Potential Correlation Between Homeostasis Control and Tumor Microenvironment Regulation of Probiotic as a Therapeutic Agent to Manage Gastrointestinal Cancer

2021 ◽  
pp. 167-189
Author(s):  
Nabendu Debnath ◽  
Ashok Kumar Yadav
Keyword(s):  
Tumor Microenvironment ◽  
Gastrointestinal Cancer ◽  
Therapeutic Agent

scholarly journals Association between Inflammation and Function of Cell Adhesion Molecules Influence on Gastrointestinal Cancer Development

Cells ◽  
2021 ◽  
Vol 10 (1) ◽  
pp. 67
Author(s):  
Hsiang-Wei Huang ◽  
Cheng-Chih Chang ◽  
Chia-Siu Wang ◽  
Kwang-Huei Lin
Keyword(s):  
Cell Adhesion ◽  
Tumor Microenvironment ◽  
Adhesion Molecules ◽  
Inflammatory Cytokines ◽  
Gastrointestinal Cancer ◽  
Cell Adhesion Molecules ◽  
Immune Cell ◽  
Immune Escape ◽  
Checkpoint Inhibitors ◽  
Cytotoxic T Cells

Gastrointestinal cancer is highly associated with inflammatory processes inducing the release of cytokines from cancer or immune cells, including interferons, interleukins, chemokines, colony-stimulating factors, and growth factors, which promote or suppress tumor progression. Inflammatory cytokines within the tumor microenvironment promote immune cell infiltration. Infiltrating immune, and tumor-surrounding stromal cells support tumor growth, angiogenesis, metastasis, and immunosuppression through communication with inflammatory cytokines and cell adhesion molecules. Notably, infiltrating immune and tumor cells present immunosuppressive molecules, such as programmed death-ligand 1 (PD-L1) and CD80/CD86. Suppression of cytotoxic T cells promotes tumor avoidance of immune surveillance and greater malignancy. Moreover, glycosylation and sialylation of proteins hyperexpressed on the cancer cell surface have been shown to enhance immune escape and metastasis. Cytokine treatments and immune checkpoint inhibitors are widely used in clinical practice. However, the tumor microenvironment is a rapidly changing milieu involving several factors. In this review, we have provided a summary of the interactions of inflammation and cell adhesion molecules between cancer and other cell types, to improve understanding of the tumor microenvironment.

scholarly journals The Roles of Hypoxia-Inducible Factors and Non-Coding RNAs in Gastrointestinal Cancer

Genes ◽  
2019 ◽  
Vol 10 (12) ◽  
pp. 1008 ◽  
Author(s):  
Hyun-Soo Cho ◽  
Tae-Su Han ◽  
Keun Hur ◽  
Hyun Seung Ban
Keyword(s):  
Transcription Factors ◽  
Tumor Microenvironment ◽  
Gastrointestinal Cancer ◽  
Cellular Responses ◽  
Regulatory Mechanisms ◽  
Hypoxia Inducible Factors ◽  
Hypoxia Response ◽  
Functional Relationships ◽  
Hypoxic Tumor ◽  
Non Coding Rnas

Hypoxia-inducible factors (HIFs) are transcription factors that play central roles in cellular responses against hypoxia. In most cancers, HIFs are closely associated with tumorigenesis by regulating cell survival, angiogenesis, metastasis, and adaptation to the hypoxic tumor microenvironment. Recently, non-coding RNAs (ncRNAs) have been reported to play critical roles in the hypoxic response in various cancers. Here, we review the roles of hypoxia-response ncRNAs in gastrointestinal cancer, with a particular focus on microRNAs and long ncRNAs, and discuss the functional relationships and regulatory mechanisms between HIFs and ncRNAs.

