Results 141 to 150 of about 156,135 (285)

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

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

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

Liposomes as Targets for Toxins [PDF]

open access: yesBiophysical Journal, 2018
Marcelo Ayllon   +3 more
openaire   +1 more source

Hijacking emergency granulopoiesis: Neutrophil ontogeny and reprogramming in cancer

open access: yesMolecular Oncology, EarlyView.
Neutrophils are highly plastic innate immune cells; their functions in cancer extend beyond the tumour microenvironment. This Review summarises current understanding of neutrophil maturation and heterogeneity and highlights tumour‐induced granulopoiesis as a systemic programme that expands immature, immunosuppressive neutrophils via tumour‐derived ...
Gabriela Marinescu, Yi Feng
wiley   +1 more source

Design of a Duplex-to-Complex Structure-Switching Approach for the Homogeneous Determination of Marine Biotoxins in Water

open access: yesToxins
In this report, we describe a fluorescent assay for the detection of six marine toxins in water. The mechanism of detection is based on a duplex-to-complex structure-switching approach.
Awatef Al-Tabban   +5 more
doaj   +1 more source

Proteasome inhibitor, ixazomib prevents topoisomerase‐I degradation and reverses irinotecan resistance in colorectal cancer

open access: yesMolecular Oncology, EarlyView.
Ixazomib inhibits proteasome‐mediated degradation of topoisomerase I induced by irinotecan, thereby restoring drug sensitivity and promoting tumor cell death in colorectal cancer. Irinotecan, a topoisomerase I (topoI) inhibitor, is widely used for colorectal cancer, but resistance remains a major clinical challenge.
Yuho Ebata   +10 more
wiley   +1 more source

Molecular cancer prevention: Intercepting disease

open access: yesMolecular Oncology, EarlyView.
Oncological practice must evolve, from treating established tumours to proactive cancer interception before clinical manifestation. This will require mechanistic insight into tumour initiation, validated biomarkers of early disease development and redesigned clinical trials, enabling cancer interception to become a core pillar of oncology with the ...
Charlotte Grieco   +2 more
wiley   +1 more source

Metastasis on pause: How dormant tumor cells stay hidden within the tumor microenvironment and evade immune surveillance

open access: yesMolecular Oncology, EarlyView.
Dormant cancer cells can hide in distant organs for years, evading treatment and the immune system. This review highlights how signals from the surrounding tissue and immune environment keep these cells inactive or trigger their reawakening. Understanding these mechanisms may help develop therapies to eliminate or control dormant cells and prevent ...
Kanishka Tiwary   +1 more
wiley   +1 more source

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