A case of squamous cell carcinoma of the head and neck producing granulocyte-colony stimulating factor with marked leukocytosis
In squamous cell carcinoma of the head and neck (SCCHN), tumor cells have been shown to secrete detectable amounts of various cytokines, such as interleukin (IL)-6, IL-10, and transforming growth factor (TGF)-β. These tumor-derived factors might be responsible for promoting malignancy. Here, we desc...
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| Veröffentlicht in: | Auris, nasus, larynx nasus, larynx, 2007-06, Vol.34 (2), p.267-271 |
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| creator | Toyoda, Minoru Chikamatsu, Kazuaki Sakakura, Koichi Fukuda, Yoichiro Takahashi, Katsumasa Miyashita, Motoaki Shimamura, Kazuo Furuya, Nobuhiko |
| description | In squamous cell carcinoma of the head and neck (SCCHN), tumor cells have been shown to secrete detectable amounts of various cytokines, such as interleukin (IL)-6, IL-10, and transforming growth factor (TGF)-β. These tumor-derived factors might be responsible for promoting malignancy. Here, we describe a SCCHN patient with tumor produced G-CSF and characterized by marked leukocytosis. In this 45-year-old man, severe leukocytosis developed in parallel with aggressive tumor growth. G-CSF production by the tumor was confirmed by immunohistochemistry (IHC). Serum G-CSF levels were elevated. The leukocyte counts and the blood G-CSF level decreased following a course of radiotherapy. Tumor cells were also positive for G-CSF receptor, suggesting autocrine growth regulation by G-CSF. Moreover, the tumor cells were also investigated by IHC with anti-p53, anti-P-glycoprotein (P-gp), anti-thymidylate synthase (TS), and anti-dihydropyrimidine dehydrogenase (DPD), which molecules are thought to contribute the acquisition of therapeutic resistance. The tumor cells were positively stained for TS and DPD, but neither p53 nor P-gp. These results suggest that a variety of molecules may be responsible for acquisition of high malignancy. |
| doi_str_mv | 10.1016/j.anl.2006.07.014 |
| format | Article |
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These tumor-derived factors might be responsible for promoting malignancy. Here, we describe a SCCHN patient with tumor produced G-CSF and characterized by marked leukocytosis. In this 45-year-old man, severe leukocytosis developed in parallel with aggressive tumor growth. G-CSF production by the tumor was confirmed by immunohistochemistry (IHC). Serum G-CSF levels were elevated. The leukocyte counts and the blood G-CSF level decreased following a course of radiotherapy. Tumor cells were also positive for G-CSF receptor, suggesting autocrine growth regulation by G-CSF. Moreover, the tumor cells were also investigated by IHC with anti-p53, anti-P-glycoprotein (P-gp), anti-thymidylate synthase (TS), and anti-dihydropyrimidine dehydrogenase (DPD), which molecules are thought to contribute the acquisition of therapeutic resistance. The tumor cells were positively stained for TS and DPD, but neither p53 nor P-gp. 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These results suggest that a variety of molecules may be responsible for acquisition of high malignancy.</description><subject>Abscess - pathology</subject><subject>Biopsy</subject><subject>Carcinoma, Squamous Cell - pathology</subject><subject>Carcinoma, Squamous Cell - radiotherapy</subject><subject>Diagnosis, Differential</subject><subject>Dihydrouracil Dehydrogenase (NADP) - metabolism</subject><subject>Disease Progression</subject><subject>Follow-Up Studies</subject><subject>G-CSF receptor</subject><subject>Granulocyte Colony-Stimulating Factor - metabolism</subject><subject>Granulocyte-colony stimulating factor (G-CSF)</subject><subject>Head and Neck Neoplasms - pathology</subject><subject>Head and Neck Neoplasms - radiotherapy</subject><subject>Humans</subject><subject>Leukocytosis</subject><subject>Leukocytosis - pathology</subject><subject>Male</subject><subject>Malignant phenotype</subject><subject>Middle Aged</subject><subject>Neck - pathology</subject><subject>Palliative Care</subject><subject>Radiotherapy Dosage</subject><subject>Squamous cell carcinoma of the head and neck (SCCHN)</subject><subject>Submandibular Gland - pathology</subject><subject>Submandibular Gland Neoplasms - pathology</subject><subject>Submandibular Gland Neoplasms - radiotherapy</subject><subject>Thymidylate Synthase - metabolism</subject><subject>Tomography, X-Ray Computed</subject><issn>0385-8146</issn><issn>1879-1476</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2007</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kE1v1DAQhi0EokvhB3BBPnFLsGMnTsSpqvioVIkLnK2JPe56N4lb26HaE38dR7sSN06WPM-8mvch5D1nNWe8-3SoYZnqhrGuZqpmXL4gO96roeