Immune Subtypes in LUAD Identify Novel Tumor Microenvironment Profiles With Prognostic and Therapeutic Implications

2021 ◽  
Author(s):  
Feng wang ◽  
Xuan Gao ◽  
Peiyuan Wang ◽  
Hao He ◽  
Peng Chen ◽  
...  
Keyword(s):  
Tumor Microenvironment ◽  
Therapeutic Implications

scholarly journals Metabolic strategies of melanoma cells: Mechanisms, interactions with the tumor microenvironment, and therapeutic implications

2017 ◽  
Vol 31 (1) ◽  
pp. 11-30 ◽  
Author(s):  
Grant M. Fischer ◽  
Y. N. Vashisht Gopal ◽  
Jennifer L. McQuade ◽  
Weiyi Peng ◽  
Ralph J. DeBerardinis ◽  
...  
Keyword(s):  
Tumor Microenvironment ◽  
Melanoma Cells ◽  
Therapeutic Implications ◽  
Metabolic Strategies

scholarly journals Tumor microenvironment complexity and therapeutic implications at a glance

2020 ◽  
Vol 18 (1) ◽  
Author(s):  
Roghayyeh Baghban ◽  
Leila Roshangar ◽  
Rana Jahanban-Esfahlan ◽  
Khaled Seidi ◽  
Abbas Ebrahimi-Kalan ◽  
...  
Keyword(s):  
Tumor Microenvironment ◽  
Therapeutic Implications

scholarly journals The Role of Extracellular Vesicles in Cancer: Cargo, Function, and Therapeutic Implications

Cells ◽  
2018 ◽  
Vol 7 (8) ◽  
pp. 93 ◽  
Author(s):  
James Jabalee ◽  
Rebecca Towle ◽  
Cathie Garnis
Keyword(s):  
Tumor Microenvironment ◽  
Tumor Cells ◽  
Extracellular Vesicles ◽  
Tumor Stroma ◽  
Therapeutic Implications ◽  
Membrane Bound ◽  
Immune Destruction ◽  
And Function ◽  
Cargo Molecule

Extracellular vesicles (EVs) are a heterogeneous collection of membrane-bound structures that play key roles in intercellular communication. EVs are potent regulators of tumorigenesis and function largely via the shuttling of cargo molecules (RNA, DNA, protein, etc.) among cancer cells and the cells of the tumor stroma. EV-based crosstalk can promote proliferation, shape the tumor microenvironment, enhance metastasis, and allow tumor cells to evade immune destruction. In many cases these functions have been linked to the presence of specific cargo molecules. Herein we will review various types of EV cargo molecule and their functional impacts in the context of oncology.

scholarly journals Characterization of a Tumor-Microenvironment-Relevant Gene Set Based on Tumor Severity in Colon Cancer and Evaluation of Its Potential for Dihydroartemisinin Targeting

2021 ◽  
Vol 2021 ◽  
pp. 1-10
Author(s):  
Bo Liang ◽  
Biao Zheng ◽  
Yan Zhou ◽  
Zheng-Quan Lai ◽  
Citing Zhang ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Tumor Microenvironment ◽  
Clinical Outcomes ◽  
Molecular Mechanisms ◽  
In Silico Analysis ◽  
Adverse Outcomes ◽  
Therapeutic Implications ◽  
Immune Infiltration ◽  
Highly Correlated

Colon cancer (COAD) is a leading cause of cancer mortality in the world. Most patients with COAD die as a result of cancer cell metastasis. However, the mechanisms underlying the metastatic phenotype of COAD remain unclear. Instead, particular features of the tumor microenvironment (TME) could predict adverse outcomes including metastasis in patients with COAD, and the role of TME in governing COAD progression is undeniable. Therefore, exploring the role of TME in COAD may help us better understand the molecular mechanisms behind COAD progression which may improve clinical outcomes and quality of patients. Here, we identified a Specific TME Regulatory Network including AEBP1, BGN, POST, and FAP (STMERN) that is highly involved in clinical outcomes of patients with COAD. Comprehensive in silico analysis of our study revealed that the STMERN is highly correlated with the severity of COAD. Meanwhile, our results reveal that the STMERN might be associated with immune infiltration in COAD. Importantly, we show that dihydroartemisinin (DHA) potentially interacts with the STMERN. We suggest that DHA might contribute to immune infiltration through regulating the STMERN in COAD. Taken together, our data provide a set of biomarkers of progression and poor prognosis in COAD. These findings could have potential prognostic and therapeutic implications in the progression of COAD.

