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Journal articles on the topic 'OncomiR (oncomiRs)'

Author: Grafiati

Published: 3 June 2025

Last updated: 1 August 2025

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1

Seo, Yoona, Sung Soo Kim, Namdoo Kim, Sungchan Cho, Jong Bae Park, and Jong Heon Kim. "Development of a miRNA-controlled dual-sensing system and its application for targeting miR-21 signaling in tumorigenesis." Experimental & Molecular Medicine 52, no. 12 (2020): 1989–2004. http://dx.doi.org/10.1038/s12276-020-00537-z.

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AbstractMicroRNAs (miRNAs) are considered to be strong prognostic markers and key therapeutic targets in human diseases, especially cancer. A sensitive monitoring platform for cancer-associated miRNA (oncomiR) action is needed for mechanistic studies, preclinical evaluation, and inhibitor screening. In this study, we developed and systemically applied a sensitive and efficient lentivirus-based system for monitoring oncomiR actions, essentially miR-21. The specificity and sensitivity of “miRDREL” against various oncomiRs were validated by checking for tight correlations between their expression

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Bollati, Valentina, Paola Monti, Davide Biganzoli, et al. "Environmental and Lifestyle Cancer Risk Factors: Shaping Extracellular Vesicle OncomiRs and Paving the Path to Cancer Development." Cancers 15, no. 17 (2023): 4317. http://dx.doi.org/10.3390/cancers15174317.

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Intercellular communication has been transformed by the discovery of extracellular vesicles (EVs) and their cargo, including microRNAs (miRNAs), which play crucial roles in intercellular signaling. These EVs were previously disregarded as cellular debris but are now recognized as vital mediators of biological information transfer between cells. Furthermore, they respond not only to internal stimuli but also to environmental and lifestyle factors. Identifying EV-borne oncomiRs, a subset of miRNAs implicated in cancer development, could revolutionize our understanding of how environmental and li

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Krsmanovic, Pavle, Heidi Mocikova, Kamila Chramostova, et al. "Circulating microRNAs in Cerebrospinal Fluid and Plasma: Sensitive Tool for Detection of Secondary CNS Involvement, Monitoring of Therapy and Prediction of CNS Relapse in Aggressive B-NHL Lymphomas." Cancers 14, no. 9 (2022): 2305. http://dx.doi.org/10.3390/cancers14092305.

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Lymphoma with secondary central nervous system (CNS) involvement represents one of the most aggressive malignancies, with poor prognosis and high mortality. New diagnostic tools for its early detection, response evaluation, and CNS relapse prediction are needed. We analyzed circulating microRNAs in the cerebrospinal fluid (CSF) and plasma of 162 patients with aggressive B-cell non-Hodgkin’s lymphomas (B-NHL) and compared their levels in CNS-involving lymphomas versus in systemic lymphomas, at diagnosis and during treatment and CNS relapse. We identified a set of five oncogenic microRNAs (miR-1

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4

Li, Jiang, Yan Yan, Lin Ang, et al. "Extracellular vesicles-derived OncomiRs mediate communication between cancer cells and cancer-associated hepatic stellate cells in hepatocellular carcinoma microenvironment." Carcinogenesis 41, no. 2 (2019): 223–34. http://dx.doi.org/10.1093/carcin/bgz096.

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Abstract Tumor microenvironment (TME) is a critical determinant for hepatocellular carcinoma (HCC). Hepatic stellate cells (HSCs) are main interstitial cells in TME and play a vital role in early intrahepatic invasion and metastasis of HCC. The potential mechanism on the interactions between HSCs and HCC cells remains unclear. In this study, the effects of extracellular vesicles (EVs)-derived OncomiRs that mediate communication between HCC cells and cancer-associated hepatic stellate cells (caHSCs) and remold TME were investigated. The results found that the HCC cells-released EVs contained mo

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5

Susanti, R., Muchamad Dafip, and Dewi Mustikaningtyas. "OncomiR Structure and Network Prediction on Adenomatosis Polyposis Coli (APC) Gene Silencing Regulation in Colorectal Cancer." Trends in Sciences 20, no. 10 (2023): 6168. http://dx.doi.org/10.48048/tis.2023.6168.

