Results 61 to 70 of about 38,805 (242)

Integrated genomic and proteomic profiling reveals insights into chemoradiation resistance in cervical cancer

open access: yesMolecular Oncology, EarlyView.
A comprehensive genomic and proteomic analysis of cervical cancer revealed STK11 and STX3 as a potential biomarkers of chemoradiation resistance. Our study demonstrated EGFR as a therapeutic target, paving the way for precision strategies to overcome treatment failure and the DNA repair pathway as a critical mechanism of resistance.
Janani Sambath   +13 more
wiley   +1 more source

Loss of the PTCH1 tumor suppressor defines a new subset of plexiform fibromyxoma. [PDF]

open access: yes, 2019
BackgroundPlexiform fibromyxoma (PF) is a rare gastric tumor often confused with gastrointestinal stromal tumor. These so-called "benign" tumors often present with upper GI bleeding and gastric outlet obstruction.
Banerjee, Sudeep   +9 more
core   +1 more source

BCL-W has a fundamental role in B cell survival and lymphomagenesis. [PDF]

open access: yes, 2017
Compromised apoptotic signaling is a prerequisite for tumorigenesis. The design of effective therapies for cancer treatment depends on a comprehensive understanding of the mechanisms that govern cell survival.
Annette S. Kim   +14 more
core   +2 more sources

Emerging role of ARHGAP29 in melanoma cell phenotype switching

open access: yesMolecular Oncology, EarlyView.
This study gives first insights into the role of ARHGAP29 in malignant melanoma. ARHGAP29 was revealed to be connected to tumor cell plasticity, promoting a mesenchymal‐like, invasive phenotype and driving tumor progression. Further, it modulates cell spreading by influencing RhoA/ROCK signaling and affects SMAD2 activity. Rho GTPase‐activating protein
Beatrice Charlotte Tröster   +3 more
wiley   +1 more source

Regulation of c-MYC transcriptional activity by transforming growth factor-beta 1-stimulated clone 22 [PDF]

open access: yes, 2018
c‐MYC stimulates cell proliferation through the suppression of cyclin‐dependent kinase (CDK) inhibitors including P15 (CDKN2B) and P21 (CDKN1A).
Kato Mitsuyasu   +6 more
core   +2 more sources

Modeling hepatic fibrosis in TP53 knockout iPSC‐derived human liver organoids

open access: yesMolecular Oncology, EarlyView.
This study developed iPSC‐derived human liver organoids with TP53 gene knockout to model human liver fibrosis. These organoids showed elevated myofibroblast activation, early disease markers, and advanced fibrotic hallmarks. The use of profibrotic differentiation medium further amplified the fibrotic signature seen in the organoids.
Mustafa Karabicici   +8 more
wiley   +1 more source

Nerve growth factor nonresponsive pheochromocytoma cells: altered internalization results in signaling dysfunction. [PDF]

open access: yes, 1992
Variant rat pheochromocytoma (PC12) cells which fail to respond to nerve growth factor (NGF) (PC12nnr5) (Green, S. H., R. E. Rydel, J. L. Connoly, and L. A. Greene. 1986. J. Cell Biol. 102:830-843) bind NGF at both high and low affinity sites.
Bradshaw, RA, Eveleth, DD
core  

Nuclear Translocation of Extradenticle Requires homothorax, which Encodes an Extradenticle-Related Homeodomain Protein [PDF]

open access: yes, 1997
We show that homothorax (hth) is required for the Hox genes to pattern the body of the fruit fly, Drosophila melanogaster. hth is necessary for the nuclear localization of an essential HOX cofactor, Extradenticle (EXD), and encodes a homeodomain protein ...
Aspland   +55 more
core   +1 more source

A synthetic benzoxazine dimer derivative targets c‐Myc to inhibit colorectal cancer progression

open access: yesMolecular Oncology, EarlyView.
Benzoxazine dimer derivatives bind to the bHLH‐LZ region of c‐Myc, disrupting c‐Myc/MAX complexes, which are evaluated from SAR analysis. This increases ubiquitination and reduces cellular c‐Myc. Impairing DNA repair mechanisms is shown through proteomic analysis.
Nicharat Sriratanasak   +8 more
wiley   +1 more source

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

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