scholarly journals Therapeutic Implications of Tumor Microenvironment in Lung Cancer: Focus on Immune Checkpoint Blockade

2022 ◽  
Vol 12 ◽  
Author(s):  
Carlo Genova ◽  
Chiara Dellepiane ◽  
Paolo Carrega ◽  
Sara Sommariva ◽  
Guido Ferlazzo ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Tumor Microenvironment ◽  
Immune Checkpoint ◽  
Cytotoxic T Lymphocyte ◽  
Checkpoint Inhibitors ◽  
Suppressor Cells ◽  
Regulatory Elements ◽  
Immune Checkpoint Blockade ◽  
Therapeutic Implications ◽  
Investigational Agents

In the last decade, the treatment of non-small cell lung cancer (NSCLC) has been revolutionized by the introduction of immune checkpoint inhibitors (ICI) directed against programmed death protein 1 (PD-1) and its ligand (PD-L1), or cytotoxic T lymphocyte antigen 4 (CTLA-4). In spite of these improvements, some patients do not achieve any benefit from ICI, and inevitably develop resistance to therapy over time. Tumor microenvironment (TME) might influence response to immunotherapy due to its prominent role in the multiple interactions between neoplastic cells and the immune system. Studies investigating lung cancer from the perspective of TME pointed out a complex scenario where tumor angiogenesis, soluble factors, immune suppressive/regulatory elements and cells composing TME itself participate to tumor growth. In this review, we point out the current state of knowledge involving the relationship between tumor cells and the components of TME in NSCLC as well as their interactions with immunotherapy providing an update on novel predictors of benefit from currently employed ICI or new therapeutic targets of investigational agents. In first place, increasing evidence suggests that TME might represent a promising biomarker of sensitivity to ICI, based on the presence of immune-modulating cells, such as Treg, myeloid derived suppressor cells, and tumor associated macrophages, which are known to induce an immunosuppressive environment, poorly responsive to ICI. Consequently, multiple clinical studies have been designed to influence TME towards a pro-immunogenic state and subsequently improve the activity of ICI. Currently, the mostly employed approach relies on the association of “classic” ICI targeting PD-1/PD-L1 and novel agents directed on molecules, such as LAG-3 and TIM-3. To date, some trials have already shown promising results, while a multitude of prospective studies are ongoing, and their results might significantly influence the future approach to cancer immunotherapy.

scholarly journals Tumor Microenvironment in Breast Cancer—Updates on Therapeutic Implications and Pathologic Assessment

Cancers ◽  
2021 ◽  
Vol 13 (16) ◽  
pp. 4233
Author(s):  
Joshua J. Li ◽  
Julia Y. Tsang ◽  
Gary M. Tse
Keyword(s):  
Breast Cancer ◽  
Tumor Microenvironment ◽  
Cancer Cells ◽  
Treatment Decision ◽  
Tumor Infiltrating Lymphocytes ◽  
Therapeutic Implications ◽  
Cancer Management ◽  
Breast Cancer Management ◽  
Pathologic Assessment ◽  
Infiltrating Lymphocytes

The tumor microenvironment (TME) in breast cancer comprises local factors, cancer cells, immune cells and stromal cells of the local and distant tissues. The interaction between cancer cells and their microenvironment plays important roles in tumor proliferation, propagation and response to therapies. There is increasing research in exploring and manipulating the non-cancerous components of the TME for breast cancer treatment. As the TME is now increasingly recognized as a treatment target, its pathologic assessment has become a critical component of breast cancer management. The latest WHO classification of tumors of the breast listed stromal response pattern/fibrotic focus as a prognostic factor and includes recommendations on the assessment of tumor infiltrating lymphocytes and PD-1/PD-L1 expression, with therapeutic implications. This review dissects the TME of breast cancer, describes pathologic assessment relevant for prognostication and treatment decision, and details therapeutic options that interacts with and/or exploits the TME in breast cancer.

