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  1. Analyzed Page
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  7. Topics
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We began analyzing https://www.nature.com/articles/1210002, but it redirected us to https://www.nature.com/articles/1210002. The analysis below is for the second page.

Title[redir]:
Transforming function of the LSM1 oncogene in human breast cancers with the 8p11–12 amplicon | Oncogene
Description:
Amplification of the 8p11–12 region occurs in 15–20% of breast cancers, but the driving oncogene at this locus has yet to be definitively identified. We mapped the 8p11–12 amplicon in breast cancer cell lines and primary human breast cancers and identified the candidate oncogene human Sm-like protein (hLsm1, LSM1) based on increases in copy number and expression level relative to human mammary epithelial cells. To examine the oncogenic role of LSM1, we overexpressed this gene in MCF10A mammary epithelial cells and inhibited its production in the SUM44 breast cancer cell line, which has a natural amplification and overexpression of LSM1. Our data confirmed that LSM1 is an oncogene from the 8p11–12 amplicon by showing that hLsm1 overexpression induced growth factor-independent proliferation and soft agar colony formation in MCF10A cells, and hLsm1 inhibition in SUM44 cells dramatically reduced soft agar growth. Little is known about hLsm1 function other than its involvement in mRNA degradation; therefore, we used expression microarray analysis to investigate how hLsm1 affects cell transformation in MCF10A and SUM44 cells. We identified numerous genes altered following hLsm1 overexpression common to SUM44 breast cancer cells that play important roles in cell cycle regulation, cell proliferation and other cancer-promoting processes. Future work will continue to characterize these important changes to achieve a more complete understanding of the mechanism of hLsm1

Matching Content Categories {πŸ“š}

  • Education
  • Science
  • Health & Fitness

Content Management System {πŸ“}

What CMS is doi.org built with?

Custom-built

No common CMS systems were detected on Doi.org, and no known web development framework was identified.

Traffic Estimate {πŸ“ˆ}

What is the average monthly size of doi.org audience?

πŸ™οΈ Massive Traffic: 50M - 100M visitors per month


Based on our best estimate, this website will receive around 96,105,781 visitors per month in the current month.

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How Does Doi.org Make Money? {πŸ’Έ}

We can't figure out the monetization strategy.

Not all websites focus on profit; some are designed to educate, connect people, or share useful tools. People create websites for numerous reasons. And this could be one such example. Doi.org might be cashing in, but we can't detect the method they're using.

Keywords {πŸ”}

article, cancer, google, scholar, cas, breast, nature, oncogene, cells, lsm, human, draghici, cell, expression, access, gene, res, amplicon, ethier, analysis, content, data, mammary, cookies, function, yang, hlsm, usa, privacy, lines, epithelial, sum, growth, genomics, open, khatri, pubmed, state, research, cancers, streicher, protein, transformation, issue, biol, watson, casm, advertising, information, subscribe,

Topics {βœ’οΈ}

nature portfolio permissions reprints privacy policy expression index computation nature advertising social media author information authors data analysis tools ontology-based tools real-time quantitative pcr author correspondence mrna-degrading enzymes dcp1/2 casm-mediated cellular transformation springerlink instant access global functional profiling model-based analysis permissions human breast cancers breast cancer identifies clinical breast cancer development web server issue cell cycle regulation pancreatic cancer cells personal data privacy hall/crc press wayne state university kelley jr cancer-promoting processes national cancer institute karmanos cancer institute cell proliferation advanced pancreatic cancer hlsm1 overexpression common altered gene expression invasive ductal carcinoma data protection explore content data confirmed subscription content expression level relative oncogene promotes transformation nrg1 gene rearrangements european economic area institutional subscriptions read distinct cytoplasmic foci transgenic mice expressing 8p11–12 region occurs

Schema {πŸ—ΊοΈ}

WebPage:
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         headline:Transforming function of the LSM1 oncogene in human breast cancers with the 8p11Ҁ“12 amplicon
         description:Amplification of the 8p11Ҁ“12 region occurs in 15Ҁ“20% of breast cancers, but the driving oncogene at this locus has yet to be definitively identified. We mapped the 8p11Ҁ“12 amplicon in breast cancer cell lines and primary human breast cancers and identified the candidate oncogene human Sm-like protein (hLsm1, LSM1) based on increases in copy number and expression level relative to human mammary epithelial cells. To examine the oncogenic role of LSM1, we overexpressed this gene in MCF10A mammary epithelial cells and inhibited its production in the SUM44 breast cancer cell line, which has a natural amplification and overexpression of LSM1. Our data confirmed that LSM1 is an oncogene from the 8p11Ҁ“12 amplicon by showing that hLsm1 overexpression induced growth factor-independent proliferation and soft agar colony formation in MCF10A cells, and hLsm1 inhibition in SUM44 cells dramatically reduced soft agar growth. Little is known about hLsm1 function other than its involvement in mRNA degradation; therefore, we used expression microarray analysis to investigate how hLsm1 affects cell transformation in MCF10A and SUM44 cells. We identified numerous genes altered following hLsm1 overexpression common to SUM44 breast cancer cells that play important roles in cell cycle regulation, cell proliferation and other cancer-promoting processes. Future work will continue to characterize these important changes to achieve a more complete understanding of the mechanism of hLsm1's effect on cancer progression.
         datePublished:2006-09-25T00:00:00Z
         dateModified:2006-09-25T00:00:00Z
         pageStart:2104
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            Cell Biology
            Human Genetics
            Oncology
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      headline:Transforming function of the LSM1 oncogene in human breast cancers with the 8p11Ҁ“12 amplicon
      description:Amplification of the 8p11Ҁ“12 region occurs in 15Ҁ“20% of breast cancers, but the driving oncogene at this locus has yet to be definitively identified. We mapped the 8p11Ҁ“12 amplicon in breast cancer cell lines and primary human breast cancers and identified the candidate oncogene human Sm-like protein (hLsm1, LSM1) based on increases in copy number and expression level relative to human mammary epithelial cells. To examine the oncogenic role of LSM1, we overexpressed this gene in MCF10A mammary epithelial cells and inhibited its production in the SUM44 breast cancer cell line, which has a natural amplification and overexpression of LSM1. Our data confirmed that LSM1 is an oncogene from the 8p11Ҁ“12 amplicon by showing that hLsm1 overexpression induced growth factor-independent proliferation and soft agar colony formation in MCF10A cells, and hLsm1 inhibition in SUM44 cells dramatically reduced soft agar growth. Little is known about hLsm1 function other than its involvement in mRNA degradation; therefore, we used expression microarray analysis to investigate how hLsm1 affects cell transformation in MCF10A and SUM44 cells. We identified numerous genes altered following hLsm1 overexpression common to SUM44 breast cancer cells that play important roles in cell cycle regulation, cell proliferation and other cancer-promoting processes. Future work will continue to characterize these important changes to achieve a more complete understanding of the mechanism of hLsm1's effect on cancer progression.
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