Results 111 to 120 of about 2,851,507 (299)

Journal of Proton Therapy: Call for Papers

open access: yes, 2015
Journal of Proton Therapy (JPT) is an international open access, peer-reviewed journal, which publishes original research, technical reports, reviews, case reports, editorials, and other materials on proton therapy with focus on radiation oncology ...
Proton Therapy, Journal of
core  

Castration‐resistant prostate cancer cells are addicted to the high activity of cyclin‐dependent kinase 2

open access: yesMolecular Oncology, EarlyView.
We show that emergence of castration‐resistant prostate (CRPC) is associated with significant upregulation of cyclins that positively regulate cyclin‐dependent kinase 2 (CDK2) and concomitant downregulation of CDK4 cyclins. This renders CRPC cells dependent on the high activity of CDK2, and CDK2 inhibitors synergistically sensitize CRPC cells to both ...
Joyeeta Chatterjee   +3 more
wiley   +1 more source

Characteristics of Users and New Initiators of Single- and Multiple-Inhaler Triple Therapy for Chronic Obstructive Pulmonary Disease in Germany

open access: yesInternational Journal of COPD
Kai-Michael Beeh,1 Kieran J Rothnie,2 Jing Claussen,3 Fränce Hardtstock,4 Rachel K Knapp,4 Thomas Wilke,5 Alexandrosz Czira,2 Chris Compton,6 Afisi S Ismaila7,8 1Insaf Respiratory Research Institute, Wiesbaden, Germany; 2Value Evidence and Outcomes, R&D ...
Beeh KM   +8 more
doaj  

Producing high-quantity and high-quality recombinant adeno-associated virus by low-cis triple transfection [PDF]

open access: yes
Recombinant adeno-associated virus (rAAV)-based gene therapy is entering clinical and commercial stages at an unprecedented pace. Triple transfection of HEK293 cells is currently the most widely used platform for rAAV manufacturing.
Liu, Hao   +19 more
core   +1 more source

Partial FAK suppression promotes tumor growth, an effect reversed by macrophage p110δ PI3K inactivation

open access: yesMolecular Oncology, EarlyView.
Partial inhibition of focal adhesion kinase (FAK) can paradoxically promote tumor growth, rather than simply producing a weaker antitumor effect than that observed with strong FAK suppression. In breast cancer and melanoma models, targeting p110δ PI3K, particularly in macrophages, counteracted these tumor‐promoting effects, highlighting the importance ...
Lydia Xenou   +4 more
wiley   +1 more source

Unraveling the epigenetic code in cancer cell–tumor microenvironment crosstalk

open access: yesMolecular Oncology, EarlyView.
Epigenetic regulation is a key driver of cancer development and progression. Diverse epigenetic alterations in cancer cells and components of the tumor microenvironment (TME) orchestrate their communication through multiple mechanisms. We discuss how the epigenetic code coordinates bidirectional cancer cell–TME crosstalk to promote cancer progression ...
Ji Hoon Park, Mi‐Young Kim
wiley   +1 more source

Clarithromycin‐based triple therapies [PDF]

open access: yesAlimentary Pharmacology & Therapeutics, 1999
J, Huang, R H, Hunt
openaire   +2 more sources

Arginine methylation as a regulatory ratchet in cancer: From substrate selection to malignant‐state stabilization

open access: yesMolecular Oncology, EarlyView.
Arginine methylation can be viewed as a persistence‐prone post‐translational modification regulated by a network of PRMTs. Competitive and compensatory interactions among PRMTs can redistribute methylation across substrate pools shaped by sequence, structural, spatial, and environmental layers, reinforcing RNA‐processing, chromatin, and signaling ...
So Hyun Kwon, Ji Min Lee
wiley   +1 more source

The role of treatment regimen and duration in treating patients with Mycobacterium avium complex lung disease: A real-world experience and case–control study

open access: yesJournal of Microbiology, Immunology and Infection
Purpose: The treatment advantage of guideline-based therapy (GBT) in Mycobacterium avium complex lung disease (MAC-LD) is well-known. However, GBT is not always feasible.
Ping-Huai Wang   +4 more
doaj   +1 more source

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

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