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LINK . SPRINGER . COM {}

  1. Analyzed Page
  2. Matching Content Categories
  3. CMS
  4. Monthly Traffic Estimate
  5. How Does Link.springer.com Make Money
  6. Keywords
  7. Topics
  8. Questions
  9. Schema
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  11. Analytics And Tracking
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We are analyzing https://link.springer.com/article/10.1007/s10549-015-3316-4.

Title:
Revisiting the estrogen receptor pathway and its role in endocrine therapy for postmenopausal women with estrogen receptor-positive metastatic breast cancer | Breast Cancer Research and Treatment
Description:
Endocrine therapy (ET) is the most commonly administered first-line systemic therapy for estrogen receptor-positive (ER+) metastatic breast cancer (MBC). Manipulation of hormone levels was one of the earliest ET approaches. However, treatment modalities have since evolved with the growing understanding of estrogen biosynthesis and ER biology. The current armamentarium of ET includes selective estrogen receptor modulation, aromatase inhibition, and selective estrogen receptor downregulation. However, intrinsic or acquired resistance to ET is frequently observed. Significant strides have been made in recent years in our understanding of the mechanisms of resistance to ET, and several targeted approaches including inhibitors against the phosphatidylinositol 3-kinase/mammalian target of rapamycin (PI3K/mTOR) pathway and cyclin-dependent kinase 4/6 (CDK4/6) have shown great promise. The mTOR inhibitor, everolimus, is already in clinical use for the treatment of resistant ER+MBC. However, multiple levels of evidence indicate that ER signaling remains as an important therapeutic target even in the resistance setting, providing the rationale for sequencing multiple lines and combinations of ET. In addition, recurrent mutations in estrogen receptor 1 (ESR1), the gene that encodes the ER, have been identified in the genomic studies of metastatic ER+ breast cancer. ESR1 mutations are an important mechanism for acquired resistance, and effective ER targeting in this setting is particularly important.
Website Age:
28 years and 1 months (reg. 1997-05-29).

Matching Content Categories {📚}

  • Health & Fitness
  • Education
  • Science

Content Management System {📝}

What CMS is link.springer.com built with?

Custom-built

No common CMS systems were detected on Link.springer.com, and no known web development framework was identified.

Traffic Estimate {📈}

What is the average monthly size of link.springer.com audience?

🌠 Phenomenal Traffic: 5M - 10M visitors per month


Based on our best estimate, this website will receive around 5,000,019 visitors per month in the current month.
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How Does Link.springer.com Make Money? {💸}

We can't figure out the monetization strategy.

Many websites are intended to earn money, but some serve to share ideas or build connections. Websites exist for all kinds of purposes. This might be one of them. Link.springer.com could be secretly minting cash, but we can't detect the process.

Keywords {🔍}

cancer, pubmed, google, scholar, breast, article, cas, estrogen, therapy, clin, central, endocrine, postmenopausal, oncol, advanced, receptor, fulvestrant, treatment, receptorpositive, kinase, cell, anastrozole, women, resistance, aromatase, res, study, tamoxifen, firstline, inhibitors, mol, versus, phase, metastatic, hormone, randomized, human, adjuvant, cyclin, trial, results, clinical, biol, pathway, abstract, survival, exemestane, patients, research, cyclindependent,

Topics {✒️}

/news/press-release/press-release-detail/pfizer_receives_u_s_fda_accelerated_approval_of_ibrance_palbociclib /publications/targeted-therapies-cancer/2013/april-2013/pi3k-inhibitors hormone-receptor-positive locally advanced month download article/chapter er/her2-positive breast cancer phosphatidylinositol 3-kinase/akt-mediated activation org/professionals/physician_gls/pdf/breast future endocrine therapies hormone-resistant breast cancer breast-cancer-derived xenografts estrogen-induced cyclin d1 er-positive breast cancer cyclin-dependent kinase activity estrogen receptor-mediated effects er+ breast cancer caused gov/ct2/show/nct01602380 gov/ct2/show/nct01953588 hormone receptor–positive hormone receptor-positive patient-level meta-analysis cancer genome atlas estrogen receptor alpha estrogen receptor-positive metastatic breast cancer constitutively active akt-3 full article pdf human breast tumours cyclin-dependent kinase 4/6 cyclin-dependent kinase phosphatidylinositol 3-kinase/mammalian target early breast cancer randomized confirm trial randomized trial comparing phase iii study estrogen-induced activation advanced breast cancer human breast cancers estrogen induces early complete cross-resistance estrogen receptor pathways important therapeutic target overcoming endocrine resistance 105th annual meeting advanced breast carcinoma estrogen receptor pathway prior endocrine therapy privacy choices/manage cookies robertson jfr anti-estrogen resistance breast cancer cells

