Results 151 to 160 of about 105,849 (264)

Ryūkyū-Rettō : Sawada, Sheet 3121-IV, AMS L791, 1952, 2e

open access: yes, 1952
Scale 1:50,000. maps : color ; 37 x 51 cm or smaller. Relief shown by contours and spot heights. Contour interval 20 meters. Japanese place names transcribed according to the modified Hepburn (Romaji) system.
United States. Army Map Service.
core  

KDM7A and KDM1A inhibition suppresses tumour promoting pathways in prostate cancer

open access: yesMolecular Oncology, EarlyView.
Treatment resistance is a major challenge for patients with advanced prostate cancer. This study examined an alternative approach to target the major prostate cancer‐promoting pathway by targeting epigenetic factors, whose levels are higher in tumours.
Jennie N Jeyapalan   +16 more
wiley   +1 more source

Ryūkyū-Rettō : Aha, Sheet 3727-II, AMS L791, 1951, 2e

open access: yes, 1951
Scale 1:50,000. maps : color ; 37 x 51 cm or smaller. Relief shown by contours and spot heights. Contour interval 20 meters. Japanese place names transcribed according to the modified Hepburn (Romaji) system.
United States. Army Map Service.
core  

Heterozygous loss‐of‐function alleles associate the conserved 3′‐5′ exoribonuclease EXOSC10 with hypersensitivity to the anticancer drug 5‐fluorouracil

open access: yesMolecular Oncology, EarlyView.
EXOSC10, an essential nuclear RNA exosome‐associated 3′‐5′ exoribonuclease, is inhibited by the anticancer drug 5‐fluorouracil (5‐FU), and EXOSC10 depletion increases 5‐FU sensitivity. The colon‐cancer variant EXOSC10S402T, located in a proteolysis motif, is stable and nuclear but nonfunctional in vivo.
Radhika Sain   +10 more
wiley   +1 more source

Sheet L-51-T

open access: yes, 1946
Scale 1:250,000. Approximately 282 maps : color ; 45 x 35 cm or smaller. Relief shown by contours, hachures, and spot heights. "Prepared under the direction of the Chief of Engineers by the Army Map Service (AM), U.S.
United States. Army Map Service.
core  

Cell‐cycle‐specific lesion evolution rather than inhibition of double‐strand‐break repair underpins cisplatin radiosensitization

open access: yesMolecular Oncology, EarlyView.
We analyze cisplatin–DNA adducts (CDAs) and double‐strand breaks (DSBs) in a cell‐cycle‐dependent manner. We find that CDAs form similarly across all cell cycle phases. DSBs arise only in S‐phase. CDAs might not directly impair DSB repair, but S‐phase DSB lesions evolve in the presence of CDAs and disrupt repair in G2, also causing radiosensitization ...
Ye Qiu   +10 more
wiley   +1 more source

Sheet K-51-F

open access: yes, 1945
Scale 1:250,000. Approximately 282 maps : color ; 45 x 35 cm or smaller. Relief shown by contours, hachures, and spot heights. "Prepared under the direction of the Chief of Engineers by the Army Map Service (AM), U.S.
United States. Army Map Service.
core  

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