scholarly journals Understanding the Role of Fibroblasts following a 3D Tumoroid Implantation for Breast Tumor Formation

2021 ◽  
Vol 8 (11) ◽  
pp. 163
Author(s):  
Girdhari Rijal
Keyword(s):  
Tumor Cells ◽  
Breast Tumor ◽  
Tumor Tissue ◽  
Review Paper ◽  
Cell Activity ◽  
Tumor Formation ◽  
Cancer Associated Fibroblasts ◽  
Technical Challenge ◽  
Signaling Systems

An understanding of the participation and modulation of fibroblasts during tumor formation and growth is still unclear. Among many speculates, one might be the technical challenge to reveal the versatile function of fibroblasts in tissue complexity, and another is the dynamics in tissue physiology and cell activity. The histology of most solid tumors shows a predominant presence of fibroblasts, suggesting that tumor cells recruit fibroblasts for breast tumor growth. In this review paper, therefore, the migration, activation, differentiation, secretion, and signaling systems that are associated with fibroblasts and cancer-associated fibroblasts (CAFs) after implantation of a breast tumoroid, i.e., a lab-generated tumor tissue into an animal, are discussed.

scholarly journals Expression of Tryptophan 2,3-Dioxygenase in Metastatic Uveal Melanoma

Cancers ◽  
2020 ◽  
Vol 12 (2) ◽  
pp. 405 ◽  
Author(s):  
Terai ◽  
Londin ◽  
Rochani ◽  
Link ◽  
Lam ◽  
...  
Keyword(s):  
Immune Responses ◽  
Tumor Cells ◽  
Uveal Melanoma ◽  
Hepatic Metastasis ◽  
Tumor Tissue ◽  
Monosomy 3 ◽  
Systemic Metastasis ◽  
T Cell Immune Responses ◽  
Tissue Specimens

Uveal melanoma (UM) is the most common primary eye malignancy in adults and up to 50% of patients subsequently develop systemic metastasis. Metastatic uveal melanoma (MUM) is highly resistant to immunotherapy. One of the mechanisms for resistance would be the immune-suppressive tumor microenvironment. Here, we have investigated the role of tryptophan 2,3-dioxygenase (TDO) in UM. Both TDO and indoleamine 2,3-dioxygenase (IDO) catalyze tryptophan and produce kynurenine, which could cause inhibition of T cell immune responses. We first studied the expression of TDO on tumor tissue specimens obtained from UM hepatic metastasis. High expression of TDO protein was confirmed in all hepatic metastasis. TDO was positive in both normal hepatocytes and the tumor cells with relatively higher expression in tumor cells. On the other hand, IDO protein remained undetectable in all of the MUM specimens. UM cell lines established from metastasis also expressed TDO protein and increasing kynurenine levels were detected in the supernatant of MUM cell culture. In TCGA database, higher TDO2 expression in primary UM significantly correlated to BAP1 mutation and monosomy 3. These results indicate that TDO might be one of the key mechanisms for resistance to immunotherapy in UM.

scholarly journals Clinical Relevance of Immune Checkpoints on Circulating Tumor Cells in Breast Cancer

Cancers ◽  
2020 ◽  
Vol 12 (2) ◽  
pp. 376 ◽  
Author(s):  
Maria A. Papadaki ◽  
Anastasios V. Koutsopoulos ◽  
Panormitis G. Tsoulfas ◽  
Eleni Lagoudaki ◽  
Despoina Aggouraki ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Tumor Cells ◽  
Circulating Tumor Cells ◽  
Peripheral Blood ◽  
Tumor Tissue ◽  
Mononuclear Cells ◽  
Immune Checkpoints ◽  
Peripheral Blood Mononuclear ◽  
Increased Risk

The role of CD47 and PD-L1 expression on circulating tumor cells (CTCs) remains unclear, and it is currently unknown whether their distribution varies between the blood and tumor tissue in breast cancer (BC). In this study, CD47 and PD-L1 expression was investigated a) on peripheral blood mononuclear cell (PBMC) cytospins from early (n = 100) and metastatic (n = 98) BC patients, by triple immunofluorescence for CD47/PD-L1/Cytokeratins, and b) on matched primary and/or metastatic tumor tissue from CTC-positive patients using immunohistochemistry. CD47+and/orPD-L1+ CTCs were detected in 11%, 16.9%, and 29.6% of early, recurrent, and de novo metastatic patients (p = 0.016). In metastatic disease, CD47highand/orPD-L1high CTCs were associated with disease progression (p = 0.005) and shorter progression-free survival (PFS) (p = 0.010), and independently predicted for an increased risk of relapse (HR: 2.719; p = 0.008) and death (HR: 2.398; p = 0.034). PD-L1 expression rates differed between CTCs and tissue tumor cells and between peripheral blood mononuclear cells (PBMCs) and tumor-infiltrating lymphocytes (TILs) (positive concordance of 3.8% and 4%, respectively). CD47 expression also differed between CTCs and tumor cells (positive concordance of 11.5%). In conclusion, CTCs expressing CD47 and PD-L1 have independent poor prognostic implications in metastatic BC, indicating a potential role of innate and adaptive immune evasion mechanisms in their metastatic potential. The clinical value of the parallel assessment of the peripheral and local immune response merits further evaluation in BC.