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The emergence of colorectal cancer cells is associated with the inactivation of the adenomatosis polyposis coli (APC) gene which increases the activity of ß-catenin, one of which is due to oncomiRNA (cancer-inducing microRNA). miR-135a/b-5p and miR-494-3p were thought to be involved in silencing the APC gene and increasing cell proliferation and could potentially be used as anti-miR targets. However, there is a need for an in-depth evaluation of the involvement of the oncomiR as a therapeutic target in preventing the formation of CRC. Therefore, this study aimed to predict the mechanism of inh

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Mumal, Iqra, Patrick Sin-Chan, Tannu Suwal, et al. "PDTM-22. A C19MC-LIN28A-MYCN ONCOGENIC CIRCUIT DRIVEN BY HIJACKED SUPER-ENHANCERS IS A DISTINCT THERAPEUTIC VULNERABILITY IN ETMRS – A LETHAL BRAIN TUMOR." Neuro-Oncology 21, Supplement_6 (2019): vi191—vi192. http://dx.doi.org/10.1093/neuonc/noz175.798.

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Abstract Embryonal tumors with multi-layered rosettes (ETMR) are aggressive brain cancers with characteristic C19MC oncomiR amplification and enrichment of pluripotency factor LIN28A. Here we investigated C19MC oncogenic mechanisms and discovered a potent C19MC-LIN28A-MYCN circuitry driven by multiple regulatory loops and super-enhancers resulting from long-range MYCN DNA interactions and C19MC gene fusions. C19MC and LIN28A targets respectively converge on critical cell cycle tumor suppressors and neo-embryonic DNMT3A/B isoforms. We identify a MYCN driven, core transcriptional network, conser

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Korać, Petra, Mariastefania Antica, and Maja Matulić. "MiR-7 in Cancer Development." Biomedicines 9, no. 3 (2021): 325. http://dx.doi.org/10.3390/biomedicines9030325.

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MicroRNAs (miRNAs) are short non-coding RNA involved in the regulation of specific mRNA translation. They participate in cellular signaling circuits and can act as oncogenes in tumor development, so-called oncomirs, as well as tumor suppressors. miR-7 is an ancient miRNA involved in the fine-tuning of several signaling pathways, acting mainly as tumor suppressor. Through downregulation of PI3K and MAPK pathways, its dominant role is the suppression of proliferation and survival, stimulation of apoptosis and inhibition of migration. Besides these functions, it has numerous additional roles in t

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8

Dogar, Afzal M., Harry Towbin та Jonathan Hall. "Suppression of Latent Transforming Growth Factor (TGF)-β1 Restores Growth Inhibitory TGF-β Signaling through microRNAs". Journal of Biological Chemistry 286, № 18 (2011): 16447–58. http://dx.doi.org/10.1074/jbc.m110.208652.

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Cancer cells secreting excess latent TGF-β are often resistant to TGF-β induced growth inhibition. We observed that RNAi against TGF-β1 led to apoptotic death in such cell lines with features that were, paradoxically, reminiscent of TGF-β signaling activity and that included transiently enhanced SMAD2 and AKT phosphorylation. A comprehensive search in Hela cells for potential microRNA drivers of this mechanism revealed that RNAi against TGF-β1 led to induction of pro-apoptotic miR-34a and to a globally decreased oncomir expression. The reduced levels of the oncomirs miR-18a and miR-24 accounte

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9

Mahmoud Ibrahim, Maryam Abdul-Kader, Ava Azizi, et al. "The miRNA-9 Isoform Story in Cancer: An OncomiR or Tumor Suppressor?" Journal of Cancer Biomoleculars and Therapeutics 2, no. 2 (2025): 13–36. https://doi.org/10.62382/jcbt.v2i2.53.

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MicroRNAs (miRNAs) are small, non-coding RNA molecules that regulate gene expression post-transcriptionally. They function by binding to newly transcribed mRNAs of protein-coding genes, suppressing gene expression at the post-transcriptional level. Thus, miRNAs play a crucial role in controlling a plethora of cellular processes, making miRNAs a unique class of regulatory RNA with defined developmental roles. Thus, these small yet powerful miRNAs have garnered the attention of many researchers due to the known biological regulatory role during chronic disease onset, including cancer. Over the p

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10

Ruiz-Plazas, Xavier, Antonio Altuna-Coy, Marta Alves-Santiago, et al. "Liquid Biopsy-Based Exo-oncomiRNAs Can Predict Prostate Cancer Aggressiveness." Cancers 13, no. 2 (2021): 250. http://dx.doi.org/10.3390/cancers13020250.

