Top 7 Biorxiv Papers Today in Cancer Biology


2.061 Mikeys
#1. Power and pitfalls of computational methods for inferring clone phylogenies and mutation orders from bulk sequencing data
Sayaka Miura, Tracy Vu, Jiamin Deng, Tiffany Buturla, Jiyeong Choi, Sudhir Kumar
Background: Tumors harbor extensive genetic heterogeneity in the form of distinct clone genotypes that arise over time and across different tissues and regions of a cancer patient. Many computational methods produce clone phylogenies from population bulk sequencing data collected from multiple tumor samples. These clone phylogenies are used to infer mutation order and clone origin times during tumor progression, rendering the selection of the appropriate clonal deconvolution method quite critical. Surprisingly, absolute and relative accuracies of these methods in correctly inferring clone phylogenies have not been consistently assessed. Methods: We evaluated the performance of seven computational methods in producing clone phylogenies for simulated datasets in which clones were sampled from multiple sectors of a primary tumor (multi-region) or primary and metastatic tumors in a patient (multi-site). We assessed the accuracy of tested methods metrics in determining the order of mutations and the branching pattern within the...
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biorxivpreprint: Power and pitfalls of computational methods for inferring clone phylogenies and mutation orders from bulk sequencing data https://t.co/8Lc4SaRUnf #bioRxiv
biorxiv_cancer: Power and pitfalls of computational methods for inferring clone phylogenies and mutation orders from bulk sequencing data https://t.co/9niUPA3n7X #biorxiv_cancer
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API for the Clone Finder application

Repository: CloneFinderAPI
User: gstecher
Language: Python
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Total Words: 11133
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1.998 Mikeys
#2. Highly multiplexed immunofluorescence images and single-cell data of immune markers in tonsil and lung cancer
Rumana Rashid, Giorgio Gaglia, Yu-An Chen, Jia-Ren Lin, Ziming Du, Zoltan Maliga, Denis Schapiro, Clarence Yapp, Jeremy Muhlich, Artem Sokolov, Peter Sorger, Sandro Santagata
In this data descriptor, we document a dataset of multiplexed immunofluorescence images and derived single-cell measurements of immune lineage and other markers in formaldehyde-fixed and paraffin-embedded (FFPE) human tonsil and lung cancer tissue. We used tissue cyclic immunofluorescence (t-CyCIF) to generate fluorescence images which we artifact corrected using the BaSiC tool, stitched and registered using the ASHLAR algorithm, and segmented using ilastik software and MATLAB. We extracted single-cell features from these images using HistoCAT software. The resulting dataset can be visualized using image browsers and analyzed using high-dimensional, single-cell methods. This dataset is a valuable resource for biological discovery of the immune system in normal and diseased states as well as for the development of multiplexed image analysis and viewing tools.
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1.996 Mikeys
#3. 3D imaging of colorectal cancer organoids identifies responses to Tankyrase inhibitors
Luned M Badder, Andrew J Hollins, Bram Herpers, Kuan Yan, Kenneth B Ewan, Jennifer R Shone, Delyth A Badder, Marc Naven, Kevin Ashelford, Rachel Hargest, Alan R Clarke, Christina Esdar, Hans-Peter Buchstaller, Dirk Wienke, Leo S Price, Paul H Shaw, Trevor Dale
Aberrant activation of the Wnt signalling pathway is required for tumour initiation and survival in the majority of colorectal cancers. The development of inhibitors of Wnt signalling has been the focus of multiple drug discovery programs targeting colorectal cancer and other malignancies associated with aberrant pathway activation. However, progression of new clinical entities targeting the Wnt pathway has been slow. One challenge lies with the limited predictive power of 2D cancer cell lines because they fail to fully recapitulate intratumoural phenotypic heterogeneity. In particular, the relationship between 2D cancer cell biology and cancer stem cell function is poorly understood. By contrast, 3D tumour organoids provide a platform in which complex cell-cell interactions can be studied. However, complex 3D models provide a challenging platform for the quantitative analysis of drug responses of therapies that have differential effects on tumour cell subpopulations. Here, we generated tumour organoids from colorectal cancer...
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Authors: 17
Total Words: 10429
Unqiue Words: 3328

