scholarly journals Evolution of sarcoma 180 in mice infected with Trypanosoma cruzi

1983 ◽  
Vol 78 (3) ◽  
pp. 237-244
Author(s):  
Fausto Edmundo Lima Pereira ◽  
William Assad Sassine ◽  
Dimith Chequer Bouhabib ◽  
Elton de Almeida Lucas
Keyword(s):  
Weight Gain ◽  
Trypanosoma Cruzi ◽  
Tumor Cells ◽  
Ascitic Fluid ◽  
Tumor Development ◽  
Sarcoma 180 ◽  
Tumor Inoculation ◽  
Time Intervals ◽  
Tumor Challenge ◽  
Ascites Formation

Mice infected with Trypanosoma cruzi were challenged with 2x10[raised to the power of 6] cells of sarcoma 180 (ascite tumor) by i.p. route, on day seven post infection. Tumor development was followed by evaluation of weight gain, by measurement of ascitic fluid produced and enumeration of tumor cells in ascitic fluid. Infected mice were more resitant to tumor development as demonstrated by reduction in ascites formation and by reduction in the number of tumor cells in ascitic fluid, at different time intervals after tumor challenge. The number of peritoneal cells exsudated after tumor inoculation was greater in infected mice than in controls. This increased resitance of mice infected with T. cruzi to tumor development could be due to the action of macrophages activated by the infection and by the action of endotoxins absorbed from the gut or produced by the own parasite.

scholarly journals Evolution of sarcoma 180 (ascitic tumor) in mice infected with Schistosoma mansoni

1986 ◽  
Vol 19 (1) ◽  
pp. 39-42
Author(s):  
Fausto Edmundo Lima Pereira ◽  
Pedro Raso ◽  
Paulo Marcos Zech Coelho
Keyword(s):  
Weight Gain ◽  
Schistosoma Mansoni ◽  
Infected Group ◽  
Sarcoma 180 ◽  
Ascites Tumor ◽  
Tumor Inoculation ◽  
Transplantable Tumor ◽  
Tumoricidal Activity ◽  
Tumor Implantation ◽  
Ascites Formation

Mice infected with 60 cercariae of Schistosoma mansoni were more resistant to the sarcoma 180 ascites tumor. Tumor inoculation was performed 50 days after schistosoma infection and the animals were observed and weighed at 48 hours intervals for development and progression of malignancy. In infected mice the weight gain (ascites formation) started later and was shorter than in uninfected Controls. Also, the number of tumor cells into the peritoneal cavity 72h after tumor implantation was shorter in infected group than incontrols. This in creased resistance against a transplantable tumor probably is related to the effect of endotoxin on tumoricidal activity of macrophages activated by the infection. The immunodepression induced by Schistosoma mansoni infection enhances the proliferation of endogenous bacteria increasing the amount of endotoxin absorbed from the gut.

Changes in cytokine production and morphology of murine lymphoma NK/Ly cells in course of tumor development

2007 ◽  
Vol 2 (1) ◽  
pp. 71-86 ◽  
Author(s):  
Rostyslav Panchuk ◽  
Natalia Boiko ◽  
Maxim Lootsik ◽  
Rostyslav Stoika
Keyword(s):  
Tumor Growth ◽  
Tumor Cells ◽  
Ascitic Fluid ◽  
Tumor Development ◽  
Pcr Analysis ◽  
Vegf Mrna ◽  
Lymphoma Cells ◽  
Extracellular Medium ◽  
Enhanced Production ◽  
Ifn Γ