Facile discovery of a therapeutic agent for NK-mediated synergistic antitumor effects using a patient-derived 3D platform

2022 ◽  
Author(s):  
Young Eun Lee ◽  
Chae Min Yuk ◽  
Min Seok Lee ◽  
Ki-Cheol Han ◽  
Eunsung Jun ◽  
...  
Keyword(s):  
Tumor Microenvironment ◽  
Cancer Treatment ◽  
Nk Cells ◽  
Natural Killer ◽  
Therapeutic Agent ◽  
Nk Cell ◽  
Physical Barrier ◽  
Antitumor Effects ◽  
Cell Dysfunction

Despite the essential roles of natural killer (NK) cells in cancer treatment, the physical barrier and biological cues of the tumor microenvironment (TME) may induce NK cell dysfunction, causing their...

scholarly journals 375 Development of thrombospondin-1 as a clinical pharmacodynamic biomarker for VT1021, a first-in-class therapeutic agent that reprograms the tumor microenvironment

2021 ◽  
Vol 9 (Suppl 3) ◽  
pp. A405-A406
Author(s):  
Jian Chen ◽  
Marsha Crochiere ◽  
Melanie Vincent ◽  
Suming Wang ◽  
Susanne Fyfe ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Tumor Microenvironment ◽  
Progressive Disease ◽  
Therapeutic Agent ◽  
Phase 1 ◽  
Mrna Levels ◽  
Rt Pcr ◽  
Tumor Biopsy ◽  
Blood Samples ◽  
Protein Levels

BackgroundVT1021 is a first-in-class therapeutic agent in Phase I clinical studies in solid tumors. In vivo preclinical studies demonstrated that VT1021 inhibited tumor growth via stimulation of p53 and Thrombospondin-1 (Tsp-1) in MDSCs. Moreover, induction of Tsp-1 reprogrammed the tumor microenvironment and induced apoptosis in tumor cells via its cell surface receptors CD36 and CD47. Here we report on the utility of Tsp-1 as a pharmacodynamic biomarker and its correlation with clinical response.MethodsTsp-1 protein levels in PBMCs, platelets and plasma were assessed by ELISA following SepMate-based fractionation of subject blood samples. Tsp-1 mRNA levels in peripheral blood cells were analyzed by quantitative RT-PCR following extraction of total RNA from subject whole blood samples via PAXgene Blood RNA kit. Tsp-1 levels in subject biopsy samples were analyzed by immunohistochemistry as described previously.ResultsUp-regulation of Tsp-1 protein was observed in PBMCs, platelets and plasma in all evaluable subjects following treatment with VT1021 across multiple indications in a phase 1 clinical study, indicating that Tsp-1 induction is a pharmacodynamic biomarker for VT1021 (figure 1). Induction of Tsp-1 by VT1021 was also shown at the transcriptional level via RT-PCR measurement of whole blood samples. Strikingly, maximum PBMC Tsp-1 levels induced by VT1021 were higher in subjects with glioblastoma (GBM) that had objective responses (complete or partial response) compared to subjects with stable disease (SD) or progressive disease (PD). Of note, pre-dose levels of Tsp-1 were predictive of response, as subjects with objective responses had higher basal levels of Tsp-1 than those that had stable or progressive disease. For subjects with pancreatic cancer, Tsp-1 induction was higher in SD subjects compared to PD subjects, suggesting that Tsp-1 induction in PBMCs can be a potential prognostic biomarker. In tumor biopsy samples from subjects with pancreatic cancer, increased colocalization of Tsp-1 and CD11b was observed in on-study samples, supporting a role of Tsp-1 in reprogramming the tumor microenvironment (figure 2).Abstract 375 Figure 1Up-regulation of Tsp-1 protein levels have been observed in PBMCs(A), platelets (B) and plasma (C) in all evaluable subjects post-dosing with VT1021 across multiple inductions in a phase 1 clinical study.Abstract 375 Figure 2Increased colocalization of Tsp-1 and CD11b was observed in tumor microenvironment in tumor biopsy samples from a subject with pancreatic cancer post-dosing with VT1021ConclusionsBased on both protein and mRNA levels, Tsp-1 induction has the potential to be a useful prognostic pharmacodynamic biomarker for VT1021 in various tumor types. In subjects with GBM, both basal and induced Tsp-1 levels in PBMCs are potential predictive and prognostic biomarkers, respectively. For subjects with pancreatic cancer, Tsp-1 protein induction in PBMCs is a potential prognostic biomarker. The predictive/prognostic utility coupled with the ability to measure levels in peripheral blood makes Tsp-1 a powerful biomarker to assess and predict clinical response to VT1021.

