Top 10 Biorxiv Papers Today in Cancer Biology


1.996 Mikeys
#1. Computational metabolism modeling predicts risk of distant relapse-free survival in breast cancer patients
Lucia Trilla-Fuertes, Angelo Gamez-Pozo, Mariana Diaz-Almiron, Guillermo Prado-Vazquez, Andrea Zapater-Moros, Rocio Lopez-Vacas, Paolo Nanni, Pilar Zamora, Enrique Espinosa, Juan Angel Fresno Vara
Aims: Differences in metabolism among breast cancer subtypes suggest that metabolism plays an important role in this disease. Flux Balance Analysis is used to explore these differences as well as drug response. Materials & Methods: Proteomics data from breast tumors were obtained by mass-spectrometry. Flux Balance Analysis was performed to study metabolic networks. Flux activities from metabolic pathways were calculated and used to build prognostic models. Results: Flux activities of vitamin A, tetrahydrobiopterin and beta-alanine metabolism pathways split our population into low- and high-risk patients. Additionally, flux activities of glycolysis and glutamate metabolism split triple negative tumors into low- and high-risk groups. Conclusions: Flux activities summarize Flux Balance Analysis data and can be associated with prognosis in cancer.
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Sample Sizes : None.
Authors: 10
Total Words: 3643
Unqiue Words: 1307

0.0 Mikeys
#2. Long non-coding RNAs defining major subtypes of B cell precursor acute lymphoblastic leukemia
Alva Rani James, Michael P Schroeder, Martin Neumann, Lorenz Bastian, Cornelia Eckert, Nicola Gökbuget, Jutta Ortiz Tanchez, Cornelia Schlee, Konstandina Isaakidis, Stefan Schwartz, Thomas Burmeister, Arend von Stackelberg, Michael A Rieger, Stefanie Göllner, Martin Horstman, Martin Schrappe, Renate Kirschner-Schwabe, Monika Brüggemann, Carsten Müller-Tidow, Hubert Serve, Altuna Akalin, Claudia D. Baldus
Recent studies implicated that long non-coding RNAs (lncRNAs) may play a role in the progression and development of acute lymphoblastic leukemia, however, this role is not yet clear. In order to unravel the role of lncRNAs associated with B-cell precursor Acute Lymphoblastic Leukemia (BCP-ALL) subtypes, we performed transcriptome sequencing and DNA methylation array across 82 BCP-ALL samples from three molecular subtypes (DUX4, Ph-like, and Near Haploid or High Hyperdiploidy). Unsupervised clustering of BCP-ALL samples on the basis of their lncRNAs on transcriptome and DNA methylation profiles revealed robust clusters separating three molecular subtypes. Using extensive computational analysis, we developed a comprehensive catalog of 1235 aberrantly dysregulated BCP-ALL subtype-specific lncRNAs with altered expression and methylation patterns from three subtypes of BCP-ALL. By analyzing the co-expression of subtype-specific lncRNAs and protein-coding genes, we inferred key molecular processes in BCP-ALL subtypes. A strong...
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biorxivpreprint: Long non-coding RNAs defining major subtypes of B cell precursor acute lymphoblastic leukemia https://t.co/w13yeU4PMq #bioRxiv
RNApreprints: James et al: Long non-coding RNAs defining major subtypes of B cell precursor acute lymphoblastic leukemia https://t.co/NYDT3fgUVW
biorxiv_cancer: Long non-coding RNAs defining major subtypes of B cell precursor acute lymphoblastic leukemia https://t.co/VYjBoQTVFw #biorxiv_cancer
GeneSCF: @GeneSCF New article citing #GeneSCF Long non-coding RNAs (#LncRNAs) defining major subtypes of #Bcell precursor acute #lymphoblastic #leukemia (#BCP-ALL) https://t.co/AWe0TCoT4d
SaubashyaSur: RT @biorxivpreprint: Long non-coding RNAs defining major subtypes of B cell precursor acute lymphoblastic leukemia https://t.co/w13yeU4PMq…
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Sample Sizes : [53]
Authors: 22
Total Words: 13125
Unqiue Words: 4211

