scholarly journals Association of cathepsin E with tumor growth arrest through angiogenesis inhibition and enhanced immune responses

2007 ◽  
Vol 388 (11) ◽  
Author(s):  
Masashi Shin ◽  
Tomoko Kadowaki ◽  
Jun-ichi Iwata ◽  
Tomoyo Kawakubo ◽  
Noriko Yamaguchi ◽  
...  
Keyword(s):  
Immune Responses ◽  
Tumor Growth ◽  
Growth Arrest ◽  
Angiogenesis Inhibition ◽  
Cathepsin E

scholarly journals Low-Dose Histone Deacetylase Inhibitor Treatment Leads to Tumor Growth Arrest and Multi-Lineage Differentiation of Malignant Rhabdoid Tumors

2016 ◽  
Vol 22 (14) ◽  
pp. 3560-3570 ◽  
Author(s):  
Andrea Muscat ◽  
Dean Popovski ◽  
W. Samantha N. Jayasekara ◽  
Fernando J. Rossello ◽  
Melissa Ferguson ◽  
...  
Keyword(s):  
Tumor Growth ◽  
Histone Deacetylase ◽  
Histone Deacetylase Inhibitor ◽  
Low Dose ◽  
Growth Arrest ◽  
Lineage Differentiation ◽  
Deacetylase Inhibitor ◽  
Rhabdoid Tumors ◽  
Inhibitor Treatment

scholarly journals Temporal Changes in Immune Responses within the Tumor Microenvironment in the 4T1.2-HER2 Mammary Tumor Model

2021 ◽  
Author(s):  
Yitong Xu ◽  
Connie Rogers
Keyword(s):  
Immune Responses ◽  
Tumor Growth ◽  
Immune Cells ◽  
Tumor Regression ◽  
Tumor Model ◽  
Second Phase ◽  
Tumor Inoculation ◽  
Cancer Model ◽  
Breast Cancer Model ◽  
Initial Tumor

Abstract Background: The murine 4T1.2 triple-negative breast cancer model is widely used, but is poorly immunogenic with no defined tumor-associated antigens. A modified 4T1.2 model has been developed that stably expresses a surrogate tumor antigen, human epidermal growth factor receptor-2 (HER2). The goal of the current study was to characterize host immune responses in the 4T1.2-HER2 tumor model, focusing on the tumor microenvironment (TME) during the early stage of tumor development. Methods: Female BALB/c mice were orthotopically inoculated with 4T1.2-HER2 tumor cells and sacrificed at day (D) 6, 9, 12, 15 and 18 post tumor inoculation. The phenotype and function of tumor-infiltrating immune cells were assessed. Results: 4T1.2 and 4T1.2-HER2 tumor cells had similar proliferation rates in vitro. In contrast to the rapid progression of the parental 4T1.2 model, the 4T1.2-HER2 model demonstrated initial tumor growth followed by spontaneous tumor regression by D18 post tumor inoculation, which was not observed in scid mice. Following tumor regression, mice demonstrated either a second phase of tumor outgrowth or complete tumor rejection. Within the TME, the percentage of T cells was reduced at D9 and increased during tumor regression through D18 (p<0.05), whereas the percentage of myeloid-derived suppressor cells (MDSCs) increased during the initial tumor growth and was reduced by D18 (p<0.01). There was a stepwise increase in the percentage of IFNg+, IL-2+ and perforin+ T cells and NK cells peaking at D12-15. Furthermore, tumor regression occurred concurrently with HER2-specific IFNg production from tumor-infiltrating immune cells at D12 and D15 (p<0.05). During the second phase of 4T1.2-HER2 tumor growth, tumor volume was negatively correlated with immune infiltration (r=0.662, p=0.052). Conclusions: These results suggest that the integration of a surrogate tumor antigen, human HER2, into the clinically relevant, yet poorly immunogenic 4T1.2 breast cancer model enhanced its immunogenicity and induced HER2-specific immune responses.

scholarly journals GRP94 (gp96) and GRP94 N-Terminal Geldanamycin Binding Domain Elicit Tissue Nonrestricted Tumor Suppression

2002 ◽  
Vol 196 (11) ◽  
pp. 1447-1459 ◽  
Author(s):  
Julie C. Baker-LePain ◽  
Marcella Sarzotti ◽  
Timothy A. Fields ◽  
Chuan-Yuan Li ◽  
Christopher V. Nicchitta
Keyword(s):  
Immune Responses ◽  
Tumor Growth ◽  
Tumor Suppression ◽  
Protective Immunity ◽  
Chemical Carcinogenesis ◽  
Binding Domain ◽  
Primary Role ◽  
Metastatic Progression ◽  
Peptide Antigens ◽  
Tissue Of Origin

