Here's how DOI.ORG makes money* and how much!

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DOI . ORG {}

  1. Analyzed Page
  2. Matching Content Categories
  3. CMS
  4. Monthly Traffic Estimate
  5. How Does Doi.org Make Money
  6. Keywords
  7. Topics
  8. Questions
  9. Schema
  10. External Links
  11. Analytics And Tracking
  12. Libraries
  13. Hosting Providers

We began analyzing https://link.springer.com/chapter/10.1007/978-3-319-42118-6_6, but it redirected us to https://link.springer.com/chapter/10.1007/978-3-319-42118-6_6. The analysis below is for the second page.

Title[redir]:
Metabolic Features of Cancer Treatment Resistance | SpringerLink
Description:
A major barrier to achieving durable remission and a definitive cure in oncology patients is the emergence of tumor resistance, a common outcome of different disease types, and independent from the therapeutic approach undertaken. In recent years, subpopulations of...

Matching Content Categories {📚}

  • Science
  • Education
  • Health & Fitness

Content Management System {📝}

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 {📈}

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

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


Based on our best estimate, this website will receive around 5,000,420 visitors per month in the current month.

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How Does Doi.org Make Money? {💸}

We can't see how the site brings in money.

Earning money isn't the goal of every website; some are designed to offer support or promote social causes. People have different reasons for creating websites. This might be one such reason. Doi.org might be making money, but it's not detectable how they're doing it.

Keywords {🔍}

pubmed, google, scholar, cas, article, cancer, cells, central, cell, resistance, wang, mitochondrial, stem, human, res, nature, leukemia, metabolism, med, tumor, dna, nat, chapter, viale, inhibition, doinature, pancreatic, drug, tumorigenic, oncol, therapeutic, tumors, autophagy, therapy, acute, melanoma, science, chen, metabolic, draetta, identification, usa, clin, doican, kim, research, expression, rev, engl, zhang,

Topics {✒️}

human colon-cancer-initiating cells month download article/chapter bone-marrow endosteal region slow-cycling cells endowed bcr-abl gene mutation abc transporter bcrp1/abcg2 cisplatin-based adjuvant chemotherapy kras-driven pancreatic cancer glutathione s-transferase p1 slow-cycling melanoma cells phagocyte ucp2 protein small-cell lung cancer author information authors resistant tumorigenic cells privacy choices/manage cookies initiating tumour growth dna damage response chromosomal instability inferred mitochondrial respiratory chain device instant download pancreatic adenocarcinoma cells human tumor cells bronchioalveolar stem cells leukaemia stem cells slow-cycling jarid1b cancer stem cells therapy-resistant cancer de carvalho fm multiple human cancers normal human cells efflux drug pumps cancer chemotherapy response warburg effect today references al-hajj glutathione-s-transferase efficient tumour formation n-ras upregulation increased mitochondrial capacity important therapeutic implications cancer stem cell 5-fluorouracil/oxaliplatin chemotherapy leukemic leukocyte populations maintain oxidative metabolism oncogenic kras addiction clin oncol official burgert eo jr tumorigenic melanoma cells genomic medicine side population cells primarily glycolytic metabolism

Questions {❓}

  • Garraway LA, Chabner B (2002) MDR1 inhibition: less resistance or less relevance?
  • Jang S, Atkins MB (2013) Which drug, and when, for patients with BRAF-mutant melanoma?
  • Jose C, Bellance N, Rossignol R (2011) Choosing between glycolysis and oxidative phosphorylation: a tumor’s dilemma?
  • Wolf DA (2014) Is reliance on mitochondrial respiration a “chink in the armor” of therapy-resistant cancer?
  • Gov What is cancer?