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Liquid biopsy-based biomarkers, including microRNAs packaged within extracellular vesicles, are promising tools for patient management. The cytokine tumor necrosis factor-like weak inducer of apoptosis (TWEAK) is related to PCa progression and is found in the semen of patients with PCa. TWEAK can induce the transfer of exo-oncomiRNAs from tumor cells to body fluids, and this process might have utility in non-invasive PCa prognosis. We investigated TWEAK-regulated exo-microRNAs in semen and in post-digital rectal examination urine from patients with different degrees of PCa aggressiveness. We f

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11

Cascione, Luciano, Eugenio Gaudio, Elena Bernasconi, et al. "BET Bromodomain Inhibitor OTX015 Affects the Expression of Micrornas Involved in the Pathogenesis of Diffuse Large B-Cell Lymphoma." Blood 124, no. 21 (2014): 4495. http://dx.doi.org/10.1182/blood.v124.21.4495.4495.

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Abstract Background. Diffuse large B-cell lymphoma (DLBCL) is the most common lymphoma, accounting for 30%-40% of all cases. Despite a major improvement in the cure rate, a large number of DLBCL patients lack therapeutic options. Aberrant changes in histone modifications, DNA methylation and expression levels of non-coding RNA, including microRNA (miRNA), contribute to DLBCL pathogenesis and represent potential therapeutic targets. OTX015 targets bromodomain and extra-terminal (BET) proteins, which are epigenetic readers contributing to gene transcription. It has shown preclinical activity in

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12

Tan, Zhibo, Min Chen, Ying Wang, et al. "CHEK1: a hub gene related to poor prognosis for lung adenocarcinoma." Biomarkers in Medicine 16, no. 2 (2022): 83–100. http://dx.doi.org/10.2217/bmm-2021-0919.

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Aim: The study aims to pinpoint hub genes and investigate their functions in order to gain insightful understandings of lung adenocarcinoma (LUAD). Methods: Bioinformatic approaches were adopted to investigate genes in databases including Gene Expression Omnibus, WebGestalt, STRING and Cytoscape, GEPIA2, Oncomine, Human Protein Atlas, TIMER2.0, UALCAN, cBioPortal, TargetScanHuman, OncomiR, ENCORI, Kaplan–Meier plotter, UCSC Xena, European Molecular Biology Laboratory – European Bioinformatics Institute Single Cell Expression Atlas and CancerSEA. Results: Five hub genes were ascertained. CHEK1

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13

Mihály, Dóra, Gergő Papp, Zsolt Mervai, et al. "The oncomir face of microRNA-206: A permanent miR-206 transfection study." Experimental Biology and Medicine 243, no. 12 (2018): 1014–23. http://dx.doi.org/10.1177/1535370218795406.

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MiR-206 is a remarkable miRNA because it functions as a suppressor miRNA in rhabdomyosarcoma while at the same time, as previously showed, it can act as an oncomiRNA in SMARCB1 immunonegative soft tissue sarcomas. The aim of this study was to investigate the effect of miR-206 on its several target genes in various human tumorous and normal cell lines. In the current work, we created miR-206-overexpressing cell lines (HT-1080, Caco2, iASC, and SS-iASC) using permanent transfection. mRNA expression of the target genes of miR-206 (SMARCB1, ACTL6A, CCND1, POLA1, NOTCH3, MET, and G6PD) and SMARCB1

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14

Peeken, Jan Caspar, Fridtjof Nüsslin, and Stephanie E. Combs. "“Radio-oncomics”." Strahlentherapie und Onkologie 193, no. 10 (2017): 767–79. http://dx.doi.org/10.1007/s00066-017-1175-0.

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15

Goga, A., and C. Benz. "Anti-Oncomir Suppression of Tumor Phenotypes." Molecular Interventions 7, no. 4 (2007): 199–202. http://dx.doi.org/10.1124/mi.7.4.6.

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16

Babu, Sunil G., Sanket Singh Ponia, Dinesh Kumar, and Sangeeta Saxena. "Cellular oncomiR orthologue in EBV oncogenesis." Computers in Biology and Medicine 41, no. 10 (2011): 891–98. http://dx.doi.org/10.1016/j.compbiomed.2011.07.007.

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17

de Almeida, Bruna, Natalia Garcia, Giovana Maffazioli, Laura Gonzalez dos Anjos, Edmund Chada Baracat, and Katia Candido Carvalho. "Oncomirs Expression Profiling in Uterine Leiomyosarcoma Cells." International Journal of Molecular Sciences 19, no. 1 (2017): 52. http://dx.doi.org/10.3390/ijms19010052.

