CRISPR/Cas9 gene editing in via visual selection in a summer classroom.

CRISPR/Cas9 methods are a powerful approach to edit the genome of . To convert existing lines to driver lines in a secondary school classroom setting, we applied the CRISPR-based genetic approach to a collection of 'driver' lines. The integration of the coat color marker into homology-assisted CRISPR knock-in (HACK) enabled visual selection of -to- conversions using brightfield stereo-microscopy available in a broader set of standard classrooms.

Sex and Circadian Timing Modulate Oxaliplatin Hematological and Hematopoietic Toxicities.

Oxaliplatin was nearly twice as hematotoxic, with optimal circadian timing differing by 6 h, in women as compared to men with colorectal cancers. Hence, we investigated sex- and timing-related determinants of oxaliplatin hematopoietic toxicities in mice. Body-weight loss (BWL), blood cell counts, bone marrow cellularity (BMC) and seven flow-cytometry-monitored hematopoietic progenitor populations were evaluated 72 h after oxaliplatin chronotherapy administration (5 mg/kg).

Crystal structure and Hirshfeld surface analysis of 5-acetyl-2-amino-4-(4-bromo-phen-yl)-6-oxo-1-phenyl-1,4,5,6-tetra-hydro-pyridine-3-carbo-nitrile.

The crystal structure of the title compound, CHBrNO, was determined using an inversion twin. Its asymmetric unit comprises two crystallographically independent mol-ecules ( and ) being the stereoisomers. Both mol-ecules are linked by pairs of N-H⋯O hydrogen bonds, forming a dimer with an (16) ring motif.

Evidence of Antitumor and Antimetastatic Potential of Induced Pluripotent Stem Cell-Based Vaccines in Cancer Immunotherapy.

Cancer is maintained by the activity of a rare population of self-renewing "cancer stem cells" (CSCs), which are resistant to conventional therapies. CSCs over-express several proteins shared with induced pluripotent stem cells (iPSCs). We show here that allogenic or autologous murine iPSCs, combined with a histone deacetylase inhibitor (HDACi), are able to elicit major anti-tumor responses in a highly aggressive triple-negative breast cancer, as a relevant cancer stemness model.

iPSC-Derived Hereditary Breast Cancer Model Reveals the -Deleted Tumor Niche as a New Culprit in Disease Progression.

Tumor progression begins when cancer cells recruit tumor-associated stromal cells to produce a vascular niche, ultimately resulting in uncontrolled growth, invasion, and metastasis. It is poorly understood, though, how this process might be affected by deletions or mutations in the breast cancer type 1 susceptibility (BRCA1) gene in patients with a lifetime risk of developing breast and/or ovarian cancer. To model the BRCA1-deleted stroma, we first generated induced pluripotent stem cells (iPSCs) from patients carrying a germline deletion of exon 17 of the BRCA1 gene (BRCA1+/- who, based on their family histories, were at a high risk for cancer.