10 results on '"tumor plasticity"'
Search Results
2. Editorial: Anakoinosis for promoting tumor tissue editing: Novel therapeutic opportunities for establishing clinically relevant tumor control by targeting tumor plasticity
- Author
-
Daniel Heudobler, Lina Ghibelli, and Albrecht Reichle
- Subjects
tumor tissue editing ,tumor plasticity ,homeostasis ,anakoinosis ,differentiation ,immunosurveillance ,Neoplasms. Tumors. Oncology. Including cancer and carcinogens ,RC254-282 - Published
- 2022
- Full Text
- View/download PDF
3. Current Advance of Therapeutic Agents in Clinical Trials Potentially Targeting Tumor Plasticity
- Author
-
Xiao-Guang Yang, Lan-Cao Zhu, Yan-Jun Wang, Yan-Yu Li, and Dun Wang
- Subjects
tumor plasticity ,cancer stem cells ,vasculogenic mimicry ,extracellular matrix ,tumor microenvironment ,targeting ,Neoplasms. Tumors. Oncology. Including cancer and carcinogens ,RC254-282 - Abstract
Tumor plasticity refers to tumor cell's inherent property of transforming one type of cell to different types of cells. Tumor plasticity is the main cause of tumor relapse, metastasis and drug resistance. Cancer stem cell (CSC) model embodies the trait of tumor plasticity. During carcinoma progression, epithelial-mesenchymal transition (EMT) plays crucial role in the formation of CSCs and vasculogenic mimicry (VM) based on epithelial-mesenchymal plasticity. And the unique tumor microenvironment (TME) not only provides suitable niche for CSCs but promotes the building of CSCs and VM that nourishes tumor tissue together with neoplasm metabolism by affecting tumor plasticity. Therapeutic strategies targeting tumor plasticity are promising ways to treat malignant tumor. In this article, we discuss the recent developments of potential drug targets related to CSCs, EMT, TME, VM, and metabolic pathways and summarize drugs that target these areas in clinical trials.
- Published
- 2019
- Full Text
- View/download PDF
4. Current Advance of Therapeutic Agents in Clinical Trials Potentially Targeting Tumor Plasticity.
- Author
-
Yang, Xiao-Guang, Zhu, Lan-Cao, Wang, Yan-Jun, Li, Yan-Yu, and Wang, Dun
- Subjects
CANCER stem cells ,CLINICAL trials ,VASCULOGENIC mimicry ,CANCER ,TUMORS - Abstract
Tumor plasticity refers to tumor cell's inherent property of transforming one type of cell to different types of cells. Tumor plasticity is the main cause of tumor relapse, metastasis and drug resistance. Cancer stem cell (CSC) model embodies the trait of tumor plasticity. During carcinoma progression, epithelial-mesenchymal transition (EMT) plays crucial role in the formation of CSCs and vasculogenic mimicry (VM) based on epithelial-mesenchymal plasticity. And the unique tumor microenvironment (TME) not only provides suitable niche for CSCs but promotes the building of CSCs and VM that nourishes tumor tissue together with neoplasm metabolism by affecting tumor plasticity. Therapeutic strategies targeting tumor plasticity are promising ways to treat malignant tumor. In this article, we discuss the recent developments of potential drug targets related to CSCs, EMT, TME, VM, and metabolic pathways and summarize drugs that target these areas in clinical trials. [ABSTRACT FROM AUTHOR]
- Published
- 2019
- Full Text
- View/download PDF
5. Microenvironment-Driven Dynamic Heterogeneity and Phenotypic Plasticity as a Mechanism of Melanoma Therapy Resistance.
- Author
-
Ahmed, Farzana and Haass, Nikolas K.
