Role of TWEAK and Fn14 in tumor biology

10.2741/2270 ◽  
2007 ◽  
Vol 12 (1) ◽  
pp. 2761 ◽  
Author(s):  
Jeffrey, A. Winkles
Keyword(s):  
Tumor Biology

scholarly journals Levels of Circulating PD-L1 Are Decreased in Patients with Resectable Cholangiocarcinoma

2021 ◽  
Vol 22 (12) ◽  
pp. 6569
Author(s):  
Christoph Roderburg ◽  
Sven H. Loosen ◽  
Jan Bednarsch ◽  
Patrick H. Alizai ◽  
Anjali A. Roeth ◽  
...  
Keyword(s):  
Tumor Recurrence ◽  
Tumor Biology ◽  
Tumor Resection ◽  
Postoperative Outcome ◽  
Serum Levels ◽  
Strong Trend ◽  
Programmed Cell Death 1 ◽  
Early Tumor ◽  
Circulating Levels

Tumor resection represents the only curative treatment option for patients with biliary tract cancers (BTCs), including intrahepatic cholangiocarcinoma (CCA), perihilar and extrahepatic CCA and gallbladder cancer. However, many patients develop early tumor recurrence and are unlikely to benefit from surgery. Therefore, markers to identify ideal surgical candidates are urgently needed. Circulating programmed cell death 1 ligand 1 (PD-L1) has recently been associated with different malignancies, including pancreatic cancer which closely resembles BTC in terms of patients’ prognosis and tumor biology. Here, we aim at evaluating a potential role of circulating PD-L1 as a novel biomarker for resectable BTC. Methods: Serum levels of PD-L1 were analyzed by ELISA in 73 BTC patients and 42 healthy controls. Results: Circulating levels of preoperative PD-L1 were significantly lower in patients with BTC compared to controls. Patients with low PD-L1 levels displayed a strong trend towards an impaired prognosis, and circulating PD-L1 was negatively correlated with experimental markers of promalignant tumor characteristics such as CCL1, CCL21, CCL25 and CCL26. For 37 out of 73 patients, postoperative PD-L1 levels were available. Interestingly, after tumor resection, circulating PD-L1 raised to almost normal levels. Notably, patients with further decreasing PD-L1 concentrations after surgery showed a trend towards an impaired postoperative outcome. Conclusion: Circulating PD-L1 levels were decreased in patients with resectable BTC. Lack of normalization of PD-L1 levels after surgery might identify patients at high risk for tumor recurrence or adverse outcome.

The Role of Cancer-associated Fibroblasts in Tumorigenesis of Gastric Cancer

2018 ◽  
Vol 24 (28) ◽  
pp. 3297-3302 ◽  
Author(s):  
Zhilong Ma ◽  
Min Chen ◽  
Xiaohu Yang ◽  
Bin Xu ◽  
Zhenshun Song ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cancer Progression ◽  
Tumor Biology ◽  
Vital Role ◽  
Cancer Associated Fibroblasts ◽  
Gastric Cancer Cells ◽  
Stromal Fibroblasts ◽  
Tumor Microenvironments ◽  
Tumorigenesis And Progression

Cancer-associated fibroblasts (CAFs) are an important cell type present in solid tumor microenvironments, including that of gastric cancer. They play a vital role in the promotion of tumorigenesis, angiogenesis, and cancer progression through paracrine signaling and modulation of the extracellular matrix. However, the exact molecular mechanism underlying the interaction between gastric cancer cells and stromal fibroblasts remains poorly understood. Recent studies have demonstrated that various factors, such as gene and microRNA variations, are involved in this process. This review discusses recent advances in understanding how these factors are regulated in CAFs and how they affect tumor biology, which may improve our understanding of their role in gastric cancer tumorigenesis and progression and provide new promising targets for therapeutic strategies.

