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Chitinase 3-like 1 as breast cancer metastasis biomarker for differential tumor progression in the intraductal versus the fat pad preclinical model

Jonas Steenbrugge (UGent) , Koen Breyne (UGent) , Sofie Denies (UGent) , Melissa Dekimpe, Kristel Demeyere (UGent) , Olivier De Wever (UGent) , Niek Sanders (UGent) and Evelyne Meyer (UGent)
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Organization
Abstract
Breast cancer starts as a primary tumor that typically spreads to the axillary lymph nodes and other organs. This process is classically studied in mice by injecting mammary tumor cells in the fat pad surrounding the mammary gland. We previously compared this classical fat pad model with an innovative intraductal mouse model, in which 4.6x10^4 triple-negative, luciferase- and E-cadherin-positive 4T1 mouse mammary tumor cells were orthotopically injected through the teat canal into the mammary gland of lactating immunocompetent mice. Primary tumor development rate was found to be slower in the intraductal model, yet similar metastasis to the liver and lungs was observed. In order to further evaluate this difference in tumor progression, we focused on the pro-inflammatory mediator YKL-40/chitinase 3-like 1 (CHI3L1). This enzymatically inactive glycoprotein is upregulated in a variety of solid tumors and plays a role both in the inflammatory process at the primary tumor site and in the systemical dissemination of tumor cells. Elevated serum levels of CHI3L1 have also been associated with poor prognosis in breast cancer patients. We found that CHI3L1 levels increased progressively both in tumor lysates and in serum, with a slower increase in the intraductal than in the fat pad model. In the mammary gland tissue a decrease of CHI3L1 levels over time was seen in both models. These results corroborate our previously observed slower onset of tumor growth and subsequent metastasis in the intraductal model and identify CHI3L1 as an interesting biomarker to evaluate tumor progression in preclinical breast cancer models.

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MLA
Steenbrugge, Jonas, Koen Breyne, Sofie Denies, et al. “Chitinase 3-like 1 as Breast Cancer Metastasis Biomarker for Differential Tumor Progression in the Intraductal Versus the Fat Pad Preclinical Model.” OncoPoint, 4th Research Seminar, Abstracts. 2016. Print.
APA
Steenbrugge, J., Breyne, K., Denies, S., Dekimpe, M., Demeyere, K., De Wever, O., Sanders, N., et al. (2016). Chitinase 3-like 1 as breast cancer metastasis biomarker for differential tumor progression in the intraductal versus the fat pad preclinical model. OncoPoint, 4th Research seminar, Abstracts. Presented at the 4th OncoPoint research seminar.
Chicago author-date
Steenbrugge, Jonas, Koen Breyne, Sofie Denies, Melissa Dekimpe, Kristel Demeyere, Olivier De Wever, Niek Sanders, and Evelyne Meyer. 2016. “Chitinase 3-like 1 as Breast Cancer Metastasis Biomarker for Differential Tumor Progression in the Intraductal Versus the Fat Pad Preclinical Model.” In OncoPoint, 4th Research Seminar, Abstracts.
Chicago author-date (all authors)
Steenbrugge, Jonas, Koen Breyne, Sofie Denies, Melissa Dekimpe, Kristel Demeyere, Olivier De Wever, Niek Sanders, and Evelyne Meyer. 2016. “Chitinase 3-like 1 as Breast Cancer Metastasis Biomarker for Differential Tumor Progression in the Intraductal Versus the Fat Pad Preclinical Model.” In OncoPoint, 4th Research Seminar, Abstracts.
Vancouver
1.
Steenbrugge J, Breyne K, Denies S, Dekimpe M, Demeyere K, De Wever O, et al. Chitinase 3-like 1 as breast cancer metastasis biomarker for differential tumor progression in the intraductal versus the fat pad preclinical model. OncoPoint, 4th Research seminar, Abstracts. 2016.
IEEE
[1]
J. Steenbrugge et al., “Chitinase 3-like 1 as breast cancer metastasis biomarker for differential tumor progression in the intraductal versus the fat pad preclinical model,” in OncoPoint, 4th Research seminar, Abstracts, Ghent, Belgium, 2016.
@inproceedings{8101089,
  abstract     = {{Breast cancer starts as a primary tumor that typically spreads to the axillary lymph nodes and other organs. This process is classically studied in mice by injecting mammary tumor cells in the fat pad surrounding the mammary gland. We previously compared this classical fat pad model with an innovative intraductal mouse model, in which 4.6x10^4 triple-negative, luciferase- and E-cadherin-positive 4T1 mouse mammary tumor cells were orthotopically injected through the teat canal into the mammary gland of lactating immunocompetent mice. Primary tumor development rate was found to be slower in the intraductal model, yet similar metastasis to the liver and lungs was observed. In order to further evaluate this difference in tumor progression, we focused on the pro-inflammatory mediator YKL-40/chitinase 3-like 1 (CHI3L1). This enzymatically inactive glycoprotein is upregulated in a variety of solid tumors and plays a role both in the inflammatory process at the primary tumor site and in the systemical dissemination of tumor cells. Elevated serum levels of CHI3L1 have also been associated with poor prognosis in breast cancer patients. We found that CHI3L1 levels increased progressively both in tumor lysates and in serum, with a slower increase in the intraductal than in the fat pad model. In the mammary gland tissue a decrease of CHI3L1 levels over time was seen in both models. These results corroborate our previously observed slower onset of tumor growth and subsequent metastasis in the intraductal model and identify CHI3L1 as an interesting biomarker to evaluate tumor progression in preclinical breast cancer models.}},
  author       = {{Steenbrugge, Jonas and Breyne, Koen and Denies, Sofie and Dekimpe, Melissa and Demeyere, Kristel and De Wever, Olivier and Sanders, Niek and Meyer, Evelyne}},
  booktitle    = {{OncoPoint, 4th Research seminar, Abstracts}},
  language     = {{eng}},
  location     = {{Ghent, Belgium}},
  title        = {{Chitinase 3-like 1 as breast cancer metastasis biomarker for differential tumor progression in the intraductal versus the fat pad preclinical model}},
  year         = {{2016}},
}