- Subjects
MELANOMA treatment ,DRUG resistance in cancer cells ,TUMOR markers - Abstract
Drug resistance constitutes a major challenge in designing melanoma therapies. Microenvironment-driven tumor heterogeneity and plasticity play a key role in this phenomenon. Melanoma is highly heterogeneous with diverse genomic alterations and expression of different biological markers. In addition, melanoma cells are highly plastic and capable of adapting quickly to changing microenvironmental conditions. These contribute to variations in therapy response and durability between individual melanoma patients. In response to changing microenvironmental conditions, like hypoxia and nutrient starvation, proliferative melanoma cells can switch to an invasive slow-cycling state. Cells in this state are more aggressive and metastatic, and show increased intrinsic drug resistance. During continuous treatment, slow-cycling cells are enriched within the tumor and give rise to a new proliferative subpopulation with increased drug resistance, by exerting their stem cell-like behavior and phenotypic plasticity. In melanoma, the proliferative and invasive states are defined by high and low microphthalmia-associated transcription factor (MITF) expression, respectively. It has been observed that in MITFhigh melanomas, inhibition of MITF increases the efficacy of targeted therapies and delays the acquisition of drug resistance. Contrarily, MITF is downregulated in melanomas with acquired drug resistance. According to the phenotype switching theory, the gene expression profile of the MITF
low state is predominantly regulated by WNT5A, AXL, and NF-κB signaling. Thus, different combinations of therapies should be effective in treating different phases of melanoma, such as the combination of targeted therapies with inhibitors of MITF expression during the initial treatment phase, but with inhibitors of WNT5A/AXL/NF-κB signaling during relapse. [ABSTRACT FROM AUTHOR]- Published
- 2018
- Full Text
- View/download PDF
6. Oncogenic micro-RNAs and Renal Cell Carcinoma
- Author
-
Cristina eGrange, Federica eCollino, Marta eTapparo, and Giovanni eCamussi
- Subjects
Kidney ,cancer stem cells ,circulating miRNAs ,EMT transition ,RCC biomarkers ,tumor plasticity ,Neoplasms. Tumors. Oncology. Including cancer and carcinogens ,RC254-282 - Abstract
Tumor formation is a complex process that occurs in different steps and involves many cell types, including tumor cells, endothelial cells, and inflammatory cells, which interact to promote growth of the tumor mass and metastasization. Epigenetic alterations occurring in transformed cells result in de-regulation of miRNA expression (a class of small non-coding RNA that regulates multiple functions) which contributes to tumorigenesis. The specific miRNAs, which have an aberrant expression in tumors, are defined as oncomiRNAs, and may be either over- or under-expressed, but down-regulation is most commonly observed.Renal cell carcinoma is a frequent form of urologic tumor, associated with an alteration of multiple signaling pathways. Many molecules involved in the progression of renal cell carcinomas, such as HIF, VEGF or mTOR, are possible targets of deregulated miRNAs. Within tumor mass, the cancer stem cell population is a fundamental component that promotes tumor growth. The cancer stem cell hypothesis postulates that cancer stem cells have the unique ability to self-renew and to maintain tumor growth and metastasis. Cancer stem cells present in renal cell carcinoma were shown to express the mesenchymal stem cell marker CD105 and to exhibit self-renewal and clonogenic properties, as well as the ability to generate serially transplantable tumors. The phenotype of cancer stem cell has been related to the potential to undergo the epithelial-mesenchymal transition, which has been linked to the expression pattern of tumorigenic miRNAs or down-regulation of anti-tumor miRNAs. In addition, the pattern of circulating miRNAs may allow discrimination between healthy and tumor patients. Therefore, a miRNA signature may be used as a tumor biomarker for cancer diagnosis, as well as to classify the risk of relapse and metastasis, and for a guide for therapy.