AbstractThe main goal of this study was to evaluate if specific cytokine expression in the NK/Ly lymphoma cells might be involved in development of intoxication in the tumor-bearing animals. RT-PCR analysis was used to study an expression of mRNA coding for IL-1α, IL-6, TNF-α, TNF-β and VEGF. ELISA was used to evaluate IL-6 and IFN-γ concentration in the ascitic fluid. Cytomorphological investigation of tumor cells was done after standard Romanovsky-Giemsa staining, and chromatin staining was performed with hematoxyline and neutral red. Lactate dehydrogenase and acid phosphatase release from tumor cells was estimated. It was revealed that the level of mRNA coding for VEGF and IL-6 was significant in the lymphoma cells. The level of VEGF mRNA was initially high and did not change during tumor progression, while the level of expression of IL6 mRNA was low at the initial stages of tumor growth and markedly increased (up to 5-fold) at the terminal stages. The obtained data on IL-6 mRNA expression were confirmed by ELISA, which showed more than 6-fold increase (from 90 to 570 pg/ml) in the IL-6 concentration in the ascitic fluid at late stages of NK/Ly tumor development. On the contrary to IL-6, concentration of IFN-γ in the ascitic fluid was very high at early stages of tumor development (1,000 pg/ml) and it markedly decreased (up to 30-fold, 30 pg/ml) at the terminal stages of tumor development. The high levels of IL-6 mRNA in tumor cells and IL-6 content in extracellular medium correlated with cell deterioration, as revealed by cytomorphologic study and the release of intracellular enzymes into extracellular medium. We suggest that an enhanced production and release of IL-6 by lymphoma cells can cause intoxication and exhaustion of the organism observed at terminal stages of tumor growth.

scholarly journals Evolution of sarcoma 180 in mice treated with hyperchlorinated water

1983 ◽  
Vol 78 (2) ◽  
pp. 209-214
Author(s):  
Fausto Edmundo Lima Pereira ◽  
Fabio Benezath Chaves
Keyword(s):  
Weight Gain ◽  
Tumor Cells ◽  
Peritoneal Cavity ◽  
Tap Water ◽  
Bactericidal Effect ◽  
Peritoneal Macrophages ◽  
Tumor Evolution ◽  
Sarcoma 180 ◽  
Tumor Implantation ◽  
Effect Of Chlorine

Mice treated with hyperchlorinated water (50 ppm of chlorine) and control mice, drinking tap water (1-3 ppm of chlorine) were inoculated with 2.5 x 10 [raised to the power of 6] sarcoma 180 cells, by intraperitoneal route. Tumor evolution was measured by enumeration of tumor cells in peritoneal cavity and by evaluation of weight gain at different time intervals after tumor implantation. In mice treated with excessive amounts of chlorine there was enhancement of tumor growth demonstrated by: (a) shorter incubation period and increased weight gain (ascites formation) after tumor implantation; (b) increased number of tumor cells in the peritoneal cavity 2, 3 and 4 days after tumor challenge. The number of peritoneal cells exsudated after tumor implantation was lower in mice treated with hyperchlorinated water than in controls. The tumor enhancement observed after excessive chlorine ingestion would be due to: (a) reduction of the number of peritoneal macrophages that migrate to the peritoneal cavity and (b) reduction of the tumoricidal capacity of peritonela macrophages induced by the direct effect of chlorine or by the reduction of the amount of endogenous endotoxins due to the bactericidal effect of chlorine.

scholarly journals Interleukin-11-expressing fibroblasts have a unique gene signature correlated with poor prognosis of colorectal cancer

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Takashi Nishina ◽  
Yutaka Deguchi ◽  
Daisuke Ohshima ◽  
Wakami Takeda ◽  
Masato Ohtsuka ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Tumor Cells ◽  
Human Cancer ◽  
Tumor Development ◽  
Gene Signature ◽  
Free Survival ◽  
Expression Of Genes ◽  
Reporter Mice ◽  
Interleukin 11

AbstractInterleukin (IL)-11 is a member of the IL-6 family of cytokines and is involved in multiple cellular responses, including tumor development. However, the origin and functions of IL-11-producing (IL-11+) cells are not fully understood. To characterize IL-11+ cells in vivo, we generate Il11 reporter mice. IL-11+ cells appear in the colon in murine tumor and acute colitis models. Il11ra1 or Il11 deletion attenuates the development of colitis-associated colorectal cancer. IL-11+ cells express fibroblast markers and genes associated with cell proliferation and tissue repair. IL-11 induces the activation of colonic fibroblasts and epithelial cells through phosphorylation of STAT3. Human cancer database analysis reveals that the expression of genes enriched in IL-11+ fibroblasts is elevated in human colorectal cancer and correlated with reduced recurrence-free survival. IL-11+ fibroblasts activate both tumor cells and fibroblasts via secretion of IL-11, thereby constituting a feed-forward loop between tumor cells and fibroblasts in the tumor microenvironment.

