Results 151 to 160 of about 1,217,808 (321)
Clinical genetics: past, present and future. [PDF]
Tromans E, Barwell J.
europepmc +1 more source
Clinical Genetics in the age of Genomics and Genome editing [PDF]
Reiner A. Veitia
openalex +1 more source
Modeling hepatic fibrosis in TP53 knockout iPSC‐derived human liver organoids
This study developed iPSC‐derived human liver organoids with TP53 gene knockout to model human liver fibrosis. These organoids showed elevated myofibroblast activation, early disease markers, and advanced fibrotic hallmarks. The use of profibrotic differentiation medium further amplified the fibrotic signature seen in the organoids.
Mustafa Karabicici +8 more
wiley +1 more source
Equity implications of patient-initiated recontact and follow-up in clinical genetics. [PDF]
Mackley MP, Chad L.
europepmc +1 more source
MOLECULAR GENETICS AND CLINICAL ASPECTS OF MONOGENIC DIABETES MELLITUS
Valentina Peterkova +6 more
openalex +2 more sources
Recontacting patients in clinical genetics services: recommendations of the European Society of Human Genetics [PDF]
Daniele Carrieri +20 more
openalex +1 more source
This study investigated how PYCR1 inhibition in bone marrow stromal cells (BMSCs) indirectly affects multiple myeloma (MM) cell metabolism and viability. Culturing MM cells in conditioned medium from PYCR1‐silenced BMSCs impaired oxidative phosphorylation and increased sensitivity to bortezomib.
Inge Oudaert +13 more
wiley +1 more source
Mosaicism in clinical genetics. [PDF]
Mefford HC.
europepmc +1 more source
Inhibition of CDK9 enhances AML cell death induced by combined venetoclax and azacitidine
The CDK9 inhibitor AZD4573 downregulates c‐MYC and MCL‐1 to induce death of cytarabine (AraC)‐resistant AML cells. This enhances VEN + AZA‐induced cell death significantly more than any combination of two of the three drugs in AraC‐resistant AML cells.
Shuangshuang Wu +18 more
wiley +1 more source