Questions {❓}

  • Bedard PL, Freedman OC, Howell A, Clemons M (2008) Overcoming endocrine resistance in breast cancer: are signal transduction inhibitors the answer?
  • Fry MJ (2001) Phosphoinositide 3-kinase signalling in breast cancer: how big a role might it play?
  • Johnston SR, Yeo B (2014) The optimal duration of adjuvant endocrine therapy for early stage breast cancer–with what drugs and for how long?
  • Miller WR, Bartlett J, Brodie AMH et al (2008) Aromatase inhibitors: are there differences between steroidal and nonsteroidal aromatase inhibitors and do they matter?
  • Muss HB (2014) Adjuvant chemotherapy in older women with breast cancer: who and what?

Schema {🗺️}

WebPage:
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         headline:Revisiting the estrogen receptor pathway and its role in endocrine therapy for postmenopausal women with estrogen receptor-positive metastatic breast cancer
         description:Endocrine therapy (ET) is the most commonly administered first-line systemic therapy for estrogen receptor-positive (ER+) metastatic breast cancer (MBC). Manipulation of hormone levels was one of the earliest ET approaches. However, treatment modalities have since evolved with the growing understanding of estrogen biosynthesis and ER biology. The current armamentarium of ET includes selective estrogen receptor modulation, aromatase inhibition, and selective estrogen receptor downregulation. However, intrinsic or acquired resistance to ET is frequently observed. Significant strides have been made in recent years in our understanding of the mechanisms of resistance to ET, and several targeted approaches including inhibitors against the phosphatidylinositol 3-kinase/mammalian target of rapamycin (PI3K/mTOR) pathway and cyclin-dependent kinase 4/6 (CDK4/6) have shown great promise. The mTOR inhibitor, everolimus, is already in clinical use for the treatment of resistant ER+MBC. However, multiple levels of evidence indicate that ER signaling remains as an important therapeutic target even in the resistance setting, providing the rationale for sequencing multiple lines and combinations of ET. In addition, recurrent mutations in estrogen receptor 1 (ESR1), the gene that encodes the ER, have been identified in the genomic studies of metastatic ER+ breast cancer. ESR1 mutations are an important mechanism for acquired resistance, and effective ER targeting in this setting is particularly important.
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      headline:Revisiting the estrogen receptor pathway and its role in endocrine therapy for postmenopausal women with estrogen receptor-positive metastatic breast cancer
      description:Endocrine therapy (ET) is the most commonly administered first-line systemic therapy for estrogen receptor-positive (ER+) metastatic breast cancer (MBC). Manipulation of hormone levels was one of the earliest ET approaches. However, treatment modalities have since evolved with the growing understanding of estrogen biosynthesis and ER biology. The current armamentarium of ET includes selective estrogen receptor modulation, aromatase inhibition, and selective estrogen receptor downregulation. However, intrinsic or acquired resistance to ET is frequently observed. Significant strides have been made in recent years in our understanding of the mechanisms of resistance to ET, and several targeted approaches including inhibitors against the phosphatidylinositol 3-kinase/mammalian target of rapamycin (PI3K/mTOR) pathway and cyclin-dependent kinase 4/6 (CDK4/6) have shown great promise. The mTOR inhibitor, everolimus, is already in clinical use for the treatment of resistant ER+MBC. However, multiple levels of evidence indicate that ER signaling remains as an important therapeutic target even in the resistance setting, providing the rationale for sequencing multiple lines and combinations of ET. In addition, recurrent mutations in estrogen receptor 1 (ESR1), the gene that encodes the ER, have been identified in the genomic studies of metastatic ER+ breast cancer. ESR1 mutations are an important mechanism for acquired resistance, and effective ER targeting in this setting is particularly important.
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External Links {🔗}(313)

Analytics and Tracking {📊}

  • Google Tag Manager

Libraries {📚}

  • Clipboard.js
  • Prism.js

CDN Services {📦}

  • Crossref

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