Results 311 to 320 of about 407,038 (348)

Identification and Drug Screening of Single Cells from Human Tumors on Semiconductor Chip for Cancer Precision Medicine

Advanced Science, EarlyView.
The study innovatively integrates single‐cell electric impedance identification and drug screening on a semiconductor chip, addressing tumor heterogeneity limitations. The system achieves label‐free cancer cell recognition while concurrently evaluating drug efficacy on cancer cells and toxicity on noncancerous cells.
Wenhao Hui, Ka‐Meng Lei, Yingying Liu, Xinru Huang, Yunlong Zhong, Xiaojun Chen, Mingji Wei, Jie Yan, Ren Shen, Pui‐In Mak, Rui P. Martins, Shuhong Yi, Ping Wang, Yanwei Jia   +13 more
wiley   +1 more source

Congenital Hyperinsulinism and Novel KDM6A Duplications -Resolving Pathogenicity With Genome and Epigenetic Analyses.

J Clin Endocrinol Metab
Männistö JME, Hopkins JJ, Hewat TI, Nasser F, Burrage J, Dastamani A, Mirante A, Murphy N, Rzasa J, Kerkhof J, Relator R, Johnson MB, Laver TW, Weymouth L, Houghton JAL, Wakeling MN, Sadikovic B, Dempster EL, Flanagan SE.   +18 more
europepmc   +1 more source

Immunologic investigations into transgene directed immune-mediated myositis following delandistrogene moxeparvovec gene therapy. [PDF]

Sci Rep
Potter RA, Moeller IH, Khan S, Haegel H, Hollenstein A, Steiner G, Wandel C, Murphy AP, Asher DR, Palatinsky E, Griffin DA, Mason S, Iannaccone ST, Zaidman CM, Rodino-Klapac LR.   +14 more
europepmc   +1 more source

C1q+ Macrophage–Tumor Cell Interaction Promoted Tumorigenesis via GPR17/PI3K/AKT Pathway Induced DNA Hypermethylation in Nasopharyngeal Carcinoma

Advanced Science, EarlyView.
In the TME of NPC, C1q secreted by C1q+ TAMs interacted with GPR17 to activate PI3K/AKT signaling through strengthening GPR17 coupling PI3K and increasing calcium levels in tumor cells. The activated PI3K/AKT signaling further induces DNA hypermethylation to promote the malignancy and stemness of tumor cells.
Yunzhi Liu, Cuicui Huang, Min Luo, Wenfu Lu, Baifeng Zhang, Lu Bai, Shuyue Zheng, Yanan Tan, Shanshan Li, Huali Wang, Lanqi Gong, Xinyuan Guan   +11 more
wiley   +1 more source

Evolution of Pineal Nonvisual Opsins in Lizards and the Tuatara and Identification of Lepidopsin: A New Opsin Gene. [PDF]

Genome Biol Evol
Romero RD, de Souza FSJ.
europepmc   +1 more source

SNORA74A Drives Self‐Renewal of Liver Cancer Stem Cells and Hepatocarcinogenesis Through Activation of Notch3 Signaling

Advanced Science, EarlyView.
Abstract Liver cancer stem cells (CSCs) account for tumor initiation, heterogeneity and therapy resistance. However, the role of small nucleolar RNAs (snoRNAs) in the regulation of liver CSCs remains largely unclear. Here, this work identifies a conserved H/ACA box snoRNA SNORA74A which is highly expressed in liver CSCs.
Ziheng Zhou, Yang Gu, Zhibin Yi, Jianyi Wang, Zhen Xiong, Hui Guo, Ying Du, Xiaoxiao Zhu, Lei He, Weizheng Ren, Yong Tian, Yanying Wang, Zusen Fan   +12 more
wiley   +1 more source

Splicing Analysis of Exonic TSC1 and TSC2 Gene Variants Causing Tuberous Sclerosis Complex. [PDF]

Hum Mutat
You Q, Liu J, Zhang R, Wang Z, Zhang B, Guo W, Xu N, Bottillo I, Shao L.   +8 more
europepmc   +1 more source

TP53‐Mutated Myeloid Neoplasms: 2024 Update on Diagnosis, Risk‐Stratification, and Management

American Journal of Hematology, EarlyView.
ABSTRACT Alterations in the tumor suppressor gene TP53 are common in human cancers and are associated with an aggressive nature. Approximately 8%–12% of myelodysplastic syndrome (MDS) and acute myeloid leukemia (AML) harbor TP53 mutations (TP53mut) and present immense challenges due to inherent chemoresistance and poor outcomes.
Mithun Vinod Shah, Daniel A. Arber, Devendra K. Hiwase   +2 more
wiley   +1 more source

Transcripts from the <i>src-1(cj293)</i> mutant can encode a SRC-1 molecule lacking the SH2 domain in <i>Caenorhabditis elegans</i>. [PDF]

MicroPubl Biol
Mahadik SS, Lundquist EA.
europepmc   +1 more source

Targeted Therapies in Myelofibrosis: Present Landscape, Ongoing Studies, and Future Perspectives

American Journal of Hematology, EarlyView.
ABSTRACT Myelofibrosis (MF) is a myeloproliferative neoplasm that is accompanied by driver JAK2, CALR, or MPL mutations in more than 90% of cases, leading to constitutive activation of the JAK–STAT pathway. MF is a multifaceted disease characterized by trilineage myeloid proliferation with prominent megakaryocyte atypia and bone marrow fibrosis, as ...
Giuseppe G. Loscocco, Paola Guglielmelli
wiley   +1 more source