- Published
- 2014
- Full Text
- View/download PDF
7. Oncogenic micro-RNAs and renal cell carcinoma.
- Author
-
Grange, Cristina, Collino, Federica, Tapparo, Marta, and Camussi, Giovanni
- Subjects
MICRORNA ,RENAL cell carcinoma ,BIOMARKERS ,CANCER cell adaptation ,RENAL cancer - Abstract
Tumor formation is a complex process that occurs in different steps and involves many cell types, including tumor cells, endothelial cells, and inflammatory cells, which interact to promote growth of the tumor mass and metastasization. Epigenetic alterations occurring in transformed cells result in de regulation of miRNA expression (a class of small non-coding RNA that regulates multiple functions), which contributes to tumorigenesis. The specific miRNAs, which have an aberrant expression in tumors, are defined as oncomiRNAs, and may be either over or under-expressed, but down-regulation is most commonly observed. Renal cell carcinoma (RCC) is a frequent form of urologic tumor, associated with an alteration of multiple signaling pathways. Many molecules involved in the progression of RCCs, such as HIF, VEGF, or mammalian target of rapamycin, are possible targets of de-regulated miRNAs.Within tumor mass, the cancer stem cell (CSC) population is a fundamental component that promotes tumor growth. The CSC hypothesis postulates that CSCs have the unique ability to self-renew and to maintain tumor growth and metastasis. CSCs present in RCC were shown to express the mesenchymal stem cell marker CD105 and to exhibit self-renewal and clonogenic properties, as well as the ability to generate serially transplantable tumors.The phenotype of CSC has been related to the potential to undergo the epithelial mesenchymal transition, which has been linked to the expression pattern of tumorigenic miRNAs or down-regulation of anti-tumor miRNAs. In addition, the pattern of circulating miRNAs may allowdiscrimination between healthy and tumor patients.Therefore, a miRNA signature may be used as a tumor biomarker for cancer diagnosis, as well as to classify the risk of relapse and metastasis, and for a guide for therapy. [ABSTRACT FROM AUTHOR]
- Published
- 2014
- Full Text
- View/download PDF
8. Current Advance of Therapeutic Agents in Clinical Trials Potentially Targeting Tumor Plasticity
- Author
-
Yan-Jun Wang, Lan-Cao Zhu, Dun Wang, Yan-Yu Li, and Xiao-Guang Yang
- Subjects
0301 basic medicine ,cancer stem cells ,Cancer Research ,Mini Review ,extracellular matrix ,Cell ,Biology ,lcsh:RC254-282 ,Metastasis ,Extracellular matrix ,03 medical and health sciences ,0302 clinical medicine ,Cancer stem cell ,Carcinoma ,medicine ,Neoplasm ,tumor microenvironment ,Vasculogenic mimicry ,vasculogenic mimicry ,targeting ,Tumor microenvironment ,tumor plasticity ,medicine.disease ,lcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogens ,030104 developmental biology ,medicine.anatomical_structure ,Oncology ,030220 oncology & carcinogenesis ,Cancer research - Abstract
Tumor plasticity refers to tumor cell's inherent property of transforming one type of cell to different types of cells. Tumor plasticity is the main cause of tumor relapse, metastasis and drug resistance. Cancer stem cell (CSC) model embodies the trait of tumor plasticity. During carcinoma progression, epithelial-mesenchymal transition (EMT) plays crucial role in the formation of CSCs and vasculogenic mimicry (VM) based on epithelial-mesenchymal plasticity. And the unique tumor microenvironment (TME) not only provides suitable niche for CSCs but promotes the building of CSCs and VM that nourishes tumor tissue together with neoplasm metabolism by affecting tumor plasticity. Therapeutic strategies targeting tumor plasticity are promising ways to treat malignant tumor. In this article, we discuss the recent developments of potential drug targets related to CSCs, EMT, TME, VM, and metabolic pathways and summarize drugs that target these areas in clinical trials.