0.0 Mikeys
#3. AKT regulates mitotic progression of mammalian cells by phosphorylating MASTL
Irfana Reshi, Misbah Un Nisa, Umer Farooq, S. Qaaifah Gillani, Sameer Ahmed Bhat, Zarka Sarwar, Khalid Fazili, Shaida Andrabi
Microtubule associated serine threonine like kinase (MASTL) has been recently identified as an important regulator of mitosis. By inhibiting protein phosphatase 2A, it plays a crucial role in activating one of the most important mitotic kinases known as cyclin dependent kinase1 (CDK1). MASTL has been seen to be up regulated in various types of cancers and is involved in tumor recurrence. It is activated by CDK1 through its auto regulatory loop but the complete mechanism of its activation is still unclear. In this study, we evaluated the regulation of MASTL via AKT during mitosis. Here we report that AKT phosphorylates MASTL at T299 which plays a critical role in its activation. Our results suggest that AKT increases CDK1 mediated phosphorylation and hence activity of MASTL which in turn promotes cell proliferation. We also show that the oncogenic potential of AKT is augmented by MASTL activation as the AKT mediated oncogenesis in colorectal cell lines can be attenuated by inhibiting and/or silencing MASTL. In brief, we report that...
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biorxiv_cancer: AKT regulates mitotic progression of mammalian cells by phosphorylating MASTL https://t.co/KQ49mpBYlP #biorxiv_cancer
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Sample Sizes : None.
Authors: 8
Total Words: 7558
Unqiue Words: 2066

0.0 Mikeys
#4. Activation of dopamine receptor 2 (DRD2) prompts transcriptomic and metabolic plasticity in glioblastoma
Seamus P. Caragher, Jack M. Shireman, Mei Huang, Jason Miska, Shivani Baisiwala, Cheol Park, Miranda Saathoff, Louisa Warnke, Ting Xiao, Maciej S. Lesniak, C. David James, Herbert Meltzer, Andrew K. Tryba, Atique U. Ahmed
Glioblastoma (GBM) is one of the most aggressive and lethal tumor types. Evidence continues to accrue indicating that the complex relationship between GBM and the brain microenvironment contributes to this malignant phenotype. However, the interaction between GBM and neurotransmitters, signaling molecules involved in neuronal communication, remains incompletely understood. Here we examined, in both sexes of humans and mice, how the monoamine dopamine influences GBM cells. We demonstrate that GBM cells express DRD2, with elevated expression in the glioma-initiating cell (GIC) population. Stimulation of DRD2 caused neuron-like depolarization exclusively in GICs. In addition, long-term activation of DRD2 heightened the sphere-forming capacity of GBM cells as well as tumor engraftment efficiency. Mechanistic investigation revealed that DRD2 signaling activates the hypoxia response and functionally alters metabolism. Finally, we found that GBM cells synthesize and secrete dopamine themselves, suggesting a potential autocrine mechanism....
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Sample Sizes : None.
Authors: 14
Total Words: 10813
Unqiue Words: 3036

0.0 Mikeys
#5. Single-cell RNA sequencing reveals a dynamic stromal niche within the evolving tumour microenvironment
Sarah Davidson, Mirjana Efremova, Angela Riedel, Bidesh Mahata, Jhuma Pramanik, Jani Huuhtanen, Gozde Kar, Roser Vento-Tormo, Tzachi Hagai, Xi Chen, Muzlifah A. Haniffa, Jacqueline D. Shields, Sarah A. Teichmann
Non-cancerous stromal cells represent a highly diverse compartment of the tumour, yet their role across tumour evolution remains unclear. We employed single-cell RNA sequencing to determine stromal adaptations in murine melanoma at different points of tumour development. Naive lymphocytes recruited from lymph nodes underwent activation and clonal expansion within the tumour, prior to PD1 and Lag3 expression, while tumour-associated myeloid cells promoted the formation of a suppressive niche through cytokine secretion and inhibitory T cell interactions. We identified three temporally distinct cancer-associated fibroblast (CAF) populations displaying unique signatures, and verified these in human datasets. In early tumours, immune CXCL12/CSF1 and complement-expressing CAFs supported recruitment of macrophages, whereas contractile CAFs became more prevalent in later tumours. This study highlights the complex interplay and increasing diversity among cells that co-evolve with the tumour, indicating that from early stages of...
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vitaliikl: Very cool study by @mirjanaefr and others. They tracked melanoma development over time and found that proportions of fibroblast populations changed as tumour evolved: recruiting macrophages to the tumour microenvironment (early) => contractile (late). https://t.co/F4XDqRdpLM
seandavis12: Single-cell RNA sequencing reveals a dynamic stromal niche within the evolving tumour microenvironment https://t.co/rNJpAa12hG
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Sample Sizes : None.
Authors: 13
Total Words: 12598
Unqiue Words: 3528

