Results 91 to 100 of about 342,417 (266)

Mutant NPM1 in Acute Myeloid Leukemia Initiation and Maintenance

open access: yesAging and Cancer, EarlyView.
NPM1 mutations drive acute myeloid leukemia by acting as neomorphic transcriptional regulators that cooperate with Menin–MLL and XPO1 to sustain HOX/MEIS1 expression and block differentiation. Targeting these mutant‐specific transcriptional dependencies provides a rational therapeutic strategy for NPM1‐mutated AML.
Yanan Jiang   +3 more
wiley   +1 more source

Oncolytic virus-mediated p53 activation boosts the antitumor immunity of a p53-transduced dendritic cell vaccine

open access: yesnpj Vaccines
Dendritic cells (DCs) transduced with replication-deficient, wild-type human p53-expressing adenovirus Ad-p53 (Ad-p53 DCs) induce p53-targeting cytotoxic T lymphocytes (CTLs).
Motohiko Yamada   +15 more
doaj   +1 more source

Unraveling the Role of TP53 in Colorectal Cancer Therapy: From Wild-Type Regulation to Mutant

open access: yesFrontiers in Bioscience-Landmark
The p53, a pivotal tumor suppressor, regulates various cellular responses, including DNA repair and apoptosis. Normally, p53 levels are low due to murine double minute clone 2 (MDM2) mediated polyubiquitination.
Wenshu Li   +6 more
doaj   +1 more source

The mutational status of p53 can influence its recognition by human T-cells

open access: yesOncoImmunology, 2017
p53 was reported to be an attractive immunotherapy target because it is mutated in approximately half of human cancers, resulting in its inactivation and often accumulation in tumor cells.
Katerina Shamalov   +3 more
doaj   +1 more source

Mitochondrially targeted p53 or DBD subdomain is superior to wild type p53 in ovarian cancer cells even with strong dominant negative mutant p53

open access: yesJournal of Ovarian Research, 2019
Background While tumor suppressor p53 functions primarily as a transcription factor in the nucleus, cellular stress can cause p53 to translocate to the mitochondria and directly trigger a rapid apoptotic response. We have previously shown that fusing p53
Phong Lu   +5 more
doaj   +1 more source

Risk Prediction Models for Recurrence After Curative Treatment of Early‐Stage or Locally Advanced Lung Cancer: A Systematic Review

open access: yesAging and Cancer, EarlyView.
This systematic review synthesizes prognostic models for survival and recurrence in resected non‐small cell lung cancer. While many models demonstrate moderate to good discrimination, few are externally validated and reporting quality is variable, limiting clinical applicability and highlighting the need for robust, transparent model development ...
Evangeline Samuel   +4 more
wiley   +1 more source

β‐Catenin/c‐Myc Axis Modulates Autophagy Response to Different Ammonia Concentrations

open access: yesAdvanced Biology, Volume 9, Issue 3, March 2025.
Ammonia, detoxified by the liver into urea and glutamine, impacts autophagy differently at varying levels. Low ammonia activates autophagy via c‐Myc and β‐catenin, while high levels suppress it. Using Huh7 cells and Spf‐ash mice, c‐Myc's role in cytoprotective autophagy is revealed, offering insights into hyperammonemia and potential therapeutic ...
S. Sergio   +11 more
wiley   +1 more source

Chromosomal Instability Drives Glioblastoma Heterogeneity and Therapeutic Opportunities

open access: yesAdvanced Science, EarlyView.
ABSTRACT Glioblastoma, the most aggressive and lethal form of brain cancer, is defined by profound genomic instability, with Chromosomal Instability (CIN) playing a central role in driving tumor progression, therapy resistance, and poor prognosis. CIN is characterized by numerical and structural alterations, is driven by mechanisms such as mitotic ...
Amarnath Pal   +3 more
wiley   +1 more source

Targeting oncogenic mutant p53 for cancer therapy

open access: yesFrontiers in Oncology, 2015
Among genetic alterations in human cancers, mutations in the tumor suppressor p53 gene are the most common, occurring in over 50% of human cancers. The majority of p53 mutations are missense mutations and result in the accumulation of dysfunctional p53 ...
Tomoo eIwakuma, Alejandro eParrales
doaj   +1 more source

PD‐1 Inhibits CD4+ TRM‐Mediated cDC1 Mobilization via Suppressing JAML in Human NSCLC

open access: yesAdvanced Science, EarlyView.
CD4+ tissue‐resident memory T cells (TRMs) in non‐small cell lung cancer recruit conventional type 1 dendritic cells via XCL1‐XCR1 signaling, orchestrating antitumor immunity. The costimulatory molecule JAML is essential for this process. PD‐1 blockade restores JAML expression and cDC1 mobilization, while JAML agonists synergize with anti‐PD‐1 therapy,
Zheyu Shao   +16 more
wiley   +1 more source

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