- Published
- 2019
9. Microenvironment-Driven Dynamic Heterogeneity and Phenotypic Plasticity as a Mechanism of Melanoma Therapy Resistance
- Author
-
Nikolas K. Haass and Farzana Ahmed
- Subjects
0301 basic medicine ,microphthalmia-associated transcription factor ,Cancer Research ,cancer drug resistance ,Mini Review ,clonality ,Drug resistance ,Biology ,lcsh:RC254-282 ,03 medical and health sciences ,slow-cycling tumor cells ,Gene expression ,tumor heterogeneity ,medicine ,melanoma ,tumor microenvironment ,Transcription factor ,Tumor microenvironment ,Melanoma ,tumor plasticity ,medicine.disease ,Microphthalmia-associated transcription factor ,lcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogens ,Phenotype ,3. Good health ,WNT5A ,030104 developmental biology ,Oncology ,Cancer research - Abstract
Drug resistance constitutes a major challenge in designing melanoma therapies. Microenvironment-driven tumor heterogeneity and plasticity play a key role in this phenomenon. Melanoma is highly heterogeneous with diverse genomic alterations and expression of different biological markers. In addition, melanoma cells are highly plastic and capable of adapting quickly to changing microenvironmental conditions. These contribute to variations in therapy response and durability between individual melanoma patients. In response to changing microenvironmental conditions, like hypoxia and nutrient starvation, proliferative melanoma cells can switch to an invasive slow-cycling state. Cells in this state are more aggressive and metastatic, and show increased intrinsic drug resistance. During continuous treatment, slow-cycling cells are enriched within the tumor and give rise to a new proliferative subpopulation with increased drug resistance, by exerting their stem cell-like behavior and phenotypic plasticity. In melanoma, the proliferative and invasive states are defined by high and low microphthalmia-associated transcription factor (MITF) expression, respectively. It has been observed that in MITF-high melanomas, inhibition of MITF increases the efficacy of targeted therapies and delays the acquisition of drug resistance. Contrarily, MITF is downregulated in melanomas with acquired drug resistance. According to the phenotype switching theory, the gene expression profile of the MITF-low state is predominantly regulated by WNT5A, AXL, and NF-kappa B signaling. Thus, different combinations of therapies should be effective in treating different phases of melanoma, such as the combination of targeted therapies with inhibitors of MITF expression during the initial treatment phase, but with inhibitors of WNT5A/AXL/NF-kappa B signaling during relapse.
- Published
- 2018
- Full Text
- View/download PDF
10. Oncogenic micro-RNAs and Renal Cell Carcinoma
- Author
-
Giovanni Camussi, Marta Tapparo, Federica Collino, and Cristina Grange
- Subjects
cancer stem cells ,Cancer Research ,Pathology ,medicine.medical_specialty ,Cell type ,kidney ,CD30 ,Cellular differentiation ,Review Article ,Biology ,medicine.disease_cause ,EMT transition ,lcsh:RC254-282 ,Metastasis ,Cancer stem cell ,medicine ,Cancer stem cells ,Circulating miRNAs ,Kidney ,RCC biomarkers ,Tumor plasticity ,Oncology ,circulating miRNAs ,Mesenchymal stem cell ,tumor plasticity ,Cancer ,lcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogens ,medicine.disease ,Cancer research ,Carcinogenesis - Abstract
Tumor formation is a complex process that occurs in different steps and involves many cell types, including tumor cells, endothelial cells, and inflammatory cells, which interact to promote growth of the tumor mass and metastasization. Epigenetic alterations occurring in transformed cells result in de-regulation of miRNA expression (a class of small non-coding RNA that regulates multiple functions) which contributes to tumorigenesis. The specific miRNAs, which have an aberrant expression in tumors, are defined as oncomiRNAs, and may be either over- or under-expressed, but down-regulation is most commonly observed.Renal cell carcinoma is a frequent form of urologic tumor, associated with an alteration of multiple signaling pathways. Many molecules involved in the progression of renal cell carcinomas, such as HIF, VEGF or mTOR, are possible targets of deregulated miRNAs. Within tumor mass, the cancer stem cell population is a fundamental component that promotes tumor growth. The cancer stem cell hypothesis postulates that cancer stem cells have the unique ability to self-renew and to maintain tumor growth and metastasis. Cancer stem cells present in renal cell carcinoma were shown to express the mesenchymal stem cell marker CD105 and to exhibit self-renewal and clonogenic properties, as well as the ability to generate serially transplantable tumors. The phenotype of cancer stem cell has been related to the potential to undergo the epithelial-mesenchymal transition, which has been linked to the expression pattern of tumorigenic miRNAs or down-regulation of anti-tumor miRNAs. In addition, the pattern of circulating miRNAs may allow discrimination between healthy and tumor patients. Therefore, a miRNA signature may be used as a tumor biomarker for cancer diagnosis, as well as to classify the risk of relapse and metastasis, and for a guide for therapy.
- Published
- 2014
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