The Role of Neuropilin in Vascular and Tumor Biology

2002 ◽  
pp. 33-48 ◽  
Author(s):  
Michael Klagsbrun ◽  
Seiji Takashima ◽  
Roni Mamluk
Keyword(s):  
Tumor Biology

scholarly journals The Role of Alternative Lengthening of Telomeres Mechanism in Cancer: Translational and Therapeutic Implications

Cancers ◽  
2020 ◽  
Vol 12 (4) ◽  
pp. 949 ◽  
Author(s):  
Marta Recagni ◽  
Joanna Bidzinska ◽  
Nadia Zaffaroni ◽  
Marco Folini
Keyword(s):  
Cancer Cells ◽  
Tumor Biology ◽  
Telomerase Activity ◽  
Telomere Maintenance ◽  
Limited Information ◽  
Adaptive Responses ◽  
Therapeutic Implications ◽  
Telomerase Inhibitors ◽  
Alternative Lengthening

Telomere maintenance mechanisms (i.e., telomerase activity (TA) and the alternative lengthening of telomere (ALT) mechanism) contribute to tumorigenesis by providing unlimited proliferative capacity to cancer cells. Although the role of either telomere maintenance mechanisms seems to be equivalent in providing a limitless proliferative ability to tumor cells, the contribution of TA and ALT to the clinical outcome of patients may differ prominently. In addition, several strategies have been developed to interfere with TA in cancer, including Imetelstat that has been the first telomerase inhibitor tested in clinical trials. Conversely, the limited information available on the molecular underpinnings of ALT has hindered thus far the development of genuine ALT-targeting agents. Moreover, whether anti-telomerase therapies may be hampered or not by possible adaptive responses is still debatable. Nonetheless, it is plausible hypothesizing that treatment with telomerase inhibitors may exert selective pressure for the emergence of cancer cells that become resistant to treatment by activating the ALT mechanism. This notion, together with the evidence that both telomere maintenance mechanisms may coexist within the same tumor and may distinctly impinge on patients’ outcomes, suggests that ALT may exert an unexpected role in tumor biology that still needs to be fully elucidated.

scholarly journals The Emerging Role of Voltage-Gated Sodium Channels in Tumor Biology

2019 ◽  
Vol 9 ◽  
Author(s):  
Weijia Mao ◽  
Jie Zhang ◽  
Heinrich Körner ◽  
Yong Jiang ◽  
Songcheng Ying
Keyword(s):  
Sodium Channels ◽  
Tumor Biology ◽  
Voltage Gated ◽  
Voltage Gated Sodium Channels

scholarly journals Age-Related Alterations in Immune Contexture Are Associated with Aggressiveness in Rhabdomyosarcoma

Cancers ◽  
2019 ◽  
Vol 11 (9) ◽  
pp. 1380 ◽  
Author(s):  
Patrizia Gasparini ◽  
Orazio Fortunato ◽  
Loris De Cecco ◽  
Michela Casanova ◽  
Maria Federica Iannó ◽  
...  
Keyword(s):  
Myogenic Differentiation ◽  
Tumor Biology ◽  
Muscle Metabolism ◽  
Γδ T Cells ◽  
Resting Cells ◽  
Over Expression ◽  
Age Related ◽  
Immune Contexture

Adolescents and young adults (AYA) with rhabdomyosarcoma (RMS) form a subgroup of patients whose optimal clinical management and access to care remain a challenge and whose survival lacks behind that of children diagnosed with histologically similar tumors. Understanding the tumor biology that differentiates children from AYA-RMS could provide critical information and drive new initiatives to improve the final outcome. MicroRNA (miRNA) and gene expression profiling (GEP) was evaluated in a RMS cohort of 49 tumor and 15 non-neoplastic tissues. miRNAs analysis identified miR-223 over-expression and miR-431 down-regulation in AYA, validated by Real-Time PCR and miRNA in situ hybridization (ISH). GEP analysis detected 793 age-correlated genes in tumors, of which 194 were anti-correlated. NOTCH2, FGFR1/2 were significantly down-modulated in AYA-RMS. miR-223 was associated with up-regulation of epithelial mesenchymal translation (EMT) and inflammatory pathways, whereas miR-431 was correlated to myogenic differentiation and muscle metabolism. GEP showed an increase in genes associated with CD4 memory resting cells and a decrease in genes associated with γδ T-cells in AYA-RMS. Immunohistochemistry (IHC) analysis demonstrated an increase of infiltrated CD4, CD8, and neutrophils in AYA-RMS tumors. Our results show that aggressiveness of AYA-RMS could be explained by differences in microenvironmental signal modulation mediated by tumor cells, suggesting a fundamental role of immune contexture in AYA-RMS development.

scholarly journals Prognostic and Predictive Implications of PTEN in Breast Cancer: Unfulfilled Promises but Intriguing Perspectives

