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Molecular & Cellular Oncology

Carlos Rovira
In a recent study published in Nature Communications, we showed that intron-encoded microRNA genes (miRNA) are frequent partners of fusion genes in the cancer genome. Analyzed from a functional rather than structural perspective, these rearrangements represent a new class of fusions we called "miRNA-convergent fusions".
2018: Molecular & Cellular Oncology
David Gilot, Marie-Dominique Galibert
microRNA (miRNA) are critical post-transcriptional regulators and key players in diseases development. We demonstrated that non-canonical microRNA Responsive Elements (here MRE-16) could sequester miR-16, dampening miR-16 tumor suppressor function. We developed small oligonucleotides, masking specifically these unusual miR-16 binding sites, that restored miR-16 function. This constitutes a promising targeted approach.
2018: Molecular & Cellular Oncology
Miriam Martini, Maria Chiara De Santis, Emilio Hirsch
Mitosis is a complex process controlling proper distribution of chromosomes and preventing genomic instability, a typical hallmark of cancer. We recently reported that that a class II isoform of Phosphoinositide 3-kinase (PI3K), PI3K-C2α, is involved in the organization of the mitotic spindle. Our study demonstrate that, differently to all other PI3K isoforms, PI3K-C2α shows an unexpected tumor suppressor function independent of its catalytic activity.
2018: Molecular & Cellular Oncology
Hélène Gaillard, Francisco García-Benítez, Andrés Aguilera
Transcription is an important source of genetic variability. A large amount of transcription-associated genome variation arises from the unscheduled formation of R loops. We have recently found that physical proximity of chromatin to nuclear pores prevents the formation of pathological R loops during transcription. Our study opens new perspectives to understand genome stability as a function of nuclear location.
2018: Molecular & Cellular Oncology
Leore T Geller, Ravid Straussman
We recently reported that bacteria can be found within pancreatic ductal adenocarcinoma (PDAC) tumors. Some of these bacteria can metabolize and thereby inactivate the nucleoside analog gemcitabine. We demonstrated that the long isoform of the bacterial enzyme cytidine deaminase (CDD) mediates the metabolism of gemcitabine. The clinical effect of overcoming this potential mechanism of drug resistance has yet to be studied.
2018: Molecular & Cellular Oncology
Lucie de Beauchamp, Pablo Baquero, Elodie M Kuntz, Eyal Gottlieb, G Vignir Helgason
We have recently uncovered an abnormal increase in mitochondrial oxidative metabolism in therapy-resistant chronic myeloid leukaemia stem cells (LSCs). By simultaneously disrupting mitochondrial respiration and inhibiting BCR-ABL kinase activity using the antibiotic tigecycline and imatinib respectively, we effectively eradicated LSCs and prevented disease relapse in pre-clinical animal models.
2018: Molecular & Cellular Oncology
Kotaro Fujimaki, Guang Yao
The regulation of cellular quiescence underlies numerous physiopathological phenomena. We recently found that quiescence depth can be tuned as to adjust a dimmer switch, by altering the expression of genes in the Retinoblastoma (Rb)-E2f pathway. Reducing quiescence depth may wake dormant cancer cells and make them susceptible to treatment.
2018: Molecular & Cellular Oncology
Manoj B Menon, Julia Gropengießer, Klaus Ruckdeschel, Matthias Gaestel
Complex posttranslational modifications determine the effects of receptor-interacting protein kinase-1 (RIPK1) on cell survival and death. Studies from us and others have revealed a p38MAPK/MK2-dependent checkpoint in RIPK1 signaling. MAPKAP kinase 2 (MK2) phosphorylates RIPK1 to suppress RIPK1-mediated apoptosis and necroptosis in response to diverse stimuli relevant to inflammation, infection, genotoxic stress and chemotherapy.
2018: Molecular & Cellular Oncology
Michael C Nicastri, Vito W Rebecca, Ravi K Amaravadi, Jeffrey D Winkler
DQ661 is a novel dimeric quinacrine that affects multiple lysosomal functions (autophagy and macropinocytosis) and mTORC1 (mechanistic target of rapamycin) activity by specifically targeting protein-palmitoyl thioesterase 1 (PPT1). DQ661 has in vivo activity in immunocompetent mouse models of cancer, and constitutes a new tool compound for the study of lysosomal function in cancer and therapeutic resistance.
2018: Molecular & Cellular Oncology
Scott David Collins, Carl Uli Bialucha, Juliet Anne Williams, Hui Gao
Despite numerous endeavors in clinical trials there are few clinically approved Antibody Drug Conjugate (ADC) therapies. Here we comment on our recent publication demonstrating the power of using panels of patient-derived xenografts (PDX) prior to Phase 1, to assess the potential heterogeneity of response a clinical candidate may show across a population. Furthermore we discuss how the same approach has been used in an additional ADC program.