0.0 Mikeys
#6. ENvironmental Dynamics Underlying Responsive Extreme Survivors (ENDURES) of Glioblastoma: a Multi-disciplinary Team-based, Multifactorial Analytical Approach
Sandra K Johnston, Paula Whitmire, Susan Christine Massey, Priya Kumthekar, Alyx B Porter, Natarajan Raghunand, Luis F Gonzalez-Cuyar, Maciej M Mrugala, Andrea Hawkins-Daarud, Pamela R Jackson, Leland S Hu, Jann N Sarkaria, Lei Wang, Robert A Gatenby, Kathleen M Egan, Peter Canoll, Kristin R Swanson
Although glioblastoma is a fatal primary brain cancer with a short median survival of 15 months, a small number of patients survive more than 5 years after diagnosis; they are known as extreme survivors (ES). Due to their rarity, very little is known about what differentiates these outliers from other glioblastoma patients. For the purpose of identifying unknown drivers of extreme survivorship in glioblastoma, we developed the ENDURES consortium (ENvironmental Dynamics Underlying Responsive Extreme Survivors of glioblastoma). This consortium is a multicenter collaborative network of investigators focused on the integration of multiple types of clinical data and the creation of patient-specific models of tumor growth informed by radiographic and histological parameters. Leveraging our combined resources, the goals of the ENDURES consortium are two-fold: (1) to build a curated, searchable, multilayered repository housing clinical and outcome data on a large cohort of ES patients with glioblastoma and (2) to leverage the ENDURES...
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biorxivpreprint: ENvironmental Dynamics Underlying Responsive Extreme Survivors (ENDURES) of Glioblastoma: a Multi-disciplinary Team-based, Multifactorial Analytical Approach https://t.co/aslrKxS4E5 #bioRxiv
Aiims1742: This is a very interesting effort by @gliomath and colleagues - creating the “ENDURES Consortium” for integrating clinical, pathological & molecular data in #glioblastoma extreme survivors. https://t.co/qj5b4J6s0k Cc: @DrAlfredYung @RonDePinho https://t.co/uJEzPRuCQt
biorxiv_cancer: ENvironmental Dynamics Underlying Responsive Extreme Survivors (ENDURES) of Glioblastoma: a Multi-disciplinary Team-based, ... https://t.co/KUR6uHT1L5 #biorxiv_cancer
Eric_Chevet: ENvironmental Dynamics Underlying Responsive Extreme Survivors (ENDURES) of Glioblastoma: a Multi-disciplinary Team-based, Multifactorial Analytical Approach https://t.co/tG8SyJxRyR
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Sample Sizes : None.
Authors: 17
Total Words: 6073
Unqiue Words: 2202

0.0 Mikeys
#7. YB-1 Is Critical For The Genesis And Progression Of KRAS Mutated Human Breast Cancer
Sylvain Lefort, Amal El-Naggar, Susanna Tan, Shane Colborne, Gian Luca Negri, Davide Pellacani, Martin Hirst, Barry Gusterson, Gregg B Morin, Poul H Sorensen, Connie J Eaves
Invasive tumors produced in immunodeficient mice from freshly isolated normal human mammary cells transduced with a KRASG12D vector showed an increased expression of the YB-1 RNA-binding protein, thus mimicking advanced human breast cancers with KRAS pathway deregulation. We also find YB-1 is upregulated in a model of human ductal carcinoma in situ obtained from xeno-transplanted myrAKT1-transduced primary human mammary cells. In the KRAS model, elevated YB-1 was evident within 2 weeks and then retained in subsequent tumor passages. Knockdown studies demonstrated YB-1 was essential for both the initial transforming activity of KRASG12D in the primary cells and the metastatic activity of an established human KRASmutant breast cancer cell line. Accompanying molecular and histological analyses indicate activation of a HIF1α response.
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Authors: 11
Total Words: 9879
Unqiue Words: 3011