scholarly journals The promising role of noncoding RNAs in cancer-associated fibroblasts: an overview of current status and future perspectives

2020 ◽  
Vol 13 (1) ◽  
Author(s):  
Zengli Fang ◽  
Jin Xu ◽  
Bo Zhang ◽  
Wei Wang ◽  
Jiang Liu ◽  
...  
Keyword(s):  
Tumor Cells ◽  
Noncoding Rnas ◽  
Current Status ◽  
Cancer Therapies ◽  
Cancer Associated Fibroblasts ◽  
Biological Processes ◽  
Future Perspectives ◽  
Metabolic Characteristics ◽  
Complex Regulatory Network

AbstractAs the most important component of the stromal cell population in the tumor microenvironment (TME), cancer-associated fibroblasts (CAFs) are crucial players in tumor initiation and progression. The interaction between CAFs and tumor cells, as well as the resulting effect, is much greater than initially expected. Numerous studies have shown that noncoding RNAs (ncRNAs) play an irreplaceable role in this interplay, and related evidence continues to emerge and advance. Under the action of ncRNAs, normal fibroblasts are directly or indirectly activated into CAFs, and their metabolic characteristics are changed; thus, CAFs can more effectively promote tumor progression. Moreover, via ncRNAs, activated CAFs can affect the gene expression and secretory characteristics of cells, alter the TME and enhance malignant biological processes in tumor cells to contribute to tumor promotion. Previously, ncRNA dysregulation was considered the main mechanism by which ncRNAs participate in the crosstalk between CAFs and tumor cells. Recently, however, exosomes containing ncRNAs have been identified as another vital mode of interaction between these two types of cells, with a more direct and clear function. Gaining an in-depth understanding of ncRNAs in CAFs and the complex regulatory network connecting CAFs with tumor cells might help us to establish more effective and safer approaches for cancer therapies targeting ncRNAs and CAFs and offer new hope for cancer patients.

The role of TGF-β production in growth inhibition of breast-tumor cells by progestins

1995 ◽  
Vol 61 (1) ◽  
pp. 80-86 ◽  
Author(s):  
Eric Kalkhoven ◽  
Linda Kwakkenbos-Isbrücker ◽  
Christine L. Mummery ◽  
Siegfried W. De Laat ◽  
Adriana J. M. Van Den Eijnden-Van Raaij ◽  
...  
Keyword(s):  
Growth Inhibition ◽  
Tumor Cells ◽  
Breast Tumor ◽  
Breast Tumor Cells

scholarly journals Loss of MYBBP1A Induces Cancer Stem Cell Activity in Renal Cancer

Cancers ◽  
2019 ◽  
Vol 11 (2) ◽  
pp. 235 ◽  
Author(s):  
Blanca Felipe-Abrio ◽  
Eva Verdugo-Sivianes ◽  
Carmen Sáez ◽  
Amancio Carnero
Keyword(s):  
Tumor Cells ◽  
Cell Lines ◽  
Cell Activity ◽  
Human Tumor ◽  
Genetic Alterations ◽  
Renal Tumors ◽  
Future Design

Tumors are cellular ecosystems where different populations and subpopulations of cells coexist. Among these cells, cancer stem cells (CSCs) are considered to be the origin of the tumor mass, being involved in metastasis and in the resistance to conventional therapies. Furthermore, tumor cells have an enormous plasticity and a phenomenon of de-differentiation of mature tumor cells to CSCs may occur. Therefore, it is essential to identify genetic alterations that cause the de-differentiation of mature tumor cells to CSCs for the future design of therapeutic strategies. In this study, we characterized the role of MYBBP1A by experiments in cell lines, xenografts and human tumor samples. We have found that MYBBP1A downregulation increases c-MYB (Avian myeloblastosis viral oncogene homolog) activity, leading to a rise in the stem-like cell population. We identified that the downregulation of MYBBP1A increases tumorigenic properties, in vitro and in vivo, in renal carcinoma cell lines that express high levels of c-MYB exclusively. Moreover, in a cohort of renal tumors, MYBBP1A is downregulated or lost in a significant percentage of tumors correlating with poor patient prognosis and a metastatic tendency. Our data support the role of MYBBP1A as a tumor suppressor by repressing c-MYB, acting as an important regulator of the plasticity of tumor cells.

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