Results 111 to 120 of about 4,670,790 (255)

The impact of a UK HIV-1 resistance database for the management and improvement of the clinical care of people living with HIV-1 [PDF]

Background: The introduction of highly active antiretroviral therapies (HAART) in 1996 to treat patients living with the human immunodeficiency virus type 1 (HIV-1), led to dramatic improvements in their mortality and morbidity.
MacRae, Eilidh
core   +3 more sources

Characteristics of HIV-1 natural drug resistance-associated mutations in former paid blood donors in Henan Province, China.

PLoS ONE, 2014
BackgroundNatural drug resistance is a major cause of antiviral treatment failure. The characteristics of HIV-1 natural drug resistance-associated mutations in former paid blood donors in Henan Province remain unclear.MethodsOne hundred and fifty HIV-1 ...
Yi Bao, Di Tian, Ying-Ying Zheng, Hong-Li Xi, Dan Liu, Min Yu, Xiao-Yuan Xu   +6 more
doaj   +1 more source

Developmental programmes drive cellular plasticity, disease progression and therapy resistance in lung adenocarcinoma

Molecular Oncology, EarlyView.
This study shows that lung adenocarcinomas exploit developmental branching morphogenesis to acquire a therapy resistant basal‐like tumour cell state. This process was found to be regulated by combined TP53 loss‐of‐function and type‐I interferon signalling, identifying a novel axis for biomarker and therapeutic target discovery.
Kamila J Bienkowska, Stephany Gallardo, Nur S. Zainal, Leena Arora, Matthew Ellis, Maria‐Antoinette Lopez, Judith Austine, Sai Pittla, Serena J Chee, Aiman Alzetani, Emily C Shaw, Christian H Ottensmeier, Gareth J Thomas, Christopher J Hanley   +13 more
wiley   +1 more source

Molecular basis of telaprevir resistance due to V36 and T54 mutations in the NS3-4A protease of the hepatitis C virus [PDF]

, 2008
Background The inhibitor telaprevir (VX-950) of the hepatitis C virus (HCV) protease NS3-4A has been tested in a recent phase 1b clinical trial in patients infected with HCV genotype 1. This trial revealed residue mutations that confer varying degrees of
Stefan Zeuzem, Albrecht, M., Hartmann, Christoph, Mayr, G., Andreas Schlicker, Welsch, C., Sarrazin, C., Susser, Simone, Sarrazin, Christoph, Lengauer, T., Albrecht, Mario, Christoph Welsch, Thomas Lengauer, Christoph Sarrazin, Antes, I., Mayr, Gabriele, Iris Antes, Simone Susser, Gabriele Mayr, Lengauer, Thomas, Susser, S., Zeuzem, S., Hartmann, C., Christoph Hartmann, Mario Albrecht, Schlicker, A., Francisco S Domingues, Domingues, Francisco S., Domingues, F., Welsch, Christoph, Schlicker, Andreas, Antes, Iris, Zeuzem, Stefan   +32 more
core   +1 more source

Stimulator of interferon genes agonist augmented antitumor immunity of osimertinib in Egfr‐mutated lung cancer

Molecular Oncology, EarlyView.
Combining osimertinib with the STING agonist ADU‐S100 activates innate and adaptive immunity to overcome the non‐inflamed microenvironment of Egfr‐mutant lung cancer. This combination increases NK and CD8+ T‐cell infiltration, associated with activation of the STING‐IRF3 pathway and local immunogenic cell death.
Jun Nishimura, Tadahiro Kuribayashi, Johannes Brägelmann, Sachi Okawa, Masataka Taoka, Shunta Mori, Tomoka Nishimura, Takaaki Tanaka, Go Makimoto, Kiichiro Ninomiya, Kammei Rai, Eiki Ichihara, Ryohei Katayama, Katsuyuki Hotta, Masahiro Tabata, Yosuke Togashi, Yoshinobu Maeda, Martin L. Sos, Katsuyuki Kiura, Kadoaki Ohashi   +19 more
wiley   +1 more source

