Results 101 to 110 of about 690,437 (335)
Promotion and inhibition of mutation in pathogens
This paper presents the research findings of a sequence of three experiments that were used to assess the impact of a cell’s stage in its life cycle on mutatability and its possible mechanism. The first experiment consisted of a modified fluctuation test
Maurice Samuel Devaraj
doaj
Chimeric diphtheria toxin–CCL8 cytotoxic peptide for breast cancer management
DTCCL8 is a recombinant fusion toxin that targets cancer cells expressing chemokine receptors. By combining diphtheria toxin with CCL8, DTCCL8 binds to multiple receptors on tumor cells and induces selective cytotoxicity. This strategy enables receptor‐mediated targeting of cancer and may support the development of chemokine‐guided therapeutics ...
Bernardo Chavez+5 more
wiley +1 more source
In prostate carcinoma, lactic acid, secreted by highly glycolytic cancer‐associated fibroblasts, is imported into tumor cells through the MCT1 transporter and prevents RSL3 and erastin‐induced ferroptosis (A). Targeting of carbonic anhydrase IX/XII, the main extracellular pH regulators, in tumor and stromal cells reduces microenvironmental acidosis and
Elisa Pardella+18 more
wiley +1 more source
STREPTOMYCIN AND DIHYDROSTREPTOMYCIN
Mode of access: Internet.
Weinstein, Louis, 1909-+1 more
openaire +3 more sources
We generated and characterized clear cell renal cell carcinoma models using the patient‐derived RCC243 cell line—including cell culture, orthotopic, and metastatic tumors—via single‐cell RNA‐sequencing for comparisons between models and patient tumor datasets.
Richard Huang+9 more
wiley +1 more source
THE QUANTITATIVE ESTIMATION OF RADIATION INDUCED MUTATIONS TO STREPTOMYCIN RESISTANCE IN ESCHERICHIA COLI [PDF]
B. A. Rubin
openalex +1 more source
Liver‐specific knockout of N6‐methyladenosine (m6A) methyltransferase METTL3 significantly accelerated hepatic tumor initiation under various oncogenic challenges, contrary to the previously reported oncogenic role of METTL3 in liver cancer cell lines or xenograft models. Mechanistically, METTL3 deficiency reduced m6A deposition on Manf transcripts and
Bo Cui+15 more
wiley +1 more source
The A3 adenosine receptors (A3ARs) are overexpressed in prostate cancer. AR 292 and AR 357, as A3AR antagonists, are capable of blocking proliferation, modulating the expression of drug transporter genes involved in chemoresistance, ferroptosis, and the hypoxia response, and inducing cell death.
Maria Beatrice Morelli+15 more
wiley +1 more source