Expression of histidine decarboxylase in human colonic cancer cells and adenomatous polyps

Boér, Katalin; Darvas, Zsuzsanna; Baki, M.; Kaszás, Ilona; Pál, Zsuzsanna; Falus, András

doi:10.1007/s000110300062

Cited by 10 publications

(4 citation statements)

References 8 publications

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“…Such results are consistent with our previous study that examined the effects of H 2 -receptor antagonists on Colon 38-tumor growth (6). In fact, 90% of human colorectal adenocarcinoma samples in one study were HDC-positive, that is, express the enzyme that synthesizes histamine, with HDC-immunoreactivity observed for different cell types, namely, tumor cells themselves and inflammatory cells infiltrating into the tumor (18). Such findings strongly suggest that endogenous histamine is involved in tumor growth.…”

Section: Discussionsupporting

confidence: 91%

Exogenous Histamine Stimulates Colorectal Cancer Implant Growth via Immunosuppression in Mice

Tomita

Okabe

2005

J Pharmacol Sci

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Abstract.Results from a limited number of studies suggest a potential role for endogenous histamine in regulating tumor growth in immunocompetent cells. The present study examined the effects of exogenous histamine on colorectal cancer growth and the immune response against tumor tissue in mice. Histamine was administered for 21 days to Colon 38 mouse colon adenocarcinoma-implanted syngeneic mice and tumor volume was measured throughout the experiment. Systemic administration of histamine for 21 days caused a significant increase in tumor implant growth compared with the vehicle. At the end of histamine administration, the interferon (IFN)-g / interleukin (IL)-4 ratio in peripheral lymphocytes, as well as histamine and cytokine levels in tumor implants were determined. Histamine levels in tumor implants remained unchanged after exogenous histamine delivery. Mice with tumor implants exhibited significantly elevated IFN-g / IL-4 ratios compared with mice lacking tumors. Nonetheless, the increased IFN-g / IL-4 ratios were markedly suppressed by histamine administration compared with vehicle. In addition, histamine delivery significantly decreased IFN-g and IL-12 mRNA expression, but increased IL-10 mRNA expression in tumor implants. It was concluded that exogenous histamine dysregulates the balance between T-helper 1 (Th1) and T-helper 2 (Th2) cells, attenuating anti-tumor cytokine expression in the tumor microenvironment, thus resulting in stimulated colorectal cancer growth.

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Section: Discussionsupporting

confidence: 91%

Exogenous Histamine Stimulates Colorectal Cancer Implant Growth via Immunosuppression in Mice

Tomita

Okabe

2005

J Pharmacol Sci

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“…Our earlier immunocytochemical results showed a difference in the distribution of the HDC positive cells in adenomas and in adenocarcinomas [7]. In this present study, some of the HDC positive cells were CD8 + T lymphocytes.…”

Section: Resultssupporting

confidence: 52%

“…It is accepted that mucosa of the colon is in constant subacute stimulated stage due to the bacteria colonizing it [6]. Previously, we demonstrated HDC immunoreactivity in both colon tumours and in adenomas [7]. Colon adenomas have a malignant potential, the villous adenomas are most likely to become malignant.…”

Section: Introductionmentioning

confidence: 99%

Histamine metabolism and CD8 + T cell infiltration in colon adenomas

Boér¹,

Darvas

Bősze

et al. 2004

Inflammation Research

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“…L‐histidine decarboxylase (HDC) is the rate‐limiting enzyme that catalyzes the formation of histamine from L‐histidine and increased expression of HDC is recognized as a specific marker for biosynthesis of histamine (15). The expression of HDC can be determined by different laboratory techniques (11, 16–20). Real‐time PCR is the most precise method for quantifying HDC at the mRNA level, whereas immunohistochemistry (IHC) is a frequently used technique to identify HDC expression in specific cells or tissues.…”

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confidence: 99%

Expression of non‐mast cell histidine decarboxylase in tumor‐associated microvessels in human esophageal squamous cell carcinomas

Liu

Fuai

et al. 2008

APMIS

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Histamine is produced by mast cells and many other types of cells. The role of histamine released from mast cells in promoting tumor angiogenesis has been intensively studied; however, the role of non-mast cell histamine in regulating tumor angiogenesis has been largely ignored. In this study, tissue specimen sections from 43 patients with esophageal squamous cell carcinoma (ESCC) and normal esophageal biopsies from 17 heath individuals obtained from a high incidence area of north China were used to assess changes in microvessel density (MVD) and non-mast cell L-histidine decarboxylase (HDC) (the only rate-limiting enzyme that catalyzes the formation of histamine from L-histidine) expression in the tumor microenvironment by immunohistochemistry (IHC). In addition, the cellular characterization of non-mast cell HDC-positive cells in microvessels was examined by double IHC combined with HDC/CD34 and HDC/PCNA antibodies. These IHC analyses revealed a significantly increased HDC-positive MVD in ESCC as compared with normal controls, which accounted for approximately 61% of CD34-labeled general MVD in ESCC. Furthermore, IHC in serial sections and double IHC showed that most of these HDC-positive cells were CD34-positive endothelial cells in microvessels with an increased proliferative capacity. Thus, our results suggest that non-mast cell histamine expressed in endothelial cells of microvessels could be an additional cellular source and might play a role in regulating angiogenesis in ESCC.

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Expression of histidine decarboxylase in human colonic cancer cells and adenomatous polyps

Cited by 10 publications

References 8 publications

Exogenous Histamine Stimulates Colorectal Cancer Implant Growth via Immunosuppression in Mice

Exogenous Histamine Stimulates Colorectal Cancer Implant Growth via Immunosuppression in Mice

Histamine metabolism and CD8 + T cell infiltration in colon adenomas

Expression of non‐mast cell histidine decarboxylase in tumor‐associated microvessels in human esophageal squamous cell carcinomas

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