Top 10 Biorxiv Papers Today in Cancer Biology


2.047 Mikeys
#1. A FIJI Macro for quantifying pattern in extracellular matrix
Esther Wershof, David J Barry, Robert P Jenkins, Antonio Rullan, Anna Wilkins, Ioannis Roxanis, Kurt I Anderson, Danielle Park, Paul A Bates, Erik Sahai
Diverse extracellular matrix patterns are observed in both normal and pathological tissue; however only piecemeal tools currently exist for quantitative analysis of matrix pattern features. Thus, there is a need for an automated pipeline for quantifying these matrix patterns. To this end we have developed an ImageJ plugin called TWOMBLI, which stands for The Workflow Of Matrix BioLogy Informatics. The aim of TWOMBLI is to quantify matrix patterns, including branch points, endpoints, curvature, gaps, and fractal dimension. It is designed to be easy-to-use, quick and versatile. TWOMBLI can be downloaded from https://github.com/wershofe/TWOMBLI together with detailed documentation. Here we present an overview of the pipeline and demonstrate its utility for quantifying extracellular matrix patterns in both experimental and clinical samples.
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biorxivpreprint: A FIJI Macro for quantifying pattern in extracellular matrix https://t.co/gHwJgunzOI #bioRxiv
biorxiv_cancer: A FIJI Macro for quantifying pattern in extracellular matrix https://t.co/csIs0VFCy9 #biorxiv_cancer
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Authors: 10
Total Words: 0
Unqiue Words: 0

2.043 Mikeys
#2. GHSR-1a is not Required for Ghrelin's Anti-inflammatory and Fat-sparing Effects in Cancer Cachexia
Haiming Liu, Jiaohua Luo, Bobby Guillory, Ji-an Chen, Pu Zang, Jordan K. Yoeli, Yamileth Hernandez, Ian (In-gi) Lee, Barbara Anderson, Mackenzie J. Storie, Alison Tewnion, Jose Garcia
Adipose tissue (AT) atrophy is a hallmark of cancer cachexia contributing to increased morbidity/mortality. Ghrelin has been proposed as a treatment for cancer cachexia partly by preventing AT atrophy. However, the mechanisms mediating ghrelin's effects are incompletely understood, including the extent to which its only known receptor, GHSR-1a, is required for these effects. This study characterizes the pathways involved in AT atrophy in the Lewis Lung Carcinoma (LLC)-induced cachexia model and those mediating the effects of ghrelin in Ghsr+/+ and Ghsr-/- mice. We show that LLC causes AT atrophy by inducing anorexia, and increasing AT inflammation, thermogenesis and energy expenditure. These changes were greater in Ghsr-/-. Ghrelin administration prevented LLC-induced anorexia only in Ghsr+/+, but prevented WAT inflammation and atrophy in both genotypes, although its effects were greater in Ghsr+/+. LLC-induced increases in BAT inflammation, WAT and BAT thermogenesis, and energy expenditure were not affected by ghrelin. In...
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biorxivpreprint: GHSR-1a is not Required for Ghrelin's Anti-inflammatory and Fat-sparing Effects in Cancer Cachexia https://t.co/ZmrpCMIzEa #bioRxiv
biorxiv_cancer: GHSR-1a is not Required for Ghrelin's Anti-inflammatory and Fat-sparing Effects in Cancer Cachexia https://t.co/jHpqCpxjQB #biorxiv_cancer
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Authors: 12
Total Words: 0
Unqiue Words: 0

2.013 Mikeys
#3. Targeting dual signaling pathways in concert with immune checkpoints for the treatment of pancreatic cancer
Erik Knudsen, Vishnu Kumarasamy, Sejin Chung, Paris Vail, Stephanie Tzetzo, Amanda Ruiz, Mukund Seshadri, Scott Abrams, Jianmin Wang, Agnieszka Witkiewicz
Pancreatic cancer harbors a poor prognosis due to the lack of effective systemic therapies. Here we interrogated means to target key effector pathways down-stream from KRAS. We found that combination treatment with MEK and CDK4/6 inhibitors was effective across a broad range of PDX models in delaying tumor progression. These effects were associated with stable cell cycle arrest, as well as the induction of multiple genes associated with interferon response and antigen presentation in an RB-dependent fashion. Using single cell sequencing and complementary approaches, we found that the combination of CDK4/6 and MEK inhibition had a significant impact on increasing T-cell infiltration and altering myeloid populations, while potently cooperating with immune checkpoint inhibitors. Together, these data indicate that there are canonical and non-canonical features of CDK4/6 and MEK inhibition that impact on the tumor and host that can contribute to durable control for tumors in combination with immune checkpoint inhibitor therapy.  
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biorxivpreprint: Targeting dual signaling pathways in concert with immune checkpoints for the treatment of pancreatic cancer https://t.co/tfXlmcSzMM #bioRxiv
biorxiv_cancer: Targeting dual signaling pathways in concert with immune checkpoints for the treatment of pancreatic cancer https://t.co/FX37NW009y #biorxiv_cancer
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Sample Sizes : [10]
Authors: 10
Total Words: 9908
Unqiue Words: 2871

