The effect of surgery and pre-treatment or posttreatment adjuvant chemotherapy on primary tumor growth in an animal model

The goal of this study was to mechanistically analyze the effects of pre-treatment or post-treatment melatonin on the metastatic spread in a mice model. Consequently, the effects on the tumor growth, angiogenesis and metastasis were evaluated with immunohistochemical and western blot analysis. 8–10 weeks-old female BALB/c mice (n = 60, 10/group) were used. Liver metastatic cells (4TLM) from 4T1 murine breast carcinoma were previously isolated. Melatonin was administrated either before or after the injection of 4TLM cells into the mammary pad. Tumor and vehicle (%6 ethanol) injections were given to vehicle groups. Tumor group consisted of the mice injected with only 4TLM cells injected to tumor group and no intervention to control group. Necropsies were performed 27 days after injection of 4TLM. Primary tumors and metastatic tissues were removed. Furthermore, changes in lung and liver metastasis and primary tumor growth and angiogenesis were evaluated. In our study neutrophil levels were noted to be increased in peripheral blood of the tumor-bearing mice. Melatonin exerted inhibitory effects on the 4TLM-induced leukocytosis. Melatonin significantly decreased lung and liver metastasis, primary tumor growth and angiogenesis. The results demonstrated that melatonin might have a therapeutic role through reducing systemic inflammatory responses, metastasis, tumor growth and angiogenesis.

Download Full-text

Cancer-associated fibroblasts stimulate primary tumor growth and metastatic spread in an orthotopic prostate cancer xenograft model

Scientific Reports ◽

10.1038/s41598-020-69424-x ◽

2020 ◽

Vol 10 (1) ◽

Author(s):

Johannes Linxweiler ◽

Turkan Hajili ◽

Christina Körbel ◽

Carolina Berchem ◽

Philip Zeuschner ◽

...

Keyword(s):

Prostate Cancer ◽

Tumor Growth ◽

Primary Tumor ◽

Xenograft Model ◽

Metastatic Spread ◽

Cancer Associated Fibroblasts ◽

Primary Tumor Growth

Download Full-text

Variability and Discontinuity of the Pathognomonic Systemic Effects Caused by Walker 256 Tumor Progression in Rats

Tumori Journal ◽

10.1177/030089169508100513 ◽

1995 ◽

Vol 81 (5) ◽

pp. 370-377 ◽

Cited By ~ 11

Author(s):

Ovidio Rettori ◽

Ana Neuza Vieira-Matos ◽

Quivo S. Tahin

Keyword(s):

Tumor Growth ◽

Primary Tumor ◽

Marked Reduction ◽

Prognostic Indicator ◽

Individual Variability ◽

Systemic Effects ◽

Primary Tumor Growth ◽

Multifocal Tumor ◽

Walker 256 ◽

Walker 256 Tumor

Cancer pathognomonic systemic effects (PSE) have high individual variability. For this reason present data were collected daily and synchronized considering four main points: inoculation day, onset of PSE, aggravation and death. The subclinical period free of PSE ranged between 15.7±2.2 days, the clinical period was less variable, 8.9±0.5 days, divided in a moderate and a grave phase of nearly the same length. PSE involved disturbances of fundamental homeostatic regulations: appetite, sodium, water, immune, etc. PSE triggering correlated highly with survival (r2=0.95, P<0.01), but poorly with primary tumor growth, and it was anticipated by metastases from 20.5±2.6 to 10.6±1.1 days (P<0.01). After multifocal simultaneous inoculations, PSE triggering was anticipated to 4.2±0.2 days (marked reduction of individual variability), in the presence of small total-tumor masses, absence of macroscopic metastases, and without changes in the following clinical period features. PSE triggering seems to be a major prognostic indicator probably related to multifocal tumor growth.

Download Full-text