scholarly journals Maternal metabolic changes with dietary intake of blueberry during pregnancy and lactation predispose adult progeny to lower mammary tumor growth rate

2013 ◽  
Vol 27 (S1) ◽  
Author(s):  
Maria Theresa E Montales ◽  
Stepan Melnyk ◽  
Ronald L Prior ◽  
Rosalia CM Simmen
Keyword(s):  
Growth Rate ◽  
Tumor Growth ◽  
Dietary Intake ◽  
Mammary Tumor ◽  
Metabolic Changes ◽  
Tumor Growth Rate ◽  
Mammary Tumor Growth ◽  
Pregnancy And Lactation

Factors that Affect Metastasis in Virus-Induced Mouse Mammary Tumors

1984 ◽  
Vol 70 (2) ◽  
pp. 131-136
Author(s):  
Fulvio Basolo ◽  
Gabriella Fontanini ◽  
Francesco Squartini
Keyword(s):  
Growth Rate ◽  
Tumor Growth ◽  
Mammary Tumor ◽  
Tumor Size ◽  
Tumor Metastasis ◽  
Lung Metastases ◽  
High Growth ◽  
High Growth Rate ◽  
Tumor Growth Rate ◽  
Tumor Virus

Two hundred and forty-one mammary tumor-bearing breeding female mice of the BALB/cf C3H and BALB/cfRIII strains, carrying milk-transmitted murine mammary tumor virus (MuMTV) of C3H and RIII origin, respectively, were studied to evaluate the factors that affect tumor metastasis. Only lung metastases were considered and the following factors taken in account: MuMTV inducing variant (C3H, RIII), number of deliveries, tumor histo-type, number of tumors per mouse, clinical duration of tumors, tumor size, and tumor growth rate. Only the number of deliveries, the tumor size and the number of tumors per mouse were found to significantly influence the rate of metastasis. The tumor growth rate affects concurrently with tumor size the metastatic process. In fact, the larger the tumor the higher the tumor growth rate. This direct relationship is significant (P < 0.01) and, in case of lung metastases at autopsy, there was a prevalence of large tumors (> 2 cm) and high growth rate (> 0.3 mm/day). The discordance of these data with those concerning mammary tumor metastasis in virgin females of the same two strains, the enhancing effect of pregnancies on metastatic spread of tumors, and the significance of results for the understanding of the general mechanisms of tumor metastasis are discussed.

scholarly journals Nutritional Folate Status Influences the Efficacy and Toxicity of Chemotherapy in Rats

Blood ◽  
1998 ◽  
Vol 92 (7) ◽  
pp. 2471-2476 ◽  
Author(s):  
Richard F. Branda ◽  
Elizabeth Nigels ◽  
Amy R. Lafayette ◽  
Miles Hacker
Keyword(s):  
Growth Rate ◽  
Tumor Growth ◽  
Folate Deficiency ◽  
Tumor Growth Rate ◽  
Fischer 344 Rats ◽  
Dietary Folate ◽  
Folate Status ◽  
Fischer 344 ◽  
Mammary Tumor Growth ◽  
Rat Mammary Tumor

Abstract The effect of folate status on the efficacy and toxicity of chemotherapy was investigated in weanling Fischer 344 rats maintained on diets of varying folate content or supplemented with daily injections of folic acid, 50 mg/kg, for 6 to 7 weeks. MADB106 rat mammary tumor growth rate was the same in folate replete and supplemented rats, but retarded in the low folate groups. The tumor growth inhibitions in low folate, replete and high folate rats treated with cyclophosphamide were: 53%, 98%, and 97% (P = .048); with 5-fluorouracil (5-FU): 46%, 49%, and 66%; and with doxorubicin: 25%, 55%, and 61%. Significant differences in survival were observed for cyclophosphamide (P = .0084) and 5-FU (P = .025) related to dietary folate content. Thus, folate deficiency impedes tumor growth rate, but supplementation does not accelerate it in folate replete animals. Correction of folate deficiency approximately doubles the efficacy of cyclophosphamide in rats with much less host toxicity. Folate repletion improves survival in 5-FU–treated animals. These studies indicate that nutritional folate status has an important influence on the efficacy and toxicity of some commonly used cancer chemotherapeutic drugs.

scholarly journals Nutritional Folate Status Influences the Efficacy and Toxicity of Chemotherapy in Rats

Blood ◽  
1998 ◽  
Vol 92 (7) ◽  
pp. 2471-2476
Author(s):  
Richard F. Branda ◽  
Elizabeth Nigels ◽  
Amy R. Lafayette ◽  
Miles Hacker
Keyword(s):  
Growth Rate ◽  
Tumor Growth ◽  
Folate Deficiency ◽  
Tumor Growth Rate ◽  
Fischer 344 Rats ◽  
Dietary Folate ◽  
Folate Status ◽  
Fischer 344 ◽  
Mammary Tumor Growth ◽  
Rat Mammary Tumor

