Results 121 to 130 of about 1,705,451 (305)

Mechanisms and therapeutic opportunities of the ribotoxic stress response in cancer

open access: yesMolecular Oncology, EarlyView.
Cancer cells' high translational demand creates opportunities to therapeutically target ribosome function. Ribosome stalling and collisions activate ZAKα and the ribotoxic stress response (RSR), which can trigger rapid, p53‐independent apoptosis in cancer.
Anastassiya Kim   +7 more
wiley   +1 more source

Combining chemotherapeutic agents and netrin‐1 interference potentiates cancer cell death

open access: yesEMBO Molecular Medicine, 2013
The secreted factor netrin‐1 is upregulated in a fraction of human cancers as a mechanism to block apoptosis induced by netrin‐1 dependence receptors DCC and UNC5H. Targeted therapies aiming to trigger tumour cell death via netrin‐1/receptors interaction
Andrea Paradisi   +12 more
doaj   +1 more source

Profiling neoadjuvant therapy response in rectal cancer using meta‐analysis of publicly available transcriptomic RNA‐seq datasets

open access: yesMolecular Oncology, EarlyView.
This study integrates publicly available transcriptomic datasets to identify molecular signatures associated with response to neoadjuvant chemoradiotherapy in locally advanced rectal cancer. By analyzing a combination of multiple cohorts with bioinformatics approaches, we reveal biological pathways and immune‐related features that may improve ...
Aleksandra Stanojevic   +10 more
wiley   +1 more source

Plasticity in growth behavior of patients' acute myeloid leukemia stem cells growing in mice

open access: yesHaematologica, 2020
Sarah Ebinger   +12 more
doaj   +1 more source

The VHL tumor suppressor at the crossroad of protein folding, aggregation, and cancer

open access: yesMolecular Oncology, EarlyView.
Mutations, environmental stress, and chaperone dysfunction can destabilize pVHL, promoting its conversion from the native folded state into amyloid‐like assemblies. This transition may contribute to protein storage, cell dormancy, survival, and drug resistance.
Lara Abad   +2 more
wiley   +1 more source

Apoptosis and Cancer

open access: yes, 2010
This is a web-based study guide on the mechanism of apoptosis, how its is activated, details on the role of caspases and extrinsic and intrinsic signalling pathways in apoptosis that are dergulated in cancer. It also includes a formative quiz, printable
Dr. Momna Hejmadi, University of Bath, UK
core  

Bufadienolide compounds sensitize human breast cancer cells to TRAIL-induced apoptosis via inhibition of STAT3/Mcl-1 pathway

open access: yes, 2011
The death receptor ligand TRAIL is considered a promising candidate for cancer therapy because of its preferential toxicity to malignant cells. However its efficacy has been challenged by a number of resistance mechanisms.
Dong, Yinhui   +11 more
core   +1 more source

Extracellular vesicle lipidomics liquid biopsy reveals systemic and tumor microenvironment metabolic reprogramming in ovarian cancer

open access: yesMolecular Oncology, EarlyView.
Extracellular vesicle (EV) lipidomic profiling of plasma and ascites from patients with high‐grade serous ovarian cancer and of ovarian cancer cell lines reveals enrichment of triglycerides (TGs), diacylglycerols (DGs), phosphatidylcholine (PCs), sphingomyelins (SMs), reflecting tumor metabolic reprogramming.
Shikha Rani   +9 more
wiley   +1 more source

Predictive and prognostic biomarkers of Bacillus Calmette‐Guérin therapy failure in bladder cancer patients: A systematic review

open access: yesMolecular Oncology, EarlyView.
High‐risk bladder cancer is typically treated with Bacillus Calmette‐Guérin (BCG), but 30–40% of patients relapse. No FDA‐ or CE‐approved biomarkers currently predict or prognosticate BCG failure. We systematically reviewed the literature and identified 72 eligible studies, revealing several promising biomarkers associated with BCG treatment response ...
Rui Ribeiro‐Pereira   +7 more
wiley   +1 more source

NAPRT loss promotes lung tumor initiation and growth through AKT signaling independently of NAD+ biosynthesis

open access: yesMolecular Oncology, EarlyView.
Loss of NAPRT promotes lung tumor initiation and growth through a noncanonical mechanism, independent of its role in NAD+ biosynthesis. Mechanistically, NAPRT depletion activates the mTORC2‐driven AKT/β‐catenin signaling axis to enhance clonogenic and invasive phenotypes. Furthermore, lung‐specific Naprt deletion significantly increases tumor burden in
Myung Joon Oh   +11 more
wiley   +1 more source

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