2018: Molecular & Cellular Oncology
David W Clark, Chinnadurai Mani, Komaraiah Palle
Mortality in ovarian cancer is predominantly due to acquired chemoresistance and tumor recurrence. UBIQUITIN CONJUGATING ENZYME E2 or RAD6 expression increases in cell lines and patient tumors in response to platinum-based chemotherapy and promotes both activation of DNA damage response pathways and expression of stemness genes and a stem cell-like phenotype driving ovarian cancer chemoresistance.
2018: Molecular & Cellular Oncology
Qing Xu, Swati Choksi, Zhengang Liu
TNFR1-mediated cell signaling involves complex molecular pathways leading to inflammation and death. Cytosolic RARγ plays a pivotal role in converting TNF-induced inflammatory responses to RIP1 initiated cell death and this finely regulated function of RARγ serves as a checkpoint to engage death pathways in response to TNF.
2018: Molecular & Cellular Oncology
Iñigo Apaolaza, Edurne San José-Eneriz, Xabier Agirre, Felipe Prósper, Francisco J Planes
The identification of therapeutic strategies exploiting the metabolic alterations of malignant cells is a relevant area in cancer research. Here, we discuss a novel computational method, based on the COBRA (COnstraint-Based Reconstruction and Analysis) framework for metabolic networks, to perform this task. Current and future steps are presented.
2018: Molecular & Cellular Oncology
Marta Kovatcheva, Mary E Klein, William D Tap, Andrew Koff
Senescence is an irreversible form of growth arrest and is generally considered a favorable outcome of cancer therapies, yet little is known about the molecular events that distinguish this state from readily reversible growth arrest (i.e. quiescence). Recently, we discovered that during therapy induced senescence the chromatin remodeling protein α-thalassemia, mental retardation, X-linked (ATRX) represses Harvey rat sarcoma viral oncogene homolog (HRAS), and repression of HRAS is necessary to establish senescence, suggesting how new clinical combinations might be used to achieve durable senescence...
2018: Molecular & Cellular Oncology
Jimok Yoon, Jonathan R Terman
MICAL Redox enzymes have recently emerged as direct regulators of cell shape and motility - working through specific reversible post-translational oxidation of actin to disassemble and remodel the cytoskeleton. Links are also now emerging between MICALs and cancer, including our recent results that regulation of MICAL sensitizes cancer cells to the cancer drug Gleevec. Targeting this new actin regulatory enzyme system may thus provide new therapeutic options for cancer treatment.
2018: Molecular & Cellular Oncology
Stephanie Bleicken, Ana J Garcia-Saez
Apoptosis regulation by Bcl-2 proteins is pivotal for mammalians, not only because it is key for development but also because aberrant apoptosis is prerequisite to severe diseases, like cancer. Recently, we quantified interactions within the Bcl-2 protein network in solution and membranes, and addressed membrane recruitment, preference of interaction partners and the consequences for Bax activation and inhibition.
2018: Molecular & Cellular Oncology
Pepijn M Schoonen, Marcel A T M van Vugt
Tumors defective in homologous recombination (HR) are highly sensitive to poly ADP-ribose polymerase (PARP) inhibition, however the cell biological mechanisms underlying this synthetic lethality remain elusive. We recently identified that PARP inhibitor-induced DNA lesions persist until mitosis, subsequently causing mitotic chromatin bridges, multinucleation and apoptosis. Here, we discuss the implications of these findings.
2018: Molecular & Cellular Oncology
Samuel J Taylor, Wallace Y Langdon
Myelosuppression is one of the most severe and limiting side effects of chemotherapy. Our recent work outlines a strategy to prevent chemotherapy-induced myelosuppression by administering a priming dose of the FMS-Like Tyrosine kinase 3 (FLT3) inhibitor quizartinib. Furthermore, by administering sequential quizartinib primed injections of fluorouracil (5-FU), we demonstrated a novel and effective strategy to eliminate disease in two mouse models of quizartinib resistant acute myeloid leukemia (AML).
2017: Molecular & Cellular Oncology
Nada Abuarab, Fangfang Li, Asipu Sivaprasadarao
In age-related diseases, rise in intracellular reactive oxygen species (ROS) causes fragmentation of mitochondrial network. Our recent study demonstrated that ROS activation of TRPM2 (transient receptor potential melastatin-2) channels triggers lysosomal Zn2+ release that, in turn, triggers mitochondrial fragmentation. The findings provide new mechanistic insights that may have therapeutic implications.
2017: Molecular & Cellular Oncology
Lang Rao, Youbao Sha, N Tony Eissa
TFEB is a master regulator for transcription of genes involved in autophagy, lysosome and mitochondrial biogenesis. Activity of TFEB is inhibited upon its phosphorylation. STUB1, a chaperone-dependent E3 ubiquitin ligase, modulates TFEB activity by preferentially targeting inactive phosphorylated TFEB for degradation by the ubiquitin proteasome pathway. Thus, the ubiquitin-proteasome pathway participates in regulating autophagy and lysosomal functions by regulating the activity of TFEB.
2017: Molecular & Cellular Oncology
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