The effect of folate status on the efficacy and toxicity of chemotherapy was investigated in weanling Fischer 344 rats maintained on diets of varying folate content or supplemented with daily injections of folic acid, 50 mg/kg, for 6 to 7 weeks. MADB106 rat mammary tumor growth rate was the same in folate replete and supplemented rats, but retarded in the low folate groups. The tumor growth inhibitions in low folate, replete and high folate rats treated with cyclophosphamide were: 53%, 98%, and 97% (P = .048); with 5-fluorouracil (5-FU): 46%, 49%, and 66%; and with doxorubicin: 25%, 55%, and 61%. Significant differences in survival were observed for cyclophosphamide (P = .0084) and 5-FU (P = .025) related to dietary folate content. Thus, folate deficiency impedes tumor growth rate, but supplementation does not accelerate it in folate replete animals. Correction of folate deficiency approximately doubles the efficacy of cyclophosphamide in rats with much less host toxicity. Folate repletion improves survival in 5-FU–treated animals. These studies indicate that nutritional folate status has an important influence on the efficacy and toxicity of some commonly used cancer chemotherapeutic drugs.

scholarly journals Tumor growth characteristics of the Walker 256 AR tumor, a regressive variant of the rat Walker 256 A tumor

2010 ◽  
Vol 53 (5) ◽  
pp. 1101-1108 ◽  
Author(s):  
Fernando Guimarães ◽  
Alessandra Soares Schanoski ◽  
Tereza Cristina Samico Cavalcanti ◽  
Priscila Bianchi Juliano ◽  
Ana Neuza Viera-Matos ◽  
...  
Keyword(s):  
Growth Rate ◽  
Tumor Growth ◽  
Wistar Rats ◽  
Tumor Regression ◽  
Growth Characteristics ◽  
Tumor Growth Rate ◽  
Continuous Growth ◽  
Tumor Bearing ◽  
Walker 256 ◽  
Complete Tumor

The present study aimed at characterizing the subcutaneous development of the Walker 256 (W256) AR tumor, a regressive variant of the rat W256 A tumor. Wistar rats were injected subcutaneously with 4x10(6) W256 A or W256 AR tumor cells. The development of tumors was evaluated daily by percutaneous measurements. None of the W256 A tumors (n=20) regressed, but 62% of the W256 AR tumor-bearing rats (n=21) underwent complete tumor regression within 35 days. Continuous growth of AR tumors was characterized by an increase of the tumor growth rate from day 12, which reached values above 1.0 g/day, and were significantly higher (p<0.05) than those of the regressive AR tumors. Immunosuppression by irradiation before subcutaneous injection of AR cells completely abrogated tumor regression and was associated with severe metastatic dissemination. Daily evaluation of the tumor growth rate enabled the discrimination, in advance, between continuously growing tumors and those that regressed later on.

Targeted Treatment of Experimental Spinal Cord Glioma With Dual Gene-Engineered Human Neural Stem Cells

Neurosurgery ◽  
2015 ◽  
Vol 79 (3) ◽  
pp. 481-491 ◽  
Author(s):  
Alexander E. Ropper ◽  
Xiang Zeng ◽  
Hariprakash Haragopal ◽  
Jamie E. Anderson ◽  
Zaid Aljuboori ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Stem Cells ◽  
Growth Rate ◽  
Neural Stem Cells ◽  
Tumor Growth ◽  
Rat Model ◽  
Weight Bearing ◽  
Tumor Growth Rate ◽  
Intramedullary Spinal Cord ◽  
Human Neural Stem Cells

Abstract BACKGROUND There are currently no satisfactory treatments or experimental models showing autonomic dysfunction for intramedullary spinal cord gliomas (ISCG). OBJECTIVE To develop a rat model of ISCG and investigate whether genetically engineered human neural stem cells (F3.hNSCs) could be developed into effective therapies for ISCG. METHODS Immunodeficient/Rowett Nude rats received C6 implantation of G55 human glioblastoma cells (10K/each). F3.hNSCs engineered to express either cytosine deaminase gene only (i.e., F3.CD) or dual genes of CD and thymidine kinase (i.e., F3.CD-TK) converted benign 5-fluorocytosine and ganciclovir into oncolytic 5-fluorouracil and ganciclovir-triphosphate, respectively. ISCG rats received injection of F3.CD-TK, F3.CD, or F3.CD-TK debris near the tumor epicenter 7 days after G55 seeding, followed with 5-FC (500 mg/kg/5 mL) and ganciclovir administrations (25 mg/kg/1 mL/day × 5/each repeat, intraperitoneal injection). Per humane standards for animals, loss of weight-bearing stepping in the hindlimb was used to determine post-tumor survival. Also evaluated were autonomic functions and tumor growth rate in vivo. RESULTS ISCG rats with F3.CD-TK treatment survived significantly longer (37.5 ± 4.78 days) than those receiving F3.CD (21.5 ± 1.75 days) or F3.CD-TK debris (19.3 ± 0.85 days; n = 4/group; P &lt;.05, median rank test), with significantly improved autonomic function and reduced tumor growth rate. F3.DC-TK cells migrated diffusively into ISCG clusters to mediate oncolytic effect. CONCLUSION Dual gene-engineered human neural stem cell regimen markedly prolonged survival in a rat model that emulates somatomotor and autonomic dysfunctions of human cervical ISCG. F3.CD-TK may provide a novel approach to treating clinical ISCG.

Sign in / Sign up

Export Citation Format

Share Document