Elevated Serum Levels of Vascular Endothelial Growth Factor Are Associated With Tumor-Associated Macrophages in Primary Breast Cancer

Vicioso, Luís; González, Francisco; Alvarez, Martina; Ribelles, Nuria; Molina, Manuel; Márquez, Antonia; Pérez, L.; Matilla, Alfredo; Alba, Emilio

doi:10.1309/0864af2u3lgpcf3j

Cited by 18 publications

(12 citation statements)

References 33 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Similar to patients with hematological malignancies (31), the tumor-bearing mice in our study had significantly higher serum VEGF-A levels than their healthy counterparts. Vicioso et al demonstrated a positive correlation between the serum VEGF levels and tumor size in primary breast cancer (32). However, the serum VEGF165 levels did not correlate with tumor size in HCC (33).…”

Section: Discussionmentioning

confidence: 99%

Vascular endothelial growth factor-A and changes in a tumor-bearing mouse model with Lewis lung cancer

et al. 2011

View full text Add to dashboard Cite

Abstract. Vascular endothelial growth factor-A (VEGF-A)affects tumor growth and metastasis through stimulation of angiogenesis. The purpose of this study was to describe features of Lewis lung cancer (LLC) in mice and compare the serum VEGF-A levels with those of normal control mice. Two groups of mice were compared: one was subcutaneously injected with LLC cells (n=16) and the other served as the normal control (n=6). The serum VEGF-A levels were measured by ELISA prior to inoculation, and at 7, 21 and 35 days post-inoculation. The tumor weight and the metastatic condition were evaluated on day 35. Changes in body weight and serum VEGF-A concentration over a period of time were compared between the groups using generalized estimating equations. The relationship between the primary tumor and the metastatic condition was analyzed using the Spearman's rank correlation test. The survival rate was 56.3% on day 35 post-tumor inoculation. No difference was found between the groups with regard to gastrocnemius muscle weight on day 35 post-inoculation [0.1315±0.0066 g vs. 0.1308±0.0069 g (normal control)]. In tumor-bearing mice, the weight gain at sacrifice was less (0.24±0.45 vs. 1.93±0.47 g, P= 0.01), the final mean tumor volume and weight were 4264.69±1038.32 mm 3 and 3.70±0.83 g, the number of nodules in the lungs and livers was 6.33 (range 0-20) and 2.22 (range 0-11), respectively, and the serum VEGF-A levels were significantly higher than those of control mice. In conclusion, lower body weight gain, metastasis in the liver and lungs, and elevated VEGF-A levels are features of LLC in mice.

show abstract

Section: Discussionmentioning

confidence: 99%

Vascular endothelial growth factor-A and changes in a tumor-bearing mouse model with Lewis lung cancer

et al. 2011

View full text Add to dashboard Cite

show abstract

“…As a major component of the leukocyte infiltrate of many solid tumors, TAMs are found to play a critical role in carcinogenesis, tumor growth, invasion, and metastasis, and induce tumor angiogenesis and lymphangiogenesis in different types of cancers such as non-small cell lung cancer (NSCLC) , breast cancer [Vicioso et al, 2006], malignant melanoma [Varney et al, 2005], and colorectal cancer [Bailey et al, 2007]. The effects of TAMs are related to a number of secreted proinflammatory cytokines, growth factors, chemotatic factors, and proteinases.…”

Section: Discussionmentioning

confidence: 99%

Alternatively activated RAW264.7 macrophages enhance tumor lymphangiogenesis in mouse lung adenocarcinoma

