Abstract
4/2012
vol. 63
Letter to the editor
Antitumor actions of human mast cells
Pol J Pathol 2012; 63: 292
Online publish date: 2013/01/24
Dear Editor,
We have read the article titled “Mast cells and cancer: enemies or allies?” by Dyduch et al. with a great interest [1]. Because of this opportunity, we want to share our in vitro experience on the anti-tumor actions of human mast cell (MC) through direct cell-mediated cytotoxicity [2]. We have also recently gotten in vivo experience on the role of tryptase-/chymase-positive MCs by working their role in the benign and malignant uterus (endometrial and cervix) carcinomas [3].
Ambiguous mounting evidence also indicates that MCs accumulate around tumors and could either promote or inhibit tumor growth probably depending on environmental conditions. First in vivo observations in the 1950s suggested their possible role as anti-tumor cells around certain solid tumors. Later, in vitro murine MC cytotoxicity (MCC) against murine tumor cells was described in 1981. Presently; believers in the inhibitory role of MCs assume them as inhibitors of tumor development through their cytotoxic pro-necrolytic/-apoptotic granules. Except for perforin, MCs indeed have been proven to have all components of cell-mediated cytotoxicity. Our recently published in vitro experiences demonstrated human MCC against human tumor cells [2]. Consistently, our in vivo experiences also showed that MCs do not account for the angiogenic process which facilitates tumor growth [3]. Our correspondences against supporters for the tumor-promoting role of MCs have also been well-documented in recent literature [4].
MC availability in tumor stroma has still been controversial, too. The important point here is whether increased tissue MC density (MCD) could be primary/secondary since MCs are also found to be increased physiologically around healing tissue. MCs might be just a reflection of generalized inflammatory reaction as well [4]. MCs also accumulate at sites of tumor growth in response to numerous chemoattractants. Such as CCL5/CXCR3 chemokines in lymphoma, and tumor-derived stem cell factor and CD30 expressions lead to tumor growth and MCD in tumor tissues [5]. Hence, it is important to find an answer to the following question: May the increased MCD be a result or a cause of tumor progression? Then, the next question is whether the MC really is an active player or an innocent passerby in a tumor stroma.
Although it is hard to explain these conflicting results in the literature, they may...
Pełna treść artykułu...
We have read the article titled “Mast cells and cancer: enemies or allies?” by Dyduch et al. with a great interest [1]. Because of this opportunity, we want to share our in vitro experience on the anti-tumor actions of human mast cell (MC) through direct cell-mediated cytotoxicity [2]. We have also recently gotten in vivo experience on the role of tryptase-/chymase-positive MCs by working their role in the benign and malignant uterus (endometrial and cervix) carcinomas [3].
Ambiguous mounting evidence also indicates that MCs accumulate around tumors and could either promote or inhibit tumor growth probably depending on environmental conditions. First in vivo observations in the 1950s suggested their possible role as anti-tumor cells around certain solid tumors. Later, in vitro murine MC cytotoxicity (MCC) against murine tumor cells was described in 1981. Presently; believers in the inhibitory role of MCs assume them as inhibitors of tumor development through their cytotoxic pro-necrolytic/-apoptotic granules. Except for perforin, MCs indeed have been proven to have all components of cell-mediated cytotoxicity. Our recently published in vitro experiences demonstrated human MCC against human tumor cells [2]. Consistently, our in vivo experiences also showed that MCs do not account for the angiogenic process which facilitates tumor growth [3]. Our correspondences against supporters for the tumor-promoting role of MCs have also been well-documented in recent literature [4].
MC availability in tumor stroma has still been controversial, too. The important point here is whether increased tissue MC density (MCD) could be primary/secondary since MCs are also found to be increased physiologically around healing tissue. MCs might be just a reflection of generalized inflammatory reaction as well [4]. MCs also accumulate at sites of tumor growth in response to numerous chemoattractants. Such as CCL5/CXCR3 chemokines in lymphoma, and tumor-derived stem cell factor and CD30 expressions lead to tumor growth and MCD in tumor tissues [5]. Hence, it is important to find an answer to the following question: May the increased MCD be a result or a cause of tumor progression? Then, the next question is whether the MC really is an active player or an innocent passerby in a tumor stroma.
Although it is hard to explain these conflicting results in the literature, they may...
Pełna treść artykułu...
Integrated with