scholarly journals Early Detection and Dynamic Changes of Circulating Tumor Cells in Transgenic NeuN Transgenic (NTTg) Mice with Spontaneous Breast Tumor Development

Cancers ◽  
2021 ◽  
Vol 13 (13) ◽  
pp. 3294
Author(s):  
Wen-Sy Tsai ◽  
Tsung-Fu Hung ◽  
Jia-Yang Chen ◽  
Shu-Huan Huang ◽  
Ying-Chih Chang
Keyword(s):  
Tumor Cells ◽  
Circulating Tumor Cells ◽  
Breast Tumor ◽  
Early Stage ◽  
Tumor Development ◽  
P Value ◽  
Vascular Density ◽  
Dynamic Changes ◽  
Tumor Bearing ◽  
Development Methods

Background: This study used NeuN transgenic (NTTg) mice with spontaneous breast tumor development to evaluate the dynamic changes of circulating tumor cells (CTCs) prior to and during tumor development. Methods: In this longitudinal, clinically uninterrupted study, we collected 75 μL of peripheral blood at the age of 8, 12, 16, and 20 weeks in the first group of five mice, and at the age of 32 weeks, the time of tumor palpability, and one week after tumor palpability in the second group of four mice. Diluted blood samples were run through a modified mouse-CMx chip to isolate the CTCs. Results: The CTC counts of the first group of mice were low (1 ± 1.6) initially. The average CTC counts were 16 ± 9.5, 29.0 ± 18.2, and 70.0 ± 30.3 cells per 75 μL blood at the age of 32 weeks, the time of tumor palpability, and one week after tumor palpability, respectively. There was a significant positive correlation between an increase in CTC levels and tumor vascular density (p-value < 0.01). This correlation was stronger than that between CTC levels and tumor size (p-value = 0.076). The captured CTCs were implanted into a non-tumor-bearing NTTg mouse for xenografting, confirming their viability and tumorigenesis. Conclusion: Serial CTCs during an early stage of tumor progression were quantified and found to be positively correlated with the later tumor vascular density and size. Furthermore, the successful generation of CTC-derived xenografts indicates the tumorigenicity of this early onset CTC population.

scholarly journals Phosphorylation of Ribosomal Proteins in Sarcoma 180 Tumor Cells

1972 ◽  
Vol 247 (17) ◽  
pp. 5345-5350
Author(s):  
Lawrence Bitte ◽  
David Kabat
Keyword(s):  
Tumor Cells ◽  
Ribosomal Proteins ◽  
Sarcoma 180

Stem-like tumor cells and proinflammatory cytokines in the ascitic fluid of ovarian cancer patients

2021 ◽  
Vol 66 (5) ◽  
pp. 297-303
Author(s):  
S. O. Gening ◽  
T. V. Abakumova ◽  
I. I. Antoneeva ◽  
A. A. Rizvanov ◽  
T. P. Gening ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Blood Serum ◽  
Tumor Cells ◽  
Ascitic Fluid ◽  
Early Stage ◽  
Abdominal Cavity ◽  
Disease Stage ◽  
Cell Populations ◽  
Benign Ovarian Tumors ◽  
Number Of Cells