Cancers ◽  
2019 ◽  
Vol 11 (9) ◽  
pp. 1401 ◽  
Author(s):  
Luisa Carbognin ◽  
Federica Miglietta ◽  
Ida Paris ◽  
Maria Vittoria Dieci
Keyword(s):  
Breast Cancer ◽  
Tumor Biology ◽  
Predictive Biomarkers ◽  
Stability Loss ◽  
Cellular Migration ◽  
Negative Regulator ◽  
Clinical Role ◽  
Growth And Survival ◽  
Tensin Homolog

The characterization of tumor biology and consequently the identification of prognostic and predictive biomarkers represent key issues for the translational research in breast cancer (BC). Phosphatase and tensin homolog deleted on chromosome ten (PTEN), the negative regulator of the proto-oncogenic phosphatidylinositol-3-kinase (PI3K)/protein kinase B (Akt) pathway, constitutes one of the most intriguing tumor suppressor genes involved in a series of biological processes, such as cell growth and survival, cellular migration and genomic stability. Loss of PTEN activity, due to protein, genetic or epigenetic alterations, was reported in up to almost half of BC cases. Recently, besides the role of PTEN in the pathogenesis of BC, investigated for over 20 years after the PTEN discovery, several retrospective and prospective translational studies, in the early and advanced setting, reported controversial results regarding the association between PTEN functional status and both clinical outcome and response to various BC treatments. This review explores the pre-clinical and clinical role of PTEN in BC with regard to the potential association of PTEN with prognosis and treatment response or resistance, underlying the complexity of the interpretation of available results and suggesting potential future perspectives.

scholarly journals Complement and Cancer—A Dysfunctional Relationship?

Antibodies ◽  
2020 ◽  
Vol 9 (4) ◽  
pp. 61
Author(s):  
Joshua M. Thurman ◽  
Jennifer Laskowski ◽  
Raphael A. Nemenoff
Keyword(s):  
Tumor Microenvironment ◽  
Complement Activation ◽  
Tumor Biology ◽  
Clinical Work ◽  
The Body ◽  
Great Promise ◽  
Cancer Therapies ◽  
Complement Inhibitors ◽  
Cell Immunity

Although it was long believed that the complement system helps the body to identify and remove transformed cells, it is now clear that complement activation contributes to carcinogenesis and can also help tumors to escape immune-elimination. Complement is activated by several different mechanisms in various types of cancer, and complement activation fragments have multiple different downstream effects on cancer cells and throughout the tumor microenvironment. Thus, the role of complement activation in tumor biology may vary among different types of cancer and over time within a single tumor. In multiple different pre-clinical models, however, complement activation has been shown to recruit immunosuppressive myeloid cells into the tumor microenvironment. These cells, in turn, suppress anti-tumor T cell immunity, enabling the tumor to grow. Based on extensive pre-clinical work, therapeutic complement inhibitors hold great promise as a new class of immunotherapy. A greater understanding of the role of complement in tumor biology will improve our ability to identify those patients most likely to benefit from this treatment and to rationally combine complement inhibitors with other cancer therapies.

Trefoil factor family peptides – friends or foes?

2015 ◽  
Vol 6 (5-6) ◽  
pp. 343-359 ◽  
Author(s):  
Maike Busch ◽  
Nicole Dünker
Keyword(s):  
Cancer Research ◽  
Tumor Suppressors ◽  
Current Knowledge ◽  
Tumor Biology ◽  
Epigenetic Mechanisms ◽  
Trefoil Factor ◽  
Protective Function ◽  
Trefoil Factor Family ◽  
Tff Peptides

AbstractTrefoil factor family (TFF) peptides are a group of molecules bearing a characteristic three-loop trefoil domain. They are mainly secreted in mucous epithelia together with mucins but are also synthesized in the nervous system. For many years, TFF peptides were only known for their wound healing and protective function, e.g. in epithelial protection and restitution. However, experimental evidence has emerged supporting a pivotal role of TFF peptides in oncogenic transformation, tumorigenesis and metastasis. Deregulated expression of TFF peptides at the gene and protein level is obviously implicated in numerous cancers, and opposing functions as oncogenes and tumor suppressors have been described. With regard to the regulation of TFF expression, epigenetic mechanisms as well as the involvement of various miRNAs are new, promising aspects in the field of cancer research. This review will summarize current knowledge about the expression and regulation of TFF peptides and the involvement of TFF peptides in tumor biology and cancerogenesis.

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