complex synapse in both memory capacity and memory consolidation is revealed by neural network simulations of face familiarity detection. Our experimental realization of the complex synapse suggests a promising approach to enhance memory capacity and to enable continual learning.

10.48550/arxiv.2401.15045

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Cerebellar c9RAN proteins associate with clinical and neuropathological characteristics of C9ORF72 repeat expansion carriers

Journal of Neurochemistry (2016)

Tania Gendron Marka van Blitterswijk Kevin F. Bieniek Lillian M. Daughrity Jie Jiang

C9ORF72

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CSNK1A1 mutations and isolated del(5q) abnormality in myelodysplastic syndrome: a retrospective mutational analysis

The Lancet Haematology (2015)

Alexander Smith Austin Kulasekararaj Jie Jiang Syed A. Mian Azim Mohamedali

10.1016/s2352-3026(15)00050-2

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Citations (20)

Immunological characteristics of human umbilical cord mesenchymal stem cells after hepatogenic differentiation

Bio-Medical Materials and Engineering (2022)

Yanfeng Yin Zongqiang Hu Zheng Guan Sha Lv Yiyin Wang

Acute liver failure is one of the most intractable clinical problems. The use of bioartificial livers may solve donor shortage problems. Human umbilical cord mesenchymal stem cells (hUCMSCs) are an excellent seed cell choice for artificial livers because they change their characteristics to resemble hepatocyte-like cells (HLCs) following artificial liver transplantation.This study aimed to determine whether the immunological characteristics of hUCMSCs are changed after being transformed into hepatocyte-like cells.HUCMSCs were isolated by the adherent method. The following hUCMSC surface markers were detected using flow cytometry: CD45, CD90, CD105, CD34, and octamer-binding transcription factor 4 (OCT-4). Functional detection of adipogenic differentiation was performed. The hUCMSCs were cultured in complete medium (control group) or induction medium (induction group), and flow cytometry was used to detect cell surface markers. Peritoneal lavage fluid was collected after intraperitoneal injection of 1 × 106 cells/mouse over 40 minutes. The leukocyte count, labeled CD45, CD3, CD4 and CD8 antibodies, and flow detection of T lymphocyte subsets were determined using the peritoneal lavage fluid.Using phenotypic and functional identification, hUCMSCs were successfully isolated using a two-step induction method. The surface markers of the hUCMSCs cells changed after HLC induction. In vivo immune results showed that hUCMSCs and HLsC induced leukocyte production.Hepatic induction of hUCMSCs changes their cell surface markers. Both HLCs and hUCMSCs cause leukocytosis in vivo, but the immune response induced by HLCs is slightly stronger.

CD90

Wharton's jelly

Cell therapy

10.3233/bme-211331

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Citations (2)

Expert consensus on perioperative immunotherapy for local advanced non-small cell lung cancer

Translational Lung Cancer Research (2021)

Bin Qiu Kaican Cai Chun Chen Jun Chen Ke‐Neng Chen

BackgroundThe treatment of lung cancer is one of the major challenges in the field of oncology.According to statistics from the National Cancer Center of China in 2015, lung cancer has the highest incidence and mortality, with 733,300 new cases and 610,200 deaths across the country (1).About 85% of lung cancers are non-small cell lung cancer (NSCLC), of which 30% to 40% are considered resectable tumors, including most stage I-II and a small portion of stage IIIA tumors (2).Very early-stage NSCLC (IA) can be cured by surgery.However, more than 50% of NSCLC patients who undergo surgical treatment will relapse or metastasize within 5 years.Even if there is no lymph node metastasis and the primary

Cancer Immunotherapy

10.21037/tlcr-21-634

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Citations (17)

Supplementary Figure 10 from Activating Point Mutations in the MET Kinase Domain Represent a Unique Molecular Subset of Lung Cancer and Other Malignancies Targetable with MET Inhibitors

Federica Pecci Seshiru Nakazawa Biagio Ricciuti Guilherme Harada Jessica Lee

MET TKD mutations in NSCLC cohort of Caris Life Sciences. (A) Flowchart of the NSCLC subgroup in the Caris Life Sciences dataset. (B) Prevalence of MET TKD mutations in NSCLC cases in the Caris Life Sciences dataset (MET TKD mutations in 280 unique patients). (C) Lollipop plot of the oncogenic / likely oncogenic MET TKD mutations detected in NSCLC cases in the Caris Life Sciences dataset (35 oncogenic / likely oncogenic MET TKD mutations in 35 unique patients). (D) concurrent driver alterations (information available for 24 cases, unavailable for 11 cases) and (E) concurrent MET amplification status (information available for 33 cases, unavailable for 2 cases) of NSCLC cases harboring oncogenic / likely oncogenic MET TKD mutations in the Caris Life Sciences dataset.

10.1158/2159-8290.26467043

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Supplementary Figure 14 from Activating Point Mutations in the MET Kinase Domain Represent a Unique Molecular Subset of Lung Cancer and Other Malignancies Targetable with MET Inhibitors

Federica Pecci Seshiru Nakazawa Biagio Ricciuti Guilherme Harada Jessica Lee

Western blot analysis of MET and ERK1/2 phosphorylation in MET R1170Q cell models. MET and ERK1/2 phosphorylation in (A) Ba/F3 cells stably transduced with MET R1170Q and (B) 293T cells transiently overexpressing MET R1170Q. Cells were treated with MET TKIs at the indicated dose for Ba/F3 cells or at 1 μM for 293T cells.

HEK 293 cells

Protein kinase domain

10.1158/2159-8290.26467025

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Data from Activating Point Mutations in the MET Kinase Domain Represent a Unique Molecular Subset of Lung Cancer and Other Malignancies Targetable with MET Inhibitors

Federica Pecci Seshiru Nakazawa Biagio Ricciuti Guilherme Harada Jessica Lee

<div>AbstractActivating point mutations in the MET tyrosine kinase domain (TKD) are oncogenic in a subset of papillary renal cell carcinomas. Here, using comprehensive genomic profiling among >600,000 patients, we identify activating MET TKD point mutations as putative oncogenic driver across diverse cancers, with a frequency of ∼0.5%. The most common mutations in the MET TKD defined as oncogenic or likely oncogenic according to OncoKB resulted in amino acid substitutions at positions H1094, L1195, F1200, D1228, Y1230, M1250, and others. Preclinical modeling of these alterations confirmed their oncogenic potential and also demonstrated differential patterns of sensitivity to type I and type II MET inhibitors. Two patients with metastatic lung adenocarcinoma harboring MET TKD mutations (H1094Y, F1200I) and no other known oncogenic drivers achieved confirmed partial responses to a type I MET inhibitor. Activating MET TKD mutations occur in multiple malignancies and may confer clinical sensitivity to currently available MET inhibitors.Significance: The identification of targetable genomic subsets of cancer has revolutionized precision oncology and offers patients treatments with more selective and effective agents. Here, we demonstrate that activating, oncogenic MET tyrosine kinase domain mutations are found across a diversity of cancer types and are responsive to MET tyrosine kinase inhibitors.</div>

Protein kinase domain

10.1158/2159-8290.c.7384706.v1

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