1.99 Mikeys
#4. Lung tumour cell-derived exosomes promote the expansion of MDSC through miR-21a/PDCD4/IL-6/STAT3 pathway
Xingju Zhang, Fei Li, Jiale Zhang, Ying Tang, Bin Xiao, Ying Wan, Jiang Shan
The percentage of MDSC population in peripheral blood is significantly increased in lung cancer patients. The accumulation of MDSC contributes to the development of a tumourassociated immune suppressive environment. But the mechanism mediating MDSC accumulation in lung cancer patients is elusive. We found that exosomes from Lewis lung cancer cells (LLC-Exo) can be taken up by the mice bone marrow cells and then promote MDSC expansion, which enhance tumour growth. Mechanistically, during the induction of MDSC from the bone marrow cells, miR-21a from LLC-Exo can stimulate BM cells to produce more IL-6 by inhibiting pdcd4 expression post-transcriptionally. Autocrine IL-6 induces tyrosine 705(Y705) of STAT3 to be phosphorylated during MDSC expansion. LLC-Exo with miR-21a deletion lost its ability to stimulate IL-6 production, STAT3 activation and MDSC expansion. These results demonstrate that lung cancer cell-derived exosomes promote functional MDSC expansion through activation of miR-21a/PDCD4/IL-6/STAT3 pathway.
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Authors: 7
Total Words: 14353
Unqiue Words: 3364

1.989 Mikeys
#5. Regulation of melanocyte development by ligand-dependent BMP signaling underlies oncogenic BMP signaling in melanoma
Alec Gramann, Arvind M Venkatesan, Melissa Guerin, Craig Ceol
Preventing terminal differentiation is important in the development and progression of many cancers including melanoma. Recent identification of GDF6 as a novel melanoma oncogene showed GDF6-activated BMP signaling suppresses differentiation of melanoma cells. Previous studies have identified roles for GDF6 orthologs during neural crest development, but have not identified direct regulation of melanocyte development. Here, we investigate gdf6a, a zebrafish ortholog of human GDF6, during the development of melanocytes. We establish that the loss of gdf6a or inhibition of BMP signaling during neural crest development disrupts normal pigment cell development, leading to shifts in pigment cell fates. This shift occurs as pigment cells arise from the neural crest and depends an MITF ortholog, mitfa, a key regulator of melanocyte development. Together, these results indicate that the oncogenic role ligand-dependent BMP signaling plays in suppressing differentiation in melanoma is a reiteration of its physiological roles during...
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1.988 Mikeys
#6. Functional plasticity and reversible growth behavior of patients acute myeloid leukemia stem cells growing in mice
Sarah Ebinger, Christina Zeller, Michela Carlet, Daniela Senft, Wen-Hsin Liu, Maja Rothenberg-Thurley, Klaus H. Metzeler, Karsten Spiekermann, Binje Vick, Irmela Jeremias
Resistance against chemotherapy remains a major obstacle in treating patients with acute myeloid leukemia (AML). Novel therapeutic concepts are especially desired to target and eliminate resistant AML stem cells. Here we show that AML stem cells harbor the plasticity to switch from a low-cycling, chemotherapy resistant state into an actively proliferating state associated with treatment response. We used patient-derived xenograft (PDX) cells from patients with high risk or relapsed AML, which were lentivirally transduced for marker expression, stained with the proliferation-sensitive dye Carboxyfluorescein succinimidyl ester (CFSE), and re-transplanted into next-recipient mice. A rare subpopulation of AML cells displayed reduced proliferation in vivo, associated with increased treatment resistance. The proportion of AML cells with stem cell potential was identical in both, the highly and lowly proliferative sub-fraction. In re-transplantation experiments, proliferation behavior proved reversible, and AML stem cells were able to...
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1.988 Mikeys
#7. STAT5-dependent regulation of CDC25A by miR-16 controls proliferation and differentiation in FLT3-ITD acute myeloid leukemia
Gabrielle Sueur, Alison Boutet, Mathilde Gotanègre, Véronique De Mas, Arnaud Besson, Stéphane Manenti, Sarah Bertoli
We recently identified the CDC25A phosphatase as a key actor in proliferation and differentiation in acute myeloid leukemia which expresses the FLT3-ITD mutation. In this paper we demonstrate that CDC25A level is controlled by a complex STAT5/miR-16 transcription and translation pathway working downstream of this receptor. First, we established by CHIP analysis that STAT5 is directly involved in FLT3-ITD-dependent CDC25A gene transcription. In addition, we determined that miR-16 expression is repressed by FLT3-ITD activity, and that STAT5 participates in this repression. In accordance with these results, miR-16 expression was significantly reduced in a panel of AML primary samples carrying the FLT3-ITD mutation when compared with FLT3wt cells. The expression of a miR-16 mimic reduced CDC25A protein and mRNA levels, and RNA interference-mediated down modulation of miR-16 restored CDC25A expression in response to FLT3-ITD inhibition. Finally, decreasing miR-16 expression partially restored the proliferation of cells treated with the...
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