2.01 Mikeys
#4. An unsupervised feature extraction and selection strategy for identifying epithelial-mesenchymal transition state metrics in breast cancer and melanoma
David J Klinke, Arezo Torang
Digital cytometry is opening up new avenues to better understand the heterogeneous cell types present within the tumor microenvironment. While the focus is towards elucidating immune and stromal cells as clinical correlates, there is still a need to better understand how a change in tumor cell phenotype, such as the epithelial-mesenchymal transition, influences the immune contexture. To complement existing digital cytometry methods, our objective was to develop an unsupervised gene signature capturing a change in differentiation state that is tailored to the specific cellular context of breast cancer and melanoma, as a illustrative example. Towards this aim, we used principal component analysis coupled with resampling to develop unsupervised gene expression-based state metrics specific for the cellular context that characterize the state of cellular differentiation within an epithelial to mesenchymal-like state space and independently correlate with metastatic potential. First developed using cell line data, the orthogonal state...
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biorxivpreprint: An unsupervised feature extraction and selection strategy for identifying epithelial-mesenchymal transition state metrics in breast cancer and melanoma https://t.co/zVZ1NhlUag #bioRxiv
biorxiv_cancer: An unsupervised feature extraction and selection strategy for identifying epithelial-mesenchymal transition state metrics in breast ... https://t.co/kBeAbAKXQ9 #biorxiv_cancer
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Authors: 2
Total Words: 0
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2.01 Mikeys
#5. Sporadic activation of an oxidative stress-dependent NRF2-p53 signaling network in breast epithelial spheroids and premalignancies
Elizabeth J. Pereira, Joseph S. Burns, Christina Y. Lee, Taylor Marohl, Delia Calderon, Lixin Wang, Kristen A. Atkins, Chun-Chao Wang, Kevin Janes
Breast-mammary epithelial cells experience different local environments during tissue development and tumorigenesis. Microenvironmental heterogeneity gives rise to distinct cell-regulatory states whose identity and importance are just beginning to be appreciated. Cellular states diversify when clonal 3D spheroids are cultured in basement membrane, and prior transcriptomic analyses identified a state associated with stress tolerance and poor response to anticancer therapeutics. Here, we examined the regulation of this state and found that it is jointly coordinated by the NRF2 and p53 pathways, which are co-stabilized by spontaneous oxidative stress within the 3D cultures. Inhibition of NRF2 or p53 individually disrupts some of the transcripts defining the regulatory state but does not yield a notable phenotype in nontransformed breast epithelial cells. In contrast, combined perturbation prevents 3D growth in an oxidative stress-dependent manner. By integrating systems models of NRF2 and p53 signaling together as a single...
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biorxivpreprint: Sporadic activation of an oxidative stress-dependent NRF2-p53 signaling network in breast epithelial spheroids and premalignancies https://t.co/vaZi5IQ8jv #bioRxiv
biorxiv_cancer: Sporadic activation of an oxidative stress-dependent NRF2-p53 signaling network in breast epithelial spheroids and premalignancies https://t.co/7rWQTeVN1f #biorxiv_cancer
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Authors: 9
Total Words: 0
Unqiue Words: 0