0.0 Mikeys
#8. Cellular acidosis triggers MondoA transcriptional activity by driving mitochondrial ATP production
Donald E Ayer, Blake R Wilde, Zhizhou Ye
MondoA and its transcriptional target thioredoxin-interacting protein (TXNIP) constitute a regulatory loop that senses glycolytic flux and controls glucose availability. Cellular stress also triggers MondoA activity and TXNIP expression. To understand how MondoA integrates glucose and stress signals, we studied its activation by acidosis. We found that acidosis drives mitochondrial ATP (mtATP) synthesis. The subsequent export of mtATP from mitochondria via adenine-nucleotide transporter and voltage-dependent anion channel, and the enzymatic activity of mitochondria-bound hexokinase results in the production of glucose-6-phosphate (G6P), a known activator of MondoA transcriptional activity. MondoA localizes to the outer-mitochondrial membrane (OMM), and in response to G6P, shuttles to the nucleus and activates transcription. Our data suggests that MondoA is a required feature of a glucose- and mtATP-dependent, OMM-localized signaling center. We propose MondoA functions as a coincidence detector and its ability to sense glucose and...
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biorxiv_cancer: Cellular acidosis triggers MondoA transcriptional activity by driving mitochondrial ATP production https://t.co/eMm8Rwr2Ob #biorxiv_cancer
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Sample Sizes : [1, 2]
Authors: 3
Total Words: 12298
Unqiue Words: 4151

0.0 Mikeys
#9. Impaired hematopoiesis and leukemia development in mice with a conditional "knock-in" allele of a mutant splicing factor gene U2af1
Dennis Liang Fei, Tao Zhen, Benjamin Durham, John Ferrarone, Tuo Zhang, Lisa Garrett, Akihide Yoshimi, Omar Abdel-Wahab, Robert Bradley, Paul Liu, Harold Varmus
Mutations affecting the spliceosomal protein U2AF1 are commonly found in myelodysplastic syndromes (MDS) and secondary acute myeloid leukemia (sAML). We have generated mice that carry Cre-dependent "knock-in" alleles of U2af1(S34F), the murine version of the most common mutant allele of U2AF1 encountered in human cancers. Cre-mediated recombination in murine hematopoietic lineages caused changes in RNA splicing, as well as multilineage cytopenia, macrocytic anemia, decreased hematopoietic stem and progenitor cells, low-grade dysplasias, and impaired transplantability, but without lifespan shortening or leukemia development. In an attempt to identify U2af1(S34F)-cooperating changes that promote leukemogenesis, we combined U2af1(S34F) with Runx1 deficiency in mice and further treated the mice with a mutagen, N-Ethyl-N-Nitrosourea (ENU). Overall, three of sixteen ENU-treated compound transgenic mice developed AML. However, AML did not arise in mice with other genotypes or without ENU treatment. Sequencing DNA from the three AMLs...
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Sample Sizes : None.
Authors: 11
Total Words: 15263
Unqiue Words: 3563

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#10. Ribosomal protein imbalance launches a C/EBP-based program to preserve tissue integrity
Ludovic Baillon
Genes encoding ribosomal proteins are expressed at rate limiting levels, rendering their biological function highly sensitive to the copy-number variation that results from genomic instability. Cells with a reduced number of ribosomal protein genes (RPGs) are eliminated, when intermingled with wild type cells, via a process known as cell competition. The mechanisms underlying this phenomenon are poorly understood. Here we report the function of a CCAAT-Enhancer-Binding Protein (C/EBP), Xrp1, that is critically required for the elimination of cells with a hemizygous RPG genotype. In such cells, Xrp1 is transcriptionally upregulated by an autoregulatory loop and is able to trigger cell elimination. Since genomic instability is likely to cause the loss of a haploinsufficient RPG, we propose a molecular model of how RPGs, together with a C/EBP-dependent transcriptional program, could preserve the genomic integrity of tissues.
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Sample Sizes : None.
Authors: 1
Total Words: 13629
Unqiue Words: 3737

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