MOLECULAR MECHANISMS OF DRUG RESISTANCE IN CANDIDA ALBICANS: ROLE OF TRANSCRIPTION FACTORS MCM1 AND ADA2 [PDF]

, 2011
Candida albicans is an opportunistic fungal pathogen responsible for localized as well as disseminated infections. C. albicans is the most commonly isolated specie from blood cultures, accounting for over 60% of all Candida isolates. The fungistatic drug
MOGAVERO, SELENE
core  

Loss of IGF‐1R impairs DNA‐PKcs recruitment to chromatin leading to defective end‐joining

Molecular Oncology, EarlyView.
IGF‐1R promotes radioresistance by facilitating DNA‐PKcs recruitment to chromatin, enabling non‐homologous end‐joining (NHEJ) repair of double‐strand breaks. Inhibition or loss of IGF‐1R disrupts this recruitment to damage sites, driving compensatory reliance on microhomology‐mediated end‐joining (MMEJ) repair.
Matthew O. Ellis, Jack V. Mills, Wojciech Niedzwiedz, Valentine M. Macaulay   +3 more
wiley   +1 more source

MITF maintains genome stability in nonmelanocyte lineages

Molecular Oncology, EarlyView.
MITF is essential for melanocyte survival and acts as an oncogene in 10%–20% of melanomas. We show that MITF depletion causes genome instability in nonmelanocytic cells, leading to LATS2‐mediated P53 activation, cell cycle arrest, and apoptosis. This study highlights the role of MITF as a genome maintenance factor beyond the melanocyte lineage. Created
Drifa H. Gudmundsdottir, Adrián López García de Lomana, Thejus B. Venkatesh, Kritika Kirty, Snaevar Sigurdsson, Linda Vidarsdottir, Ramile Dilshat, Erla Sveinbjornsdottir, Snaedis Ragnarsdottir, Daniel H Magnusson, Maria R. Bustos, Eirikur Steingrimsson, Thorkell Gudjonsson, Stefan Sigurdsson   +13 more
wiley   +1 more source

Concurrence of Plasmodium falciparum dhfr and crt mutations in northern Ghana. [PDF]

, 2005
BACKGROUND: Both chloroquine (CQ) and sulfadoxine-pyrimethamine (SP) are failing drugs in much of sub-Saharan Africa. Previous findings suggest an association between resistance to CQ and to SP in vivo, in vitro, and on the molecular level.
Bousema J Teun, Sauerwein, Robert W, Teunis A Eggelte, Bousema, J. Teun, Bienzle Ulrich, Bousema, J Teun, Ehrhardt, Stephan, Eggelte Teunis A, Mockenhaupt Frank P, Otchwemah, Rowland N., Ehrhardt Stephan, Otchwemah, Rowland N, Bienzle, Ulrich, Mockenhaupt, Frank P., Mockenhaupt, Frank P, J Teun Bousema, Rowland N Otchwemah, Eggelte, Teunis A, Eggelte, Teunis A., Ulrich Bienzle, Stephan Ehrhardt, Otchwemah Rowland N, Sauerwein Robert W, Frank P Mockenhaupt, Robert W Sauerwein, Sauerwein, Robert W.   +25 more
core   +1 more source

A novel quinazolinone insulin receptor inhibitor and its synergy with an EGFR inhibitor in glucose‐driven glioblastoma

Molecular Oncology, EarlyView.
The novel styrylquinazolinone‐based molecule W1B effectively suppresses glioblastoma by inhibiting IGF1R and EGFR. In high‐glucose microenvironments driving tumor resistance, W1B acts synergistically with the EGFR inhibitor dacomitinib. This combination safely blocks compensatory survival signaling in zebrafish xenograft models. Showcasing promising in
Patryk Rurka, Wioleta Cieślik, Wojciech Płaziński, Katarzyna Stępnik, Anna Boguszewska‐Czubara, Elżbieta Kot, Robert Musioł, Mateusz Jasica, Anna Mrozek‐Wilczkiewicz, Katarzyna Malarz   +9 more
wiley   +1 more source