Results 161 to 170 of about 8,072,886 (297)

Differential expression of cancer‐related genes supports prediction of poor response to first‐line treatments in T‐ALL pediatric patients with high minimal residual disease

open access: yesMolecular Oncology, EarlyView.
In the present work, we have identified a transcriptional signature based on the differential expression of six genes (BCL2&MAST4, HSH2D&LAT2, METRN&PITPNM2) that would facilitate the early detection of T‐cell acute lymphoblastic leukemia (T‐ALL) patients prone to a poor treatment response and could be implemented at diagnosis, along with other risk ...
Antonio Lahera   +11 more
wiley   +1 more source

Commentary: Less is more in thoracic surgeryCentral Message

open access: yesJTCVS Techniques, 2022
Shoji Okado, MD   +1 more
doaj   +1 more source

Less is more: downsampling x-ray images improves pose estimation accuracy. [PDF]

open access: yesMed Eng Phys
Williams DE   +4 more
europepmc   +1 more source

CCDC80 suppresses high‐grade serous ovarian cancer migration via negative regulation of B7‐H3

open access: yesMolecular Oncology, EarlyView.
PAX8 is a lineage‐specific master regulator of transcription in high‐grade serous ovarian cancer (HGSC) progression. We show for the first time that PAX8 facilitates proliferation and metastasis by repressing the cell autonomous tumor suppressor CCDC80 and inducing B7‐H3 expression.
Aya Saleh   +12 more
wiley   +1 more source

Less is more: inverting the paradigm across the cancer care continuum. [PDF]

open access: yesEClinicalMedicine
Vos JAM   +2 more
europepmc   +1 more source

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

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

Hepatitis C therapy in 2011: is less more, is more less?

open access: yesBrazilian Journal of Infectious Diseases
Evaldo Stanislau Affonso de Araújo
doaj   +1 more source

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