I read with great interest the recent article by Chan et al. Citation[1]. Interestingly, recent data suggests that vasohibin-1 (VASH1) may be involved in the development and progression of a number of systemic malignancies besides renal cell carcinomas.
For instance, the VASH1 positive ratio is a measure of neovascularization in breast tissue. In certain breast cancers such as ductal carcinoma in situ, VASH1 levels are a strong predictor of accentuated aggressive behaviors and microvascular invasion Citation[1]. The response to adjuvant chemotherapy such as tamoxifen is significantly influenced by the VASH1 positive ratio Citation[2]. Higher levels of VASH1 are associated with higher histological grades. Hence, VASH1 can be used for predicting treatment outcomes in breast cancer patients. In fact, Tamaki et al. have shown that a close association exists between VASH1 and ‘disease free survival' and ‘overall survival' in breast carcinoma patients Citation[3].
Similarly, a poor clinical outcome after curative surgery is seen in hepatocellular carcinomas that exhibit increased expression of VASH1 Citation[4]. This is because of the accentuated angiogenesis as a result of VASH1 upregulation. A close relationship exists between microvessel density and VASH1 levels. In fact, Wang et al. in a recent study have shown that upregulated VASH1 levels are an independent prognostic indicator of ‘shorter disease-free survival' and ‘overall survival' in hepatocellular carcinomas following surgery. Similarly, gastric carcinomas express VASH1. The expression of VASH1 in gastric carcinomas is significantly influenced by hypoxia.
The above examples clearly illustrate the significant role of VASH1 in systemic carcinogenesis and the need for further studies to fully evaluate its role in the development of other systemic tumors.
Declaration of interest
H Sasano has received the educational grant from Pfizer Oncology, Japan. The authors declare no other conflicts of interest or any other support in the completion of their original research paper entitled ‘Effects of estrogen depletion on angiogenesis in estrogen-receptor-positive breast carcinoma – an immunohistochemical study of vasohibin-1 and CD31 with correlation to pathobiological response of the patients in neoadjuvant aromatase inhibitor therapy' published in the journal.
Declaration of interest
The author states no conflict of interest and has received no payment in preparation of this manuscript.
Bibliography
- Chan MS, Wang L, Chanplakorn N, Effects of estrogen depletion on angiogenesis in estrogen-receptor-positive breast carcinoma--an immunohistochemical study of vasohibin-1 and CD31 with correlation to pathobiological response of the patients in neoadjuvant aromatase inhibitor therapy. Expert Opin Ther Targets 2012;16(Suppl 1):S69-78
- Tamaki K, Sasano H, Maruo Y, Vasohibin-1 as a potential predictor of aggressive behavior of ductal carcinoma in situ of the breast. Cancer Sci 2010;101:1051-8
- Tamaki K, Moriya T, Sato Y, Vasohibin-1 in human breast carcinoma: a potential negative feedback regulator of angiogenesis. Cancer Sci 2009;100:88-94
- Wang Q, Tian X, Zhang C, Wang Q. Upregulation of vasohibin-1 expression with angiogenesis and poor prognosis of hepatocellular carcinoma after curative surgery. Med Oncol 2011. In press
Author's response
Dear Dr Kapoor,
As informed by the Commissioning Editor for Expert Opinion on Therapeutic Targets on October 10, 2012, you have sent a letter commenting on our recent publication of our original research entitled ‘Effects of estrogen depletion on angiogenesis in estrogen-receptor-positive breast carcinoma – an immunohistochemical study of vasohibin-1 and CD31 with correlation to pathobiological response of the patients in neoadjuvant aromatase inhibitor therapy' that was published in Expert Opinion on Therapeutic Targets in 2012; Volume 16 Supplement 1:S69–S78.
On behalf of Professor Sasano, my supervisor in the above-stated original research and our team of co-authors, we very much appreciate your generous comments in our work and will continue to work in this particular field of vasohibin-1 from the standpoint of pathology.
Once again thank you for your comments and we wish you all the best in your work and research.