Zhang

Wang

Gao

et al. 2009

J of Cellular Biochemistry

View full text Add to dashboard Cite

Tumor-associated macrophages (TAMs) have been implicated in promoting tumor progression and invasion. The onset and maintenance of tumor angiogenesis and lymphangiogenesis also seem to be partly driven by a group of polarized alternatively activated macrophages (aaMphi) in lung adenocarcinoma. Here, the aaMphi and classically activated macrophages (caMphi) were obtained using RAW264.7 cells via IL-4 and IFN-gamma + LPS treatment, respectively. Co-inoculation of aaMphi with Lewis lung carcinoma (LLC) cells promoted tumor growth, increased lymph node metastasis, and reduced the survival in C57BL/6 mice bearing LLC. Furthermore, the effects of the activated macrophages on the lymphangiogenesis-related properties of lymphatic endothelial cells (LECs) were investigated in vitro. When LECs were cultured in macrophages conditioned medium or in a co-culture system of macrophages and LECs, aaMphi significantly promoted proliferation, migration, and tube-like formation of LECs. We identified high VEGF-C expression in aaMphi and low expression in caMphi as well as unactivated macrophages by ELISA and Western blotting. In LECs, co-culture with aaMphi resulted in a significant increase of mRNA levels of specific lymphatic marker VEGF receptor-3 and the homeobox gene Prox-1, as well as lymphangiogenic factor VEGF-C rather than VEGF-D by quantitative RT-PCR. Furthermore, enhanced LECs migration and capillary formation by co-culture with aaMphi were significantly inhibited by rVEGF receptor-3/Fc chimera. In conclusion, these data show that aaMphi play a critical role in tumor-induced lymphangiogenesis through up-regulating VEGF-C and increasing lymphangiogenesis-related behavior of LECs, which may contribute to lymphatic invasion in lung adenocarcinoma.

show abstract

“…During breast cancer development the TAMs enhance cancer metastasis and promote resistance to chemotherapeutic agents [Gabrilovich et al, ; De Palma and Lewis, ]. Several evidence indicated that the level of high circulating VEGF was depending on the number of TAMs infiltration in primary tumor and p53 that relationship enhanced the angiogenesis in breast cancer [Vicioso et al, ]. However, the metastatic effect of VEGF and macrophage in tumor further need to the investigation.…”

Section: Tumor‐associated Macrophagesmentioning

confidence: 99%

Macrophage Polarization: Anti-Cancer Strategies to Target Tumor-Associated Macrophage in Breast Cancer

et al. 2017

View full text Add to dashboard Cite

Tumor-associated macrophages (TAMs) are the most abundant inflammatory cells and orchestrate different stages of breast cancer development. TAMs participate in the tumor angiogenesis, matrix remodeling, invasion, immunosuppression, metastasis, and chemoresistance in breast cancer. Several clinical studies indicate the association between the high influx of TAMs in tumor with poor prognosis in hepatocellular, ovarian, cervical, and breast cancer. Previously developed hypotheses have proposed that TAMs participate in antitumor responses of the body, while recently many clinical and experimental studies have revealed that TAMs in tumor microenvironment predominantly resemble with M2-like polarized macrophages and produce a high amount of anti-inflammatory factors which are directly responsible for the development of tumor. Various studies have shown that TAMs in tumor either enhance or antagonize the anti-tumor efficacy of cytotoxic agents, antibodies-targeting cancer cells, and therapeutic agents depending on the nature of treatment. Thereby, multiple roles of TAMs suggests that it is very important to develop novel therapeutic strategies to target TAMs in breast tumor. In this review, we have discussed the functional role of TAMs in breast cancer and summarized available recent advances potential therapeutic strategies that effectively target to TAMs cells. J. Cell. Biochem. 118: 2484-2501, 2017. © 2017 Wiley Periodicals, Inc.

show abstract

Elevated Serum Levels of Vascular Endothelial Growth Factor Are Associated With Tumor-Associated Macrophages in Primary Breast Cancer

Cited by 18 publications

References 33 publications

Vascular endothelial growth factor-A and changes in a tumor-bearing mouse model with Lewis lung cancer

Vascular endothelial growth factor-A and changes in a tumor-bearing mouse model with Lewis lung cancer

Alternatively activated RAW264.7 macrophages enhance tumor lymphangiogenesis in mouse lung adenocarcinoma

Macrophage Polarization: Anti-Cancer Strategies to Target Tumor-Associated Macrophage in Breast Cancer

Contact Info

Product

Resources

About