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18

Esquela-Kerscher, Aurora, and Frank J. Slack. "Oncomirs — microRNAs with a role in cancer." Nature Reviews Cancer 6, no. 4 (2006): 259–69. http://dx.doi.org/10.1038/nrc1840.

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19

Bobbili, Madhusudhan Reddy, Robert M. Mader, Johannes Grillari, and Hanna Dellago. "OncomiR-17-5p: alarm signal in cancer?" Oncotarget 8, no. 41 (2017): 71206–22. http://dx.doi.org/10.18632/oncotarget.19331.

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20

Thompson, Patricia A. "Navigating the Maize between Red Meat and Oncomirs." Cancer Prevention Research 7, no. 8 (2014): 777–80. http://dx.doi.org/10.1158/1940-6207.capr-14-0196.

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21

Delancey, Craig. "Teleofunctions and Oncomice." Environmental Ethics 26, no. 2 (2004): 171–88. http://dx.doi.org/10.5840/enviroethics200426228.

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22

Mocellin, Simone, Sandro Pasquali, and Pierluigi Pilati. "Oncomirs: From Tumor Biology to Molecularly Targeted Anticancer Strategies." Mini-Reviews in Medicinal Chemistry 9, no. 1 (2009): 70–80. http://dx.doi.org/10.2174/138955709787001802.

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23

Reshmi, G., and M. Radhakrishna Pillai. "Beyond HPV: Oncomirs as new players in cervical cancer." FEBS Letters 582, no. 30 (2008): 4113–16. http://dx.doi.org/10.1016/j.febslet.2008.11.011.

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24

Bhattacharyya, Malay, and Sanghamitra Bandyopadhyay. "In Silico Identification of OncomiRs in Different Cancer Types." Journal of The Institution of Engineers (India): Series B 93, no. 1 (2012): 15–23. http://dx.doi.org/10.1007/s40031-012-0003-2.

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25

Cho, William CS. "OncomiRs: the discovery and progress of microRNAs in cancers." Molecular Cancer 6, no. 1 (2007): 60. http://dx.doi.org/10.1186/1476-4598-6-60.

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26

Olive, Virginie, Qijing Li, and Lin He. "mir-17-92: a polycistronic oncomir with pleiotropic functions." Immunological Reviews 253, no. 1 (2013): 158–66. http://dx.doi.org/10.1111/imr.12054.

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27

Kincaid, R. P., J. M. Burke, and C. S. Sullivan. "RNA virus microRNA that mimics a B-cell oncomiR." Proceedings of the National Academy of Sciences 109, no. 8 (2012): 3077–82. http://dx.doi.org/10.1073/pnas.1116107109.

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28

Folini, Marco, Paolo Gandellini, Nicole Longoni, et al. "miR-21: an oncomir on strike in prostate cancer." Molecular Cancer 9, no. 1 (2010): 12. http://dx.doi.org/10.1186/1476-4598-9-12.

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29

Taïbi, Fatiha, Valérie Metzinger-Le Meuth, Ziad A. Massy, and Laurent Metzinger. "miR-223: An inflammatory oncomiR enters the cardiovascular field." Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease 1842, no. 7 (2014): 1001–9. http://dx.doi.org/10.1016/j.bbadis.2014.03.005.

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30

Vestergaard, Lau K., Douglas N. P. Oliveira, Tim S. Poulsen, Claus K. Høgdall, and Estrid V. Høgdall. "Oncomine™ Comprehensive Assay v3 vs. Oncomine™ Comprehensive Assay Plus." Cancers 13, no. 20 (2021): 5230. http://dx.doi.org/10.3390/cancers13205230.

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The usage of next generation sequencing in combination with targeted gene panels has enforced a better understanding of tumor compositions. The identification of key genomic biomarkers underlying a disease are crucial for diagnosis, prognosis, treatment and therapeutic responses. The Oncomine™ Comprehensive Assay v3 (OCAv3) covers 161 cancer-associated genes and is routinely employed to support clinical decision making for a therapeutic course. An improved version, Oncomine™ Comprehensive Assay Plus (OCA-Plus), has been recently developed, covering 501 genes (144 overlapping with OCAv3) in add

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31

Kang, K. Connie. "Escaping the Oncoming Communists." Manoa 14, no. 2 (2002): 133–37. http://dx.doi.org/10.1353/man.2003.0022.