scholarly journals Angiogenic Properties of NK Cells in Cancer and Other Angiogenesis-Dependent Diseases

Cells ◽  
2021 ◽  
Vol 10 (7) ◽  
pp. 1621
Author(s):  
Dorota M. Radomska-Leśniewska ◽  
Agata Białoszewska ◽  
Paweł Kamiński
Keyword(s):  
Tumor Microenvironment ◽  
Tumor Growth ◽  
Nk Cells ◽  
Natural Killer ◽  
Target Cells ◽  
Therapeutic Implications ◽  
Angiogenesis Process ◽  
Tumor Growth And Metastasis

The pathogenesis of many serious diseases, including cancer, is closely related to disturbances in the angiogenesis process. Angiogenesis is essential for the progression of tumor growth and metastasis. The tumor microenvironment (TME) has immunosuppressive properties, which contribute to tumor expansion and angiogenesis. Similarly, the uterine microenvironment (UME) exerts a tolerogenic (immunosuppressive) and proangiogenic effect on its cells, promoting implantation and development of the embryo and placenta. In the TME and UME natural killer (NK) cells, which otherwise are capable of killing target cells autonomously, enter a state of reduced cytotoxicity or anergy. Both TME and UME are rich with factors (e.g., TGF-β, glycodelin, hypoxia), which support a conversion of NK cells to the low/non-cytotoxic, proangiogenic CD56brightCD16low phenotype. It is plausible that the phenomenon of acquiring proangiogenic and low cytotoxic features by NK cells is not only limited to cancer but is a common feature of different angiogenesis-dependent diseases (ADDs). In this review, we will discuss the role of NK cells in angiogenesis disturbances associated with cancer and other selected ADDs. Expanding the knowledge of the mechanisms responsible for angiogenesis and its disorders contributes to a better understanding of ADDs and may have therapeutic implications.

scholarly journals The Acidic Brain—Glycolytic Switch in the Microenvironment of Malignant Glioma

2021 ◽  
Vol 22 (11) ◽  
pp. 5518
Author(s):  
Anna Maria Reuss ◽  
Dominik Groos ◽  
Michael Buchfelder ◽  
Nicolai Savaskan
Keyword(s):  
Tumor Microenvironment ◽  
Malignant Glioma ◽  
Cancer Cells ◽  
Hypoxia Inducible Factor ◽  
Resistance Mechanisms ◽  
Adaptation To Hypoxia ◽  
Therapeutic Implications ◽  
Angiogenic Switch ◽  
Functional Consequences ◽  
Energy Deprivation

Malignant glioma represents a fatal disease with a poor prognosis and development of resistance mechanisms against conventional therapeutic approaches. The distinct tumor zones of this heterogeneous neoplasm develop their own microenvironment, in which subpopulations of cancer cells communicate. Adaptation to hypoxia in the center of the expanding tumor mass leads to the glycolytic and angiogenic switch, accompanied by upregulation of different glycolytic enzymes, transporters, and other metabolites. These processes render the tumor microenvironment more acidic, remodel the extracellular matrix, and create energy gradients for the metabolic communication between different cancer cells in distinct tumor zones. Escape mechanisms from hypoxia-induced cell death and energy deprivation are the result. The functional consequences are more aggressive and malignant behavior with enhanced proliferation and survival, migration and invasiveness, and the induction of angiogenesis. In this review, we go from the biochemical principles of aerobic and anaerobic glycolysis over the glycolytic switch, regulated by the key transcription factor hypoxia-inducible factor (HIF)-1α, to other important metabolic players like the monocarboxylate transporters (MCTs)1 and 4. We discuss the metabolic symbiosis model via lactate shuttling in the acidic tumor microenvironment and highlight the functional consequences of the glycolytic switch on glioma malignancy. Furthermore, we illustrate regulation by micro ribonucleic acids (miRNAs) and the connection between isocitrate dehydrogenase (IDH) mutation status and glycolytic metabolism. Finally, we give an outlook about the diagnostic and therapeutic implications of the glycolytic switch and the relation to tumor immunity in malignant glioma.

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