journal
MENU ▼
Read by QxMD icon Read
search

Molecular & Cellular Oncology

journal
https://www.readbyqxmd.com/read/29487898/corrigendum
#1
(no author information available yet)
[This corrects the article DOI: 10.1080/23723556.2017.1285385.].
2018: Molecular & Cellular Oncology
https://www.readbyqxmd.com/read/29487897/cellular-quiescence-how-tgf%C3%AE-protects-cancer-cells-from-chemotherapy
#2
Jessie A Brown, Markus Schober
Using a functional proliferation reporter we identified quiescent tumor propagating cancer cells (TPCs) in intact squamous cell carcinomas, and found that TGFβ signaling controls their reversible entry into a growth arrested state, which protects TPCs from chemotherapy. TPCs with compromised TGFβ/Smad signaling can't enter quiescence and subsequently die from chemotherapy.
2018: Molecular & Cellular Oncology
https://www.readbyqxmd.com/read/29487896/a-path-from-melanocyte-stem-cells-to-cutaneous-melanoma-illuminated-by-uvb
#3
Hyeongsun Moon, Andrew C White
The relationship between melanocyte stem cells (MCSCs) and melanoma has been unclear. We recently demonstrated that melanoma-prone MCSCs are able to initiate cutaneous melanoma following stem cell activation through ultraviolet-B (UVB) exposure or natural stem cell cycling. Conversely, MCSC quiescence is sufficient to suppress tumorigenesis. This provides new insight into the role of environmental factors in tumor initiation from adult stem cells.
2018: Molecular & Cellular Oncology
https://www.readbyqxmd.com/read/29487895/mhc-i-genotype-drives-early-immune-selection-of-oncogenic-mutations
#4
Rachel Marty, Nicola de Prisco, Hannah Carter, Joan Font-Burgada
MHC-I exposes the intracellular contents to immune cells for surveillance of cellular health. Due to high genomic variation, individuals' immune systems differ in their ability to expose and eliminate cancer-causing mutations. These personalized immune blind spots create specific oncogenic mutation predispositions within patients and influence their prevalence across populations.
2018: Molecular & Cellular Oncology
https://www.readbyqxmd.com/read/29487894/autophagy-and-mitophagy-in-hepatocarcinogenesis
#5
Kai Liu, Jiyoung Lee, Jing-Hsiung James Ou
Autophagy is required for benign hepatic tumors to progress into malignant hepatocellular carcinoma. In our recent studies, we found that autophagy, or more specifically mitophagy, was required to suppress TP53 and induce the expression of the transcription factor NANOG to maintain hepatic cancer stem cells and promote hepatocarcinogenesis.
2018: Molecular & Cellular Oncology
https://www.readbyqxmd.com/read/29487893/ubash3b-mediated-silencing-of-the-mitotic-checkpoint-therapeutic-perspectives-in-cancer
#6
Ksenia Krupina, Charlotte Kleiss, Sushil Awal, Irene Rodriguez-Hernandez, Victoria Sanz-Moreno, Izabela Sumara
Defects in mitosis can lead to aneuploidy, which is a common feature of human cancers. Spindle Assembly Checkpoint (SAC) controls fidelity of chromosome segregation in mitosis to prevent aneuploidy. The ubiquitin receptor protein Ubiquitin Associated and SH3 Domain Containing B (UBASH3B) was recently found to control SAC silencing and faithful chromosome segregation by relocalizing Aurora B kinase to the mitotic microtubules. Accordingly, loss and gain of function of UBASH3B have strong effects on mitotic progression...
2018: Molecular & Cellular Oncology
https://www.readbyqxmd.com/read/29487892/predicting-human-clinical-trial-responses-in-mice
#7
Hui Gao, Juliet Anne Williams
Preclinical modeling of human Phase II oncology trials by traditional methods has failed to be highly predictive. Here, we comment on our data showing that much better prediction of clinical trial results can be achieved using a broad-based patient-derived xenograft (PDX) panel.
2018: Molecular & Cellular Oncology
https://www.readbyqxmd.com/read/29404401/mirna-convergent-gene-fusions
#8
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
https://www.readbyqxmd.com/read/29404400/mirna-displacement-as-a-promising-approach-for-cancer-therapy
#9
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
https://www.readbyqxmd.com/read/29404399/the-turtle-and-the-rabbit-story-in-a-modern-pi3-key
#10
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
https://www.readbyqxmd.com/read/29404398/gene-gating-at-nuclear-pores-prevents-the-formation-of-r-loops
#11
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
https://www.readbyqxmd.com/read/29404397/intratumoral-bacteria-may-elicit-chemoresistance-by-metabolizing-anticancer-agents
#12
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
https://www.readbyqxmd.com/read/29404396/auto-commentary-on-targeting-mitochondrial-oxidative-phosphorylation-eradicates-therapy-resistant-chronic-myeloid-leukemia-stem-cells
#13
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
https://www.readbyqxmd.com/read/29404395/crack-the-state-of-silence-tune-the-depth-of-cellular-quiescence-for-cancer-therapy
#14
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
https://www.readbyqxmd.com/read/29404394/to-die-or-not-to-die-regulatory-feedback-phosphorylation-circuits-determine-receptor-interacting-protein-kinase-1-ripk1-function
#15
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
https://www.readbyqxmd.com/read/29404393/dimeric-quinacrines-as-chemical-tools-to-identify-ppt1-a-new-regulator-of-autophagy-in-cancer-cells
#16
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
https://www.readbyqxmd.com/read/29404392/utilizing-panels-of-patient-derived-xenografts-to-aid-the-development-of-antibody-drug-conjugates
#17
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
https://www.readbyqxmd.com/read/29404391/rad6-promotes-chemoresistance-in-ovarian-cancer
#18
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
https://www.readbyqxmd.com/read/29404390/switching-from-tnf-induced-inflammation-to-death-signaling
#19
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
https://www.readbyqxmd.com/read/29404389/cobra-methods-and-metabolic-drug-targets-in-cancer
#20
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
journal
journal
49572
1
2
Fetch more papers »
Fetching more papers... Fetching...
Read by QxMD. Sign in or create an account to discover new knowledge that matter to you.
Remove bar
Read by QxMD icon Read
×

Search Tips

Use Boolean operators: AND/OR

diabetic AND foot
diabetes OR diabetic

Exclude a word using the 'minus' sign

Virchow -triad

Use Parentheses

water AND (cup OR glass)

Add an asterisk (*) at end of a word to include word stems

Neuro* will search for Neurology, Neuroscientist, Neurological, and so on

Use quotes to search for an exact phrase

"primary prevention of cancer"
(heart or cardiac or cardio*) AND arrest -"American Heart Association"