scholarly journals Silymarin (milk thistle extract) as a therapeutic agent in gastrointestinal cancer

2021 ◽  
Vol 142 ◽  
pp. 112024
Author(s):  
Maryam Fallah ◽  
Amirhossein Davoodvandi ◽  
Shahin Nikmanzar ◽  
Sarehnaz Aghili ◽  
Seyed Mohammad Ali Mirazimi ◽  
...  
Keyword(s):  
Gastrointestinal Cancer ◽  
Therapeutic Agent ◽  
Milk Thistle

ACE2 as therapeutic agent

2020 ◽  
Vol 134 (19) ◽  
pp. 2581-2595
Author(s):  
Qiuhong Li ◽  
Maria B. Grant ◽  
Elaine M. Richards ◽  
Mohan K. Raizada
Keyword(s):  
Therapeutic Agent ◽  
Renin Angiotensin System ◽  
Peptide Hormone ◽  
Experimental Models ◽  
Electrolyte Balance ◽  
Ang Ii ◽  
Angiotensin Converting Enzyme 2 ◽  
Beneficial Effects ◽  
Overwhelming Evidence ◽  
Future Challenges

Abstract The angiotensin-converting enzyme 2 (ACE2) has emerged as a critical regulator of the renin–angiotensin system (RAS), which plays important roles in cardiovascular homeostasis by regulating vascular tone, fluid and electrolyte balance. ACE2 functions as a carboxymonopeptidase hydrolyzing the cleavage of a single C-terminal residue from Angiotensin-II (Ang-II), the key peptide hormone of RAS, to form Angiotensin-(1-7) (Ang-(1-7)), which binds to the G-protein–coupled Mas receptor and activates signaling pathways that counteract the pathways activated by Ang-II. ACE2 is expressed in a variety of tissues and overwhelming evidence substantiates the beneficial effects of enhancing ACE2/Ang-(1-7)/Mas axis under many pathological conditions in these tissues in experimental models. This review will provide a succinct overview on current strategies to enhance ACE2 as therapeutic agent, and discuss limitations and future challenges. ACE2 also has other functions, such as acting as a co-factor for amino acid transport and being exploited by the severe acute respiratory syndrome coronaviruses (SARS-CoVs) as cellular entry receptor, the implications of these functions in development of ACE2-based therapeutics will also be discussed.

Expression of splice variants; The human cholecystokinin-B receptor in association with gastrointestinal cancer

2001 ◽  
Vol 120 (5) ◽  
pp. A507-A507
Author(s):  
D KANG ◽  
Y WHANG ◽  
J YOO ◽  
I SONG ◽  
J OH ◽  
...  
Keyword(s):  
Gastrointestinal Cancer ◽  
Splice Variants

CD9 negatively regulates growth signaling of the gastrointestinal cancer cells

2001 ◽  
Vol 120 (5) ◽  
pp. A660-A660
Author(s):  
Y MURAYAMA ◽  
Y SHINOMURA ◽  
J MIYAGAWA ◽  
H YOSHIDA ◽  
T KIYOHARA ◽  
...  
Keyword(s):  
Cancer Cells ◽  
Gastrointestinal Cancer

The Gastrointestinal Cancer Committee of the National Advisory Cancer Council

1955 ◽  
Vol 29 (4) ◽  
pp. 492-493
Author(s):  
George T. Pack ◽  
Morris K. Barrett
Keyword(s):  
Gastrointestinal Cancer ◽  
Cancer Council
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