Results 111 to 120 of about 19,205,329 (382)

The c-MYC-AP4-p21 cascade [PDF]

Cell Cycle, 2009
The p21 gene encodes a CDK-inhibitor, which is induced by p53 and many other anti-proliferative factors. The mechanism of transcriptional repression of p21 by c-MYC has been a subject of intensive study for several years, as it may explain how c-MYC promotes cell cycle progression.
Peter, Jung, Heiko, Hermeking
openaire   +2 more sources

Intein‐based modular chimeric antigen receptor platform for specific CD19/CD20 co‐targeting

Molecular Oncology, EarlyView.
CARtein is a modular CAR platform that uses split inteins to splice antigen‐recognition modules onto a universal signaling backbone, enabling precise, scarless assembly without re‐engineering signaling domains. Deployed here against CD19 and CD20 in B‐cell malignancies, the design supports flexible multi‐antigen targeting to boost T‐cell activation and
Pablo Gonzalez‐Garcia, Noelia Moares, Wenjie Yi‐He, Rosa Luna‐Espejo, Ricardo Fernandez‐Cisnal, Javier Ocaña‐Cuesta, Juan P. Muñoz‐Miranda, Antonio Gabucio, Cecilia M. Fernandez‐Ponce, Francisco Garcia‐Cozar   +9 more
wiley   +1 more source

Glutathione Depletion Induced by c-Myc Downregulation Triggers Apoptosis on Treatment with Alkylating Agents

Neoplasia: An International Journal for Oncology Research, 2004
Here we investigate the mechanism(s) involved in the c-Myc-dependent drug response of melanoma cells. By using three M14-derived c-Myc low-expressing clones, we demonstrate that alkylating agents, cisplatin and melphalan, trigger apoptosis in the c-Myc ...
Annamaria Biroccio, Barbara Benassi, Francesco Fiorentino, Gabriella Zupi   +3 more
doaj   +1 more source

Brief report: RRx-001 is a c-Myc inhibitor that targets cancer stem cells. [PDF]

, 2018
The goal of anticancer therapy is to selectively eradicate all malignant cells. Unfortunately for the majority of patients with metastatic disease, this goal is consistently thwarted by the nearly inevitable development of therapeutic resistance; the ...
Cabrales, Pedro, Caroen, Scott, Carter, Corey A, Oronsky, Arnold, Oronsky, Bryan, Reid, Tony R   +5 more
core   +2 more sources

Class IIa HDACs forced degradation allows resensitization of oxaliplatin‐resistant FBXW7‐mutated colorectal cancer

Molecular Oncology, EarlyView.
HDAC4 is degraded by the E3 ligase FBXW7. In colorectal cancer, FBXW7 mutations prevent HDAC4 degradation, leading to oxaliplatin resistance. Forced degradation of HDAC4 using a PROTAC compound restores drug sensitivity by resetting the super‐enhancer landscape, reprogramming the epigenetic state of FBXW7‐mutated cells to resemble oxaliplatin ...
Vanessa Tolotto, Nicolò Gualandi, Ylenia Cortolezzis, Raffaella Picco, Monica Colitti, Francesca D'Este, Mariachiara Gani, Wayne W. Hancock, Giovanni Terrosu, Cristina Degrassi, Francesca Agostini, Claudio Brancolini, Luigi E. Xodo, Eros Di Giorgio   +13 more
wiley   +1 more source

Novel Indolocarbazole Derivative 12-(α-L-arabinopyranosyl)indolo[2,3-a]pyrrolo[3,4-c]carbazole-5,7-dione Is a Preferred c-Myc Guanine Quadruplex Ligand

Journal of Nucleic Acids, 2011
The indolocarbazole derivative 12-(α-L-arabinopyranosyl)indolo[2,3-a]pyrrolo[3,4-c]carbazole-5,7-dione (AIC) has demonstrated a high potency (at nanomolar to submicromolar concentrations) towards the NCI panel of human tumor cell lines and transplanted ...
Dmitry N. Kaluzhny, Anna K. Shchyolkina, Nikolay S. Ilyinsky, Olga F. Borisova, Alexander A. Shtil   +4 more
doaj   +1 more source

The role of c-Myc-RBM38 loop in the growth suppression in breast cancer

Journal of Experimental & Clinical Cancer Research, 2017
Background RNA-binding protein 38 (RBM38) is a member of the RNA recognition motif (RRM) family of RNA-binding proteins (RBPs). RBM38 often exerts its function by forming regulatory loops with relevant genes.
Xiao-Xia Li, Liang Shi, Xu-Jie Zhou, Jing Wu, Tian-Song Xia, Wen-Bin Zhou, Xi Sun, Lei Zhu, Ji-Fu Wei, Qiang Ding   +9 more
doaj   +1 more source

Dual targeting of p53 and c-Myc selectively eliminates leukaemic stem cells

Nature, 2016
Chronic myeloid leukaemia (CML) arises after transformation of a haemopoietic stem cell (HSC) by the protein-tyrosine kinase BCR–ABL. Direct inhibition of BCR–ABL kinase has revolutionized disease management, but fails to eradicate leukaemic stem cells ...
Sheela A. Abraham, L. Hopcroft, Emma Carrick, M. Drotar, Karen M. Dunn, A. Williamson, Koorosh Korfi, Pablo Baquero, Laura Park, M. Scott, F. Pellicanò, A. Pierce, M. Copland, C. Nourse, S. Grimmond, D. Vetrie, A. Whetton, T. Holyoake   +17 more
semanticscholar   +1 more source

Systems-pharmacology dissection of a drug synergy in imatinib-resistant CML [PDF]

, 2012
Occurrence of the BCR-ABL[superscript T315I] gatekeeper mutation is among the most pressing challenges in the therapy of chronic myeloid leukemia (CML). Several BCR-ABL inhibitors have multiple targets and pleiotropic effects that could be exploited for ...
A Quintás-Cardama, A Seth, A Subramanian, AA Borisy, AL Hopkins, André C Müller, B Benassi, B Luo, B Palsson, BJ Druker, C Pan, CA Eide, CI Bliss, CL Sawyers, D Bixby, F Grebien, Florian Grebien, Florian P Breitwieser, Forest M White, FP Breitwieser, FX Mahon, G Dennis Jr., Georg E Winter, Giulio Superti-Furga, H Kitano, IJ Griswold, J Dopazo, J Lamb, J Lehár, J Zhang, Jacques Colinge, JE Cortes, JE Delmore, Karoline V Gleixner, Keiryn L Bennett, LM Packer, M Albajar, M Azam, M Schuhmacher, Manuela Gridling, Martin Bilban, ME Gorre, N Meyer, NJ Donato, O Hantschel, P Filippakopoulos, Peter Valent, PL Ross, S Adhikary, S Gupta, S Pelengaris, Scott M Carlson, SR Hann, T O′Hare, U Rix, U Rix, Uwe Rix, X Chen, ZA Knight   +58 more
core   +1 more source

Strength through diversity: how cancers thrive when clones cooperate

Molecular Oncology, EarlyView.
Intratumor heterogeneity can offer direct benefits to the tumor through cooperation between different clones. In this review, Kuiken et al. discuss existing evidence for clonal cooperativity to identify overarching principles, and highlight how novel technological developments could address remaining open questions.
Marije C. Kuiken, Maartje Witsen, Emile E. Voest, Krijn K. Dijkstra   +3 more
wiley   +1 more source