In chemical carcinogenesis models, GRP94 (gp96) elicits tumor-specific protective immunity. The tumor specificity of this response is thought to reflect immune responses to GRP94-bound peptide antigens, the cohort of which uniquely identifies the GRP94 tissue of origin. In this study, we examined the apparent tissue restriction of GRP94-elicited protective immunity in a 4T1 mammary carcinoma model. We report that the vaccination of BALB/c mice with irradiated fibroblasts expressing a secretory form of GRP94 markedly suppressed 4T1 tumor growth and metastasis. In addition, vaccination with irradiated cells secreting the GRP94 NH2-terminal geldanamycin-binding domain (NTD), a region lacking canonical peptide-binding motifs, yielded a similar suppression of tumor growth and metastatic progression. Conditioned media from cultures of GRP94 or GRP94 NTD-secreting fibroblasts elicited the up-regulation of major histocompatibility complex class II and CD86 in dendritic cell cultures, consistent with a natural adjuvant function for GRP94 and the GRP94 NTD. Based on these findings, we propose that GRP94-elicited tumor suppression can occur independent of the GRP94 tissue of origin and suggest a primary role for GRP4 natural adjuvant function in antitumor immune responses.

scholarly journals In vivo anti‐V‐ATPase antibody treatment delays ovarian tumor growth by increasing antitumor immune responses

2020 ◽  
Vol 14 (10) ◽  
pp. 2436-2454
Author(s):  
Arpita Kulshrestha ◽  
Gajendra K. Katara ◽  
Safaa A. Ibrahim ◽  
Valerie E. Riehl ◽  
Sylvia Schneiderman ◽  
...  
Keyword(s):  
Immune Responses ◽  
Tumor Growth ◽  
Ovarian Tumor ◽  
Antibody Treatment ◽  
Treatment Delays

scholarly journals Knockdown of DCAMKL-1 Results in Liver Cancer Tumor Growth Arrest Through Inhibition of c-MYC via Let-7a MicroRNA; Inhibits EMT via Mir-200a MicroRNA Dependent Mechanisms

2011 ◽  
Vol 140 (5) ◽  
pp. S-890
Author(s):  
Sripathi M. Sureban ◽  
Dongfeng Qu ◽  
Randal May ◽  
Sima Asfa ◽  
Shrikant Anant ◽  
...  
Keyword(s):  
Liver Cancer ◽  
Tumor Growth ◽  
Growth Arrest ◽  
Cancer Tumor

scholarly journals Tumor growth inhibition by mSTEAP peptide nanovaccine inducing augmented CD8+ T cell immune responses

2019 ◽  
Vol 9 (6) ◽  
pp. 1095-1105 ◽  
Author(s):  
Qiuqiang Chen ◽  
Ying Bao ◽  
Danielle Burner ◽  
Sharmeela Kaushal ◽  
Yu Zhang ◽  
...  
Keyword(s):  
T Cell ◽  
Immune Responses ◽  
Tumor Growth ◽  
Growth Inhibition ◽  
Cd8 T Cell ◽  
Tumor Growth Inhibition ◽  
T Cell Immune Responses

scholarly journals QUANTITATIVE EFFECTS OF NUTRITIONAL ESSENTIAL AMINO ACID DEFICIENCY UPON IMMUNE RESPONSES TO TUMORS IN MICE

1973 ◽  
Vol 137 (1) ◽  
pp. 1-9 ◽  
Author(s):  
David G. Jose ◽  
Robert A. Good
Keyword(s):  
Amino Acids ◽  
Amino Acid ◽  
Immune Responses ◽  
Tumor Growth ◽  
Essential Amino Acid ◽  
Cell Mediated Immunity ◽  
Host Animal ◽  
Vitro Assay ◽  
Cytotoxic Cell

Mice were fed diets deficient in a single essential amino acid, and the primary immune responses to inoculation of allogenic tumor cells was measured by in vitro assay of cellular immunity. Moderate reduction of the amino acids phenylalanine-tyrosine, valine, threonine, methionine-cystine, isoleucine, and tryptophane in the diet produced profound depression of hemagglutinating and blocking antibody responses, although cytotoxic cell-mediated immunity remained intact. These diets had previously been shown to result in a selective depression of tumor growth in mice. Limitation of the amino acids arginine, histidine, and lysine in the diets gave rise to only slight depression of the immune responses. These diets had previously been shown to produce a proportional decrease in both tumor growth and host body weight. Moderate leucine restriction resulted in a paradoxical depression of cytotoxic cell-mediated immunity with little effect on serum blocking activity. Slight increases had previously been noted in the weight of tumors in mice fed leucine-restricted diets. Deficiency or imbalance of essential amino acids in the diet may produce profound depression of immune responses and apparent, marked changes in the immune resistance of the host animal to tumors.

Chronic bacterial osteomyelitis suppression of tumor growth requires innate immune responses

2009 ◽  
Vol 59 (3) ◽  
pp. 367-378 ◽  
Author(s):  
Joseph L. Sottnik ◽  
Lance W. U’Ren ◽  
Douglas H. Thamm ◽  
Stephen J. Withrow ◽  
Steven W. Dow
Keyword(s):  
Immune Responses ◽  
Tumor Growth ◽  
Innate Immune ◽  
Innate Immune Responses
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