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32

Rana, Muhit, Mustafa Balcioglu, Maya Kovach, et al. "Reprogrammable multiplexed detection of circulating oncomiRs using hybridization chain reaction." Chemical Communications 52, no. 17 (2016): 3524–27. http://dx.doi.org/10.1039/c5cc09910b.

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Coupling the DNA polymerization capability of HCR with the plasmonic properties of AuNP for reprogrammable, multiplexed and visual detection of three different circulating oncomiRs in seven different combinations.

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33

Krutovskikh, Vladimir A., and Zdenko Herceg. "Oncogenic microRNAs (OncomiRs) as a new class of cancer biomarkers." BioEssays 32, no. 10 (2010): 894–904. http://dx.doi.org/10.1002/bies.201000040.

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34

Chakraborty, Saikat, and Yamuna Krishnan. "A structural map of oncomiR-1 at single-nucleotide resolution." Nucleic Acids Research 45, no. 16 (2017): 9694–705. http://dx.doi.org/10.1093/nar/gkx613.

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35

Potrich, Cristina, Valentina Vaghi, Lorenzo Lunelli, et al. "OncomiR detection in circulating body fluids: a PDMS microdevice perspective." Lab Chip 14, no. 20 (2014): 4067–75. http://dx.doi.org/10.1039/c4lc00630e.

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36

Kort, Eric J., Leslie Farber, Maria Tretiakova, et al. "The E2F3-Oncomir-1 Axis Is Activated in Wilms' Tumor." Cancer Research 68, no. 11 (2008): 4034–38. http://dx.doi.org/10.1158/0008-5472.can-08-0592.

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37

Svoronos, Alexander A., Donald M. Engelman, and Frank J. Slack. "OncomiR or Tumor Suppressor? The Duplicity of MicroRNAs in Cancer." Cancer Research 76, no. 13 (2016): 3666–70. http://dx.doi.org/10.1158/0008-5472.can-16-0359.

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38

Phoebe M, Grace Lydia, and Jemmy Christy H. "Utilizing OncomiR and TSmiR as Biomarkers for Screening Breast Cancer." Current Trends in Biotechnology and Pharmacy 18, no. 4s (2024): 18–30. https://doi.org/10.5530/ctbp.2024.4s.2.

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39

Wong, Nathan W., Yuhao Chen, Shuai Chen, and Xiaowei Wang. "OncomiR: an online resource for exploring pan-cancer microRNA dysregulation." Bioinformatics 34, no. 4 (2017): 713–15. http://dx.doi.org/10.1093/bioinformatics/btx627.

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40

He, Chengcheng, Bo Luo, Nan Jiang, et al. "OncomiR or antioncomiR: Role of miRNAs in Acute Myeloid Leukemia." Leukemia & Lymphoma 60, no. 2 (2018): 284–94. http://dx.doi.org/10.1080/10428194.2018.1480769.

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41

Chaudhuri, A. A., A. Y. L. So, A. Mehta, et al. "Oncomir miR-125b regulates hematopoiesis by targeting the gene Lin28A." Proceedings of the National Academy of Sciences 109, no. 11 (2012): 4233–38. http://dx.doi.org/10.1073/pnas.1200677109.

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42

Menon, Amrutha, Noraini Abd-Aziz, Kanwal Khalid, Chit Laa Poh, and Rakesh Naidu. "miRNA: A Promising Therapeutic Target in Cancer." International Journal of Molecular Sciences 23, no. 19 (2022): 11502. http://dx.doi.org/10.3390/ijms231911502.

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microRNAs are small non-coding RNAs that regulate several genes post-transcriptionally by complementarity pairing. Since discovery, they have been reported to be involved in a variety of biological functions and pathologies including cancer. In cancer, they can act as a tumor suppressor or oncomiR depending on the cell type. Studies have shown that miRNA-based therapy, either by inhibiting an oncomiR or by inducing a tumor suppressor, is effective in cancer treatment. This review focusses on the role of miRNA in cancer, therapeutic approaches with miRNAs and how they can be effectively deliver

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43

Pospisil, Vit, Heidi Mocikova, Magdalena Klanova, et al. "Oncogenic Micrornas In Cerebrospinal Fluid and Sera Reflect Therapy Efficacy and Their Reappearance Precedes Clinical Relapse In Primary and Secondary CNS Lymphoma." Blood 122, no. 21 (2013): 1777. http://dx.doi.org/10.1182/blood.v122.21.1777.1777.

