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We are analyzing https://link.springer.com/article/10.1007/s10555-021-09988-w.

Title:
The tumor microenvironment in pancreatic ductal adenocarcinoma: current perspectives and future directions | Cancer and Metastasis Reviews
Description:
Pancreatic ductal adenocarcinoma (PDAC) is among the most lethal malignancies and is characterized by a unique tumor microenvironment (TME) consisting of an abundant stromal component. Many features contained with the PDAC stroma contribute to resistance to cytotoxic and immunotherapeutic regimens, as well as the propensity for this tumor to metastasize. At the cellular level, PDAC cells crosstalk with a complex mixture of non-neoplastic cell types including fibroblasts, endothelial cells, and immune cells. These intricate interactions fuel the progression and therapeutic resistance of this aggressive cancer. Moreover, data suggest the polarization of these cell types, in particular immune and fibroblast populations, dictate how PDAC tumors grow, metastasize, and respond to therapy. As a result, current research is focused on how to best target these populations to render tumors responsive to treatment. Herein, we summarize the cell populations implicated in providing a supporting role for the development and progression of PDAC. We focus on stromal fibroblasts and immune subsets that have been widely researched. We discuss factors which govern the phenotype of these populations and provide insight on how they have been targeted therapeutically. This review provides an overview of the tumor microenvironment and postulates that cellular and soluble factors within the microenvironment can be specifically targeted to improve patient outcomes.
Website Age:
28 years and 1 months (reg. 1997-05-29).

Matching Content Categories {πŸ“š}

  • Education
  • Health & Fitness
  • Science

Content Management System {πŸ“}

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 {πŸ“ˆ}

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? {πŸ’Έ}

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

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 {πŸ”}

pubmed, pancreatic, cancer, article, google, scholar, cas, central, adenocarcinoma, cells, ductal, cell, journal, tumor, research, microenvironment, nature, immunology, immune, clinical, fibroblasts, stromal, immunotherapy, human, pdac, promote, macrophages, patients, development, pancreas, cancerassociated, signaling, oncology, immunity, metastasis, lesinski, progression, discovery, myeloid, myeloidderived, suppressor, therapy, tumour, gastroenterology, metastatic, stellate, gut, targeting, science, promotes,

Topics {βœ’οΈ}

nab-paclitaxel/gemcitabine versus nab-paclitaxel/gemcitabine cross-species single-cell analysis month download article/chapter c-met-targeting antibody-drug conjugate anti-alpha-enolase antibody limits cell-dependent antitumor immunity tumour cell-derived debris single-center retrospective analysis myeloid-derived suppressor cells tumor-induced stat3 activation pd-1/pd-l1 checkpoint activation lymphocyte-mediated immune suppression tumor-stromal interactions contributes blocking cxcls-cxcr2 axis nab-paclitaxel/gemcitabine enabling anti-tumor immunity ink4a/arf deficiency cooperate beta-catenin expression correlate fibroblasts promote angiogenesis immune-inflammatory microenvironment pancreatic tumor microenvironment febs open bio kras-induced pancreatic tumorigenesis unique tumor microenvironment vitamin a-storing cell il-1beta recruit stroma-rich xenograft model full article pdf collagen i-mediated reduced cell invasion/migration stromal microenvironment shapes pancreatic tumour cells orthotopic murine models tumor-infiltrating cd8 anti-pd-l1 immunotherapy il-6 signaling blockade cell mediated immunity analogue calcipotriol promotes jak-stat3 signaling promote tumor progression regulatory il-10 phenotype tumor cell proliferation tumour-host interface pancreatic neoplastic transformation privacy choices/manage cookies n-cadherin expression pancreatic ductal adenocarcinoma advanced pancreatic adenocarcinoma anti-inflammatory properties prognostic factors related

Questions {❓}

  • Pancreatic ductal adenocarcinoma epidemiology and risk assessment: Could we prevent?
  • Acinar?

Schema {πŸ—ΊοΈ}

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         headline:The tumor microenvironment in pancreatic ductal adenocarcinoma: current perspectives and future directions
         description:Pancreatic ductal adenocarcinoma (PDAC) is among the most lethal malignancies and is characterized by a unique tumor microenvironment (TME) consisting of an abundant stromal component. Many features contained with the PDAC stroma contribute to resistance to cytotoxic and immunotherapeutic regimens, as well as the propensity for this tumor to metastasize. At the cellular level, PDAC cells crosstalk with a complex mixture of non-neoplastic cell types including fibroblasts, endothelial cells, and immune cells. These intricate interactions fuel the progression and therapeutic resistance of this aggressive cancer. Moreover, data suggest the polarization of these cell types, in particular immune and fibroblast populations, dictate how PDAC tumors grow, metastasize, and respond to therapy. As a result, current research is focused on how to best target these populations to render tumors responsive to treatment. Herein, we summarize the cell populations implicated in providing a supporting role for the development and progression of PDAC. We focus on stromal fibroblasts and immune subsets that have been widely researched. We discuss factors which govern the phenotype of these populations and provide insight on how they have been targeted therapeutically. This review provides an overview of the tumor microenvironment and postulates that cellular and soluble factors within the microenvironment can be specifically targeted to improve patient outcomes.
         datePublished:2021-09-30T00:00:00Z
         dateModified:2021-09-30T00:00:00Z
         pageStart:675
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            Oncology
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            general
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      headline:The tumor microenvironment in pancreatic ductal adenocarcinoma: current perspectives and future directions
      description:Pancreatic ductal adenocarcinoma (PDAC) is among the most lethal malignancies and is characterized by a unique tumor microenvironment (TME) consisting of an abundant stromal component. Many features contained with the PDAC stroma contribute to resistance to cytotoxic and immunotherapeutic regimens, as well as the propensity for this tumor to metastasize. At the cellular level, PDAC cells crosstalk with a complex mixture of non-neoplastic cell types including fibroblasts, endothelial cells, and immune cells. These intricate interactions fuel the progression and therapeutic resistance of this aggressive cancer. Moreover, data suggest the polarization of these cell types, in particular immune and fibroblast populations, dictate how PDAC tumors grow, metastasize, and respond to therapy. As a result, current research is focused on how to best target these populations to render tumors responsive to treatment. Herein, we summarize the cell populations implicated in providing a supporting role for the development and progression of PDAC. We focus on stromal fibroblasts and immune subsets that have been widely researched. We discuss factors which govern the phenotype of these populations and provide insight on how they have been targeted therapeutically. This review provides an overview of the tumor microenvironment and postulates that cellular and soluble factors within the microenvironment can be specifically targeted to improve patient outcomes.
      datePublished:2021-09-30T00:00:00Z
      dateModified:2021-09-30T00:00:00Z
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         Cancer-associated fibroblasts
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         general
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