Results 131 to 140 of about 221,871 (288)

Adaptaquin is selectively toxic to glioma stem cells through disruption of iron and cholesterol metabolism

open access: yesMolecular Oncology, EarlyView.
Adaptaquin selectively kills glioma stem cells while sparing differentiated brain cells. Transcriptomic and proteomic analyses show Adaptaquin disrupts iron and cholesterol homeostasis, with iron chelation amplifying cytotoxicity via cholesterol depletion, mitochondrial dysfunction, and elevated reactive oxygen species.
Adrien M. Vaquié   +16 more
wiley   +1 more source

Patient‐specific pharmacogenomics demonstrates xCT as predictive therapeutic target in colon cancer with possible implications in tumor connectivity

open access: yesMolecular Oncology, EarlyView.
This study integrates transcriptomic profiling of matched tumor and healthy tissues from 32 colorectal cancer patients with functional validation in patient‐derived organoids, revealing dysregulated metabolic programs driven by overexpressed xCT (SLC7A11) and SLC3A2, identifying an oncogenic cystine/glutamate transporter signature linked to ...
Marco Strecker   +16 more
wiley   +1 more source

Predictors of response and rational combinations for the novel MCL‐1 inhibitor MIK665 in acute myeloid leukemia

open access: yesMolecular Oncology, EarlyView.
This study characterizes the responses of primary acute myeloid leukemia (AML) patient samples to the MCL‐1 inhibitor MIK665. The results revealed that monocytic differentiation is associated with MIK665 sensitivity. Conversely, elevated ABCB1 expression is a potential biomarker of resistance to the treatment, which can be overcome by the combination ...
Joseph Saad   +17 more
wiley   +1 more source

Feasibility of a ctDNA multigenic panel for non‐small‐cell lung cancer early detection and disease surveillance

open access: yesMolecular Oncology, EarlyView.
Plasma‐based detection of actionable mutations is a promising approach in lung cancer management. Analysis of ctDNA with a multigene NGS panel identified TP53, KRAS, and EGFR as the most frequently altered, with TP53 and KRAS in treatment‐naïve patients and TP53 and EGFR in previously treated patients.
Giovanna Maria Stanfoca Casagrande   +11 more
wiley   +1 more source

Aggressive prostate cancer is associated with pericyte dysfunction

open access: yesMolecular Oncology, EarlyView.
Tumor‐produced TGF‐β drives pericyte dysfunction in prostate cancer. This dysfunction is characterized by downregulation of some canonical pericyte markers (i.e., DES, CSPG4, and ACTA2) while maintaining the expression of others (i.e., PDGFRB, NOTCH3, and RGS5).
Anabel Martinez‐Romero   +11 more
wiley   +1 more source

Comparison of Maternal Anxiety between Primigravid Women and Pregnant Women with the History of Previous Fetal or Neonatal Death

open access: yesنشریه پرستاری ایران, 2006
Background & Aim: Pregnancy is a significant event for pregnant women who need to adapt physiologically and psychologically, though it is a normal phase of a woman’s life.
M. Ahadi   +3 more
doaj  

Tumor and germline testing with next generation sequencing in epithelial ovarian cancer: a prospective paired comparison using an 18‐gene panel

open access: yesMolecular Oncology, EarlyView.
Genetic testing in epithelial ovarian cancer includes both germline and tumor‐testing. This approach often duplicates resources. The current prospective study assessed the feasibility of tumor‐first multigene testing by comparing tumor tissue with germline testing of peripheral blood using an 18‐gene NGS panel in 106 patients.
Elisabeth Spenard   +12 more
wiley   +1 more source

Survivin and Aurora Kinase A control cell fate decisions during mitosis

open access: yesMolecular Oncology, EarlyView.
Aurora A interacts with survivin during mitosis and regulates its centromeric role. Loss of Aurora A activity mislocalises survivin, the CPC and BubR1, leading to disruption of the spindle checkpoint and triggering premature mitotic exit, which we refer to as ‘mitotic slippage’.
Hana Abdelkabir   +2 more
wiley   +1 more source

CDK11 inhibition induces cytoplasmic p21WAF1 splice variant by p53 stabilisation and SF3B1 inactivation

open access: yesMolecular Oncology, EarlyView.
CDK11 inhibition stabilises the tumour suppressor p53 and triggers the production of an alternative p21WAF1 splice variant p21L, through the inactivation of the spliceosomal protein SF3B1. Unlike the canonical p21WAF1 protein, p21L is localised in the cytoplasm and has reduced cell cycle‐blocking activity.
Radovan Krejcir   +12 more
wiley   +1 more source

Improving statistical reporting in psychology. [PDF]

open access: yesCommun Psychol
Schubert AL   +3 more
europepmc   +1 more source

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