Ovarian cancer (OC) is able to develop implantation metastases in the abdominal cavity. Ascites is potentially useful for evaluating cancer features. The aim of the study was to assess the content of stem-like tumor cells and inflammatory mediators in ascites of OC. The prospective study included 11 patients with primary OC having ascites, 8 patients with benign ovarian tumors having ascites and 22 healthy women. In ascitic fluid obtained by laparocentesis, the populations of tumor stem-like cells were determined on a Cytoflex S` flow cytometer (Beckman Coulter, USA) and CytExpert Software using monoclonal antibodies to CD45, CD44 and CD133. The cytokine profiles of ascitic fluid and blood serum (IL-1β, IL-18, IL-4, IL-10 and VEGF) were assessed by ELISA. Stem-like cells were found in all samples. 5 cell populations were evaluated. The number of cells expressing both markers: CD44 + and CD133+, was the lowest. The highest, about 32%, was the number of CD44+ cells. The number of cells CD45-CD44+CD133- in ascites strongly positively correlated with the content of IL-10 in ascites, and the numbers of CD45-CD133+ and CD45-CD44-CD133+ - with the level of VEGF in blood serum. No correlations were found between the numbers of stem-like cells and the disease stage or the level of CA125 in blood. The combination of IL-4 and IL-10 in ascites had the greatest significance in predicting the disease stage. These results suggest a relationship between the levels of VEGF, IL-10, and cancer stem cells in the OC ascites. Stem-like cells in OC ascites are heterogeneous and are present even at an early stage of the disease. It seems promising to study cell populations and cytokine profile of ascites together, to assess the biomarker potential of their combination.

scholarly journals Cellular context-dependent consequences of Apc mutations on gene regulation and cellular behavior

2017 ◽  
Vol 114 (4) ◽  
pp. 758-763 ◽  
Author(s):  
Kyoichi Hashimoto ◽  
Yosuke Yamada ◽  
Katsunori Semi ◽  
Masaki Yagi ◽  
Akito Tanaka ◽  
...  
Keyword(s):  
Gene Regulation ◽  
Tumor Cells ◽  
Critical Role ◽  
Tumor Development ◽  
Cell Lineage ◽  
Genetic Rescue ◽  
Cellular Behavior ◽  
Cellular Context ◽  
Context Dependent

The spectrum of genetic mutations differs among cancers in different organs, implying a cellular context-dependent effect for genetic aberrations. However, the extent to which the cellular context affects the consequences of oncogenic mutations remains to be fully elucidated. We reprogrammed colon tumor cells in an ApcMin/+ (adenomatous polyposis coli) mouse model, in which the loss of the Apc gene plays a critical role in tumor development and subsequently, established reprogrammed tumor cells (RTCs) that exhibit pluripotent stem cell (PSC)-like signatures of gene expression. We show that the majority of the genes in RTCs that were affected by Apc mutations did not overlap with the genes affected in the intestine. RTCs lacked pluripotency but exhibited an increased expression of Cdx2 and a differentiation propensity that was biased toward the trophectoderm cell lineage. Genetic rescue of the mutated Apc allele conferred pluripotency on RTCs and enabled their differentiation into various cell types in vivo. The redisruption of Apc in RTC-derived differentiated cells resulted in neoplastic growth that was exclusive to the intestine, but the majority of the intestinal lesions remained as pretumoral microadenomas. These results highlight the significant influence of cellular context on gene regulation, cellular plasticity, and cellular behavior in response to the loss of the Apc function. Our results also imply that the transition from microadenomas to macroscopic tumors is reprogrammable, which underscores the importance of epigenetic regulation on tumor promotion.

On hormonal control of tumor growth

1934 ◽  
Vol 30 (5) ◽  
pp. 466-467
Author(s):  
М. Reiss ◽  
U. Druckrey ◽  
А. Hochwald
Keyword(s):  
Growth Hormone ◽  
Tumor Growth ◽  
Tumor Development ◽  
Hormonal Control ◽  
Tumor Inoculation ◽  
Hormone Injection

In rats in which Jensen's sarcoma usually grows rapidly, pituitaryectomy performed at least 3 weeks before tumor inoculation causes tumor growth to stop and even develop backwards. The fact that growth hormone injection again causes the tumor to stop growing further emphasizes the role of growth hormone in tumor development.

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