p53 pathway dysfunction in AML: beyond mutations.

Oncotarget

Alfonso Quintás-Cardama: TCR2 Therapeutics, Cambridge, MA, USA.

Published: December 2017


Category Ranking

98%

Total Visits

921

Avg Visit Duration

2 minutes

Citations

20

Article Abstract

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5752443PMC
http://dx.doi.org/10.18632/oncotarget.22713DOI Listing

Publication Analysis

Top Keywords

p53 pathway
4
pathway dysfunction
4
dysfunction aml
4
aml mutations
4
p53
1
dysfunction
1
aml
1
mutations
1

Similar Publications

Background: Gastric cancer (GC) is the fourth leading cause of cancer-related death globally. Tumor profiling has revealed actionable gene alterations that guide treatment strategies and enhance survival. Among Hispanics living in Puerto Rico (PRH), GC ranks among the top 10 causes of cancer-related death.

View Article and Find Full Text PDF

Aurora kinase A (AURKA) is a serine/threonine kinase that plays a critical role in cell cycle regulation, particularly during mitosis. Recent studies have identified AURKA as an oncogene overexpressed in various cancers, including gastric cancer (GC). This review summarizes the molecular mechanisms by which AURKA contributes to GC pathogenesis, including its roles in cell proliferation, apoptosis inhibition, epithelial-mesenchymal transition (EMT), and cancer stemness.

View Article and Find Full Text PDF

Ovarian cancer remains a major health threat with limited treatment options available. It is characterized by immunosuppressive tumor microenvironment (TME) maintained by tumor-associated macrophages (TAMs) hindering anti-tumor responses and immunotherapy efficacy. Here we show that targeting retinoblastoma protein (Rb) by disruption of its LxCxE cleft pocket causes preferential cell death in Rbhigh M2 polarized or M2-like Rbhigh immunosuppressive TAMs by induction of ER stress, p53 and mitochondria-related cell death pathways.

View Article and Find Full Text PDF

Patients with metastatic colorectal cancer (mCRC) to the liver exhibit poor survival rates. Chemotherapy combined with anti-vascular therapy has emerged as the standard treatment, but resistance to anti-VEGFA therapy inevitably develops. The metabolic reprogramming of tumor vascular endothelial cells (TECs) plays a crucial, yet still poorly understood, role in the development of therapeutic resistance.

View Article and Find Full Text PDF

Tumor antigen PRAME promotes melanoma growth by inactivating p53 through the SIRT1-DBC1 axis.

Oncogene

September 2025

Department of Integrative Bioscience and Biotechnology, Sejong University, 209 Neungdong-ro, Gwangjin-gu, Seoul, 05006, South Korea.

Preferentially expressed antigen in melanoma (PRAME), which is highly expressed in melanoma, is associated with tumor progression and malignancy. Notably, melanoma cells often exhibit inactivation of the tumor suppressor p53 despite carrying the wild-type p53 gene. Here, we investigated the functional interplay between PRAME and p53.

View Article and Find Full Text PDF