Results 91 to 100 of about 198,228 (265)

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

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

Study on Algorithm for Flight Plan Pairing Based on SSR Code Set

open access: yes工程科学与技术, 2016
:Aiming at the pairing issue for flight plan which contains a airspace phase but without SSR(secondary surveillance radar) code,a novel method based on SSR code set for matching plan and track was proposed.Firstly,the boundary search algorithm was used ...
林毅, 张建伟, 刘洪
doaj  

CD47 promotes mitogen‐activated protein kinase and epithelial‐to‐mesenchymal transition molecular programs to drive prometastatic phenotypes in non‐small cell lung cancer

open access: yesMolecular Oncology, EarlyView.
Beyond its role in immune evasion, this study identified that CD47 drives tumor‐intrinsic signaling in non‐small cell lung cancer (NSCLC). Transcriptomic profiling and functional studies revealed that CD47 regulates cell adhesion, migration, and metastasis through an ERK–EMT signaling axis.
Asa P.Y. Lau   +8 more
wiley   +1 more source

Lifting Bailey pairs to WP-Bailey pairs

open access: yesDiscrete Mathematics, 2009
A pair of sequences $(α_{n}(a,k,q),β_{n}(a,k,q))$ such that $α_0(a,k,q)=1$ and \[ β_{n}(a,k,q) = \sum_{j=0}^{n} \frac{(k/a; q)_{n-j}(k; q)_{n+j}}{(q;q)_{n-j}(aq;q)_{n+j}}α_{j}(a,k,q) \] is termed a \emph{WP-Bailey Pair}. Upon setting $k=0$ in such a pair we obtain a \emph{Bailey pair}.
McLaughlin, James   +2 more
openaire   +4 more sources

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

A pair of pandemics

open access: yesNew Scientist, 2020
In our fights against covid-19 and obesity, our best weapon is research.
openaire   +2 more sources

The capacity pairing.

open access: yesJournal für die reine und angewandte Mathematik (Crelles Journal), 1993
This paper constructs a new pairing on the Arakelov divisor class group of a regular arithmetic surface, the capacity pairing. It has the same functoriality properties as Arakelov's intersection pairing, but is not in general symmetric. It is normalized by requiring that on sections its value is given by an expression arising in capacity theory; on a ...
Rumely, Robert, CHINBURG, Ted
openaire   +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

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