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Abstract Introduction MicroRNAs (miRNAs) are single-stranded non-coding RNAs (21-25nt) that negatively regulate gene expression at post-transcriptional level by blocking translation and mRNA destabilization. Diffuse large B cell lymphomas (DLBCL) overexpress oncogenic microRNAs (including miR-17-92 and miR-155) that regulate tumor growth and spreading. Unlike longer species of RNA, microRNAs are stable and detectable in body fluids including serum/plasma and cerebrospinal fluid (CSF), however their kinetics in body fluids upon course the therapy of DLBCL has not been fully explored. Notably DL

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Jurkovicova, Dana, Bozena Smolkova, Monika Magyerkova, et al. "Down-regulation of traditional oncomiRs in plasma of breast cancer patients." Oncotarget 8, no. 44 (2017): 77369–84. http://dx.doi.org/10.18632/oncotarget.20484.

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Manikandan, Jayapal, Joseph Jude Aarthi, Srinivasan Dinesh Kumar, and Peter Natesan Pushparaj. "Oncomirs: The potential role of non-coding microRNAs in understanding cancer." Bioinformation 2, no. 8 (2008): 330–34. http://dx.doi.org/10.6026/97320630002330.

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Guizard, C., P. Amblard, and X. Bouisson. "Oncoming Developments in Membrane Standardization." Key Engineering Materials 61-62 (January 1992): 399–402. http://dx.doi.org/10.4028/www.scientific.net/kem.61-62.399.

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Rajabi, H., C. Jin, R. Ahmad, A. C. McClary, M. D. Joshi, and D. Kufe. "Mucin 1 Oncoprotein Expression Is Suppressed by the miR-125b Oncomir." Genes & Cancer 1, no. 1 (2010): 62–68. http://dx.doi.org/10.1177/1947601909357933.

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48

Kim, Hyunsoo, Wei Huang, Xiuli Jiang, Brenton Pennicooke, Peter J. Park, and Mark D. Johnson. "Integrative genome analysis reveals an oncomir/oncogene cluster regulating glioblastoma survivorship." Proceedings of the National Academy of Sciences 107, no. 5 (2010): 2183–88. http://dx.doi.org/10.1073/pnas.0909896107.

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Using a multidimensional genomic data set on glioblastoma from The Cancer Genome Atlas, we identified hsa-miR-26a as a cooperating component of a frequently occurring amplicon that also contains CDK4 and CENTG1, two oncogenes that regulate the RB1 and PI3 kinase/AKT pathways, respectively. By integrating DNA copy number, mRNA, microRNA, and DNA methylation data, we identified functionally relevant targets of miR-26a in glioblastoma, including PTEN, RB1, and MAP3K2/MEKK2. We demonstrate that miR-26a alone can transform cells and it promotes glioblastoma cell growth in vitro and in the mouse bra

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Barnaś, Edyta, Joanna Ewa Skręt-Magierło, Sylwia Paszek, et al. "Two oncomiRs, miR-182-5p and miR-103a-3p, Involved in Intravenous Leiomyomatosis." Genes 14, no. 3 (2023): 712. http://dx.doi.org/10.3390/genes14030712.

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Leiomyomas, also referred to as fibroids, belong to the most common type of benign tumors developing in the myometrium of the uterus. Intravenous leiomyomatosis (IVL) tends to be regarded as a rare type of uterine leiomyoma. IVL tumors are characterized by muscle cell masses developing within the uterine and extrauterine venous system. The underlying mechanism responsible for the proliferation of these lesions is still unknown. The aim of the study was to investigate the expression of the two epigenetic factors, oncomiRs miR-182-5p and miR-103a-3p, in intravenous leiomyomatosis. This study was

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50

Wu, Yu, Shun Ying Zhu, Hong Wang, Fei Yao, and Huai Zhong Zhu. "Crossing Roads Safely: Influence of Various Vehicle Types in Gap Selection by Pedestrians." Applied Mechanics and Materials 361-363 (August 2013): 2152–55. http://dx.doi.org/10.4028/www.scientific.net/amm.361-363.2152.

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This paper analyzed the relationship between the gap selection and the types of oncoming vehicle in the process of pedestrians crossing the road. The oncoming vehicles were divided into large and small vehicle; six groups of pedestrians were recorded, young-male, mid-aged-male, old-male, young-female, mid-aged-female and old-female. The accepted gaps were recorded and analyzed using one-way ANOVA analysis. The results showed that, oncoming vehicles type had significant impact upon gap selection of pedestrians. A large oncoming vehicle had a shorter selected gap than a small oncoming vehicle. I

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