2.01 Mikeys
#6. DECR1 is an androgen-repressed survival factor that regulates PUFA oxidation to protect prostate tumor cells from ferroptosis
Zeyad D Nassar, Chui Yan Mah, Jonas Dehairs, Ingrid J.G. Burvenich, Swati Irani, Margaret M Centenera, Raj K Shrestha, Max Moldovan, Anthony S Don, Andrew M Scott, Lisa G Horvath, David J Lynn, Luke A Selth, Andrew J Hoy, Johannes V Swinnen, Lisa M Butler
Fatty acid β-oxidation (FAO) is the main bioenergetic pathway in prostate cancer (PCa) and a promising novel therapeutic vulnerability. Here we demonstrate therapeutic efficacy of targeting FAO in clinical prostate tumors cultured ex vivo, and identify DECR1, which encodes the rate-limiting enzyme for oxidation of polyunsaturated fatty acids (PUFAs), as robustly overexpressed in PCa tissues and associated with shorter relapse-free survival. DECR1 is a negatively-regulated androgen receptor (AR) target gene and, therefore, may promote PCa cell survival and resistance to AR targeting therapeutics. DECR1 knockdown in PCa cells selectively inhibited β-oxidation of PUFAs, inhibited proliferation and migration of PCa cells, including treatment resistant lines, and suppressed tumor cell proliferation in vivo. Mechanistically, targeting of DECR1 caused cellular accumulation of linoleic acid, enhanced mitochondrial oxidative stress and lipid peroxidation, and ferroptosis. These findings implicate PUFA oxidation via DECR1 as a previously...
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shanicemah: i’m excited to share that my PhD work and our lab’s first ever #preprint is online now at #bioRxiv! @UniofAdelaide @scienceatsahmri @FFCMHMensHealth @Lipids_and_PCa https://t.co/MZ7WMLAyIC
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Authors: 16
Total Words: 0
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1.998 Mikeys
#7. PIM Kinases Alter Mitochondrial Dynamics and Chemosensitivity in Lung Cancer
Shailender S Chauhan, Rachel K Toth, Corbin C Jensen, Andrea L Casillas, David S Kashatus, Noel A Warfel
Resistance to chemotherapy represents a major obstacle 35 to the successful treatment of non-small cell lung cancer (NSCLC). The goal of this study was to determine how PIM kinases impact mitochondrial dynamics, ROS production, and response to chemotherapy in lung cancer. Live cell imaging and microscopy were used to determine the effect of PIM loss or inhibition on mitochondrial phenotype and ROS. Inhibition of PIM kinases caused excessive mitochondrial fission and significant upregulation of mitochondrial superoxide, increasing intercellular ROS. Mechanistically, we define a signaling axis linking PIM1 to Drp1 and mitochondrial fission in lung cancer. PIM inhibition significantly increased the protein levels and mitochondrial localization of Drp1, causing marked fragmentation of mitochondria. An inverse correlation between PIM1 and Drp1 was confirmed in NSCLC patient samples. Inhibition of PIM sensitized NSCLC to chemotherapy and produced a synergistic anti-tumor response in vitro and in vivo. Immunohistochemistry and...
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ISCaM18: RT @biorxiv_cancer: PIM Kinases Alter Mitochondrial Dynamics and Chemosensitivity in Lung Cancer https://t.co/UKTuLqeahY #biorxiv_cancer
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Authors: 6
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1.998 Mikeys
#8. Integrated analyses of early responses to radiation in glioblastoma identify new alterations in RNA processing and candidate target genes to improve treatment outcomes
Saket Choudhary, Suzanne C Burns, Hoda Mirsafian, Wenzheng Li, Dat T Vo, Mei Qiao, Andrew D Smith, Luiz O Penalva
Background: High-dose radiation is the main component of glioblastoma therapy. Unfortunately, radio-resistance is a common problem and a major contributor to tumor relapse. Understanding the molecular mechanisms driving response to radiation is critical for identifying regulatory routes that could be targeted to improve treatment response. Methods: We conducted an integrated analysis in the U251 and U343 glioblastoma cell lines to map early alterations in the expression of genes at three levels: transcription, splicing, and translation in response to ionizing radiation. Results: Changes at the transcriptional level were the most prevalent response. Downregulated genes are strongly associated with cell cycle and DNA replication and linked to a coordinated module of expression. Alterations in this group are likely driven by decreased expression of the transcription factor FOXM1 and members of the E2F family. Genes involved in RNA regulatory mechanisms were affected at the mRNA, splicing, and translation levels, highlighting their...
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Authors: 8
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1.997 Mikeys
#9. The significance of microRNA genes expression in ovarian cancer cell lines resistant to cytotoxic drugs
Dominika Kazmierczak, Karol Jopek, Karolina Sterzynska, Marcin Rucinski, Radoslaw Januchowski
Ovarian cancer is the most fatal type of gynecological cancer. The main reason for high mortality is the development of drug resistance. It can be related to increased expression of drug transporters and increased expression of extracellular matrix (ECM) proteins. miRNA is a short noncoding RNA that regulates expression of about 60% of genes in the human genome and plays a crucial role in developing cancer, including resistance to chemotherapy. Our foremost aim was to exhibit alterations in the miRNA expression levels in the cisplatin (CIS), paclitaxel (PAC), doxorubicin (DOX), and topotecan (TOP) - resistant variants of W1 sensitive ovarian cancer cell line using miRNA microarray. The second goal was to identify miRNAs responsible for the regulation of drug-resistant genes. According to our observation, alterations in the expression of 40 miRNA genes. The level of expression of 21 genes was upregulated in at least one drug-resistant cell line. The expression of 19 genes was downregulated in at least one drug-resistant cell line....
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Authors: 5
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1.997 Mikeys
#10. Measurement and models accounting for cell death capture hidden variation in compound response
Song Yi Bae, Ning Guan, Rui Yan, Katrina Warner, Aaron Samuel Meyer
Cancer cell sensitivity or resistance is almost universally quantified through a direct or surrogate measure of cell number. However, compound responses can occur through many distinct phenotypic outcomes including changes in cell growth, apoptosis, and non-apoptotic cell death. These outcomes have distinct effects on the tumor microenvironment, immune responses, and resistance mechanisms. Here, we show that quantifying cell viability alone is insufficient to distinguish between these compound responses. Using an alternative assay and drug response analysis amenable to high-throughput measurement, we find that compounds with identical viability outcomes can have very different effects on cell growth and death. Moreover, compound pairs with additive cell growth and death effects can appear synergistic when only assessed by viability. Overall, these results demonstrate an approach to incorporating measurements of cell death when characterizing a pharmacologic response.
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biorxivpreprint: Measurement and models accounting for cell death capture hidden variation in compound response https://t.co/CgX5FyMLeo #bioRxiv
biorxiv_cancer: Measurement and models accounting for cell death capture hidden variation in compound response https://t.co/PhkD3jz1vR #biorxiv_cancer
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Sample Sizes : None.
Authors: 5
Total Words: 7227
Unqiue Words: 2446

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