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Title:
Tumor dormancy: potential therapeutic target in tumor recurrence and metastasis prevention | Experimental Hematology & Oncology
Description:
In past decades, cancer patient survival has been improved with earlier detection and advancements in therapy. However, many patients who exhibit no clinical symptoms after frontline therapy subsequently suffer, often many years later, aggressive tumor recurrence. Cancer recurrence represents a critical clinical challenge in effectively treating malignancies and for patients’ quality of life. Tumor cell dormancy may help to explain treatment resistance and recurrence or metastatic reactivation. Understanding the dormant stage of tumor cells may help in discovering ways to maintain the dormant state or permanently eliminate dormant residual disseminated tumor cells. Over the past decade, numerous studies indicate that various mechanisms of tumor dormancy exist, including cellular dormancy (quiescence), angiogenic dormancy, and immunologic dormancy. In this short review, we summarize recent experimental and clinical evidence for these three mechanisms and other possible tumor microenvironment mechanisms that may influence tumor dormancy.
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Keywords {🔍}
dormancy, tumor, cells, pubmed, cancer, article, cell, google, scholar, cas, growth, dormant, central, quiescence, protein, microenvironment, recurrence, complex, expression, angiogenic, dtcs, metastasis, niches, cycle, bone, factor, factors, clinical, state, mechanisms, figure, dream, signaling, genes, breast, immunity, quiescent, pathway, patients, escape, kinase, therapeutic, cellular, immunologic, balance, immune, muvb, bmp, treatment, proliferation,
Topics {✒️}
apc/cdh1-skp-p27kip1/p21 signaling pathway shiaw-yih lin typical rb-cyclin/cdk-dependent complex tumor-specific homing-regulated receptors tgf-β/bone morphogenetic protein extracellular signal-regulated kinase cytotoxic t-lymphocyte-induced apoptosis myeloid-derived suppressor cells mitogen-activated protein kinase gap junction-mediated import article download pdf platelet-derived growth factor aguirre-ghiso ja oct4hi/cd44hi/med/cd24-/+ cell cycle-dependent repression cytotoxic t-lymphocyte response dna double-strand breaks small-cell lung cancer evade anti-tumor immunity estrogen receptor-negative tumor slow-cycling bc cells estrogen receptor-positive tumors multi-subunit dream complex downregulating cyclin/cdk activation apc/cdh1 increased tgf-β/bmp signaling long-term hazard open access license summarize recent experimental tumor-derived secreted factors host-protective immune response angiogenic-dormant tumor cells muvb-bmyb-foxm1 complex hodgkin b-cell lymphomas cyclin-dependent kinase cancer stem cells reducing t-cell activation full size image nontraditional rb/p27 pathway lee-lim ap privacy choices/manage cookies limited tumor size fibroblast growth factor disseminating tumour cells article wang authors’ original file sosa ms enhance imatinib-induced apoptosis p21/p27/p57 inhibitor disseminated tumor cells
Questions {❓}
- Allgayer H, Aguirre-Ghiso JA: The urokinase receptor (u-PAR)–a link between tumor cell dormancy and minimal residual disease in bone marrow?
- Quesnel B: Dormant tumor cells as a therapeutic target?
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headline:Tumor dormancy: potential therapeutic target in tumor recurrence and metastasis prevention
description:In past decades, cancer patient survival has been improved with earlier detection and advancements in therapy. However, many patients who exhibit no clinical symptoms after frontline therapy subsequently suffer, often many years later, aggressive tumor recurrence. Cancer recurrence represents a critical clinical challenge in effectively treating malignancies and for patients’ quality of life. Tumor cell dormancy may help to explain treatment resistance and recurrence or metastatic reactivation. Understanding the dormant stage of tumor cells may help in discovering ways to maintain the dormant state or permanently eliminate dormant residual disseminated tumor cells. Over the past decade, numerous studies indicate that various mechanisms of tumor dormancy exist, including cellular dormancy (quiescence), angiogenic dormancy, and immunologic dormancy. In this short review, we summarize recent experimental and clinical evidence for these three mechanisms and other possible tumor microenvironment mechanisms that may influence tumor dormancy.
datePublished:2013-10-16T00:00:00Z
dateModified:2013-10-16T00:00:00Z
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Tumor dormancy
Quiescence
Immunologic dormancy
Angiogenic dormancy
Tumor microenvironment
Hematology
Oncology
Cancer Research
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headline:Tumor dormancy: potential therapeutic target in tumor recurrence and metastasis prevention
description:In past decades, cancer patient survival has been improved with earlier detection and advancements in therapy. However, many patients who exhibit no clinical symptoms after frontline therapy subsequently suffer, often many years later, aggressive tumor recurrence. Cancer recurrence represents a critical clinical challenge in effectively treating malignancies and for patients’ quality of life. Tumor cell dormancy may help to explain treatment resistance and recurrence or metastatic reactivation. Understanding the dormant stage of tumor cells may help in discovering ways to maintain the dormant state or permanently eliminate dormant residual disseminated tumor cells. Over the past decade, numerous studies indicate that various mechanisms of tumor dormancy exist, including cellular dormancy (quiescence), angiogenic dormancy, and immunologic dormancy. In this short review, we summarize recent experimental and clinical evidence for these three mechanisms and other possible tumor microenvironment mechanisms that may influence tumor dormancy.
datePublished:2013-10-16T00:00:00Z
dateModified:2013-10-16T00:00:00Z
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Tumor dormancy
Quiescence
Immunologic dormancy
Angiogenic dormancy
Tumor microenvironment
Hematology
Oncology
Cancer Research
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