Schema {🗺️}

ScholarlyArticle:
      headline:Metabolic Features of Cancer Treatment Resistance
      pageEnd:156
      pageStart:135
      image:https://media.springernature.com/w153/springer-static/cover/book/978-3-319-42118-6.jpg
      genre:
         Medicine
         Medicine (R0)
      isPartOf:
         name:Metabolism in Cancer
         isbn:
            978-3-319-42118-6
            978-3-319-42116-2
         type:Book
      publisher:
         name:Springer International Publishing
         logo:
            url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
            type:ImageObject
         type:Organization
      author:
            name:Andrea Viale
            affiliation:
                  name:The University of Texas MD Anderson Cancer Center
                  address:
                     name:Department of Genomic Medicine, The University of Texas MD Anderson Cancer Center, Houston, USA
                     type:PostalAddress
                  type:Organization
            email:[email protected]
            type:Person
            name:Giulio F. Draetta
            affiliation:
                  name:The University of Texas MD Anderson Cancer Center
                  address:
                     name:Department of Genomic Medicine, The University of Texas MD Anderson Cancer Center, Houston, USA
                     type:PostalAddress
                  type:Organization
                  name:The University of Texas MD Anderson Cancer Center
                  address:
                     name:Department of Molecular and Cellular Oncology, The University of Texas MD Anderson Cancer Center, Houston, USA
                     type:PostalAddress
                  type:Organization
            type:Person
      keywords:Tumor resistance, Relapse, Cancer stem cell, Quiescence, Metabolism, Mitochondria, Oxidative phosphorylation
      description:A major barrier to achieving durable remission and a definitive cure in oncology patients is the emergence of tumor resistance, a common outcome of different disease types, and independent from the therapeutic approach undertaken. In recent years, subpopulations of slow-cycling cells endowed with enhanced tumorigenic potential and multidrug resistance have been isolated in different tumors, and mounting experimental evidence suggests these resistant cells are responsible for tumor relapse. An in-depth metabolic characterization of resistant tumor stem cells revealed that they rely more on mitochondrial respiration and less on glycolysis than other tumor cells, a finding that challenges the assumption that tumors have a primarily glycolytic metabolism and defective mitochondria. The demonstration of a metabolic program in resistant tumorigenic cells that may be present in the majority of tumors has important therapeutic implications and is a critical consideration as we address the challenge of identifying new vulnerabilities that might be exploited therapeutically.
      datePublished:2016
      isAccessibleForFree:
      hasPart:
         isAccessibleForFree:
         cssSelector:.main-content
         type:WebPageElement
      context:https://schema.org
Book:
      name:Metabolism in Cancer
      isbn:
         978-3-319-42118-6
         978-3-319-42116-2
Organization:
      name:Springer International Publishing
      logo:
         url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
         type:ImageObject
      name:The University of Texas MD Anderson Cancer Center
      address:
         name:Department of Genomic Medicine, The University of Texas MD Anderson Cancer Center, Houston, USA
         type:PostalAddress
      name:The University of Texas MD Anderson Cancer Center
      address:
         name:Department of Genomic Medicine, The University of Texas MD Anderson Cancer Center, Houston, USA
         type:PostalAddress
      name:The University of Texas MD Anderson Cancer Center
      address:
         name:Department of Molecular and Cellular Oncology, The University of Texas MD Anderson Cancer Center, Houston, USA
         type:PostalAddress
ImageObject:
      url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
Person:
      name:Andrea Viale
      affiliation:
            name:The University of Texas MD Anderson Cancer Center
            address:
               name:Department of Genomic Medicine, The University of Texas MD Anderson Cancer Center, Houston, USA
               type:PostalAddress
            type:Organization
      email:[email protected]
      name:Giulio F. Draetta
      affiliation:
            name:The University of Texas MD Anderson Cancer Center
            address:
               name:Department of Genomic Medicine, The University of Texas MD Anderson Cancer Center, Houston, USA
               type:PostalAddress
            type:Organization
            name:The University of Texas MD Anderson Cancer Center
            address:
               name:Department of Molecular and Cellular Oncology, The University of Texas MD Anderson Cancer Center, Houston, USA
               type:PostalAddress
            type:Organization
PostalAddress:
      name:Department of Genomic Medicine, The University of Texas MD Anderson Cancer Center, Houston, USA
      name:Department of Genomic Medicine, The University of Texas MD Anderson Cancer Center, Houston, USA
      name:Department of Molecular and Cellular Oncology, The University of Texas MD Anderson Cancer Center, Houston, USA
WebPageElement:
      isAccessibleForFree:
      cssSelector:.main-content

External Links {🔗}(425)

Analytics and Tracking {📊}

  • Google Tag Manager

Libraries {📚}

  • Clipboard.js

Emails and Hosting {✉️}

Mail Servers:

  • mx.zoho.eu
  • mx2.zoho.eu
  • mx3.zoho.eu

Name Servers:

  • josh.ns.cloudflare.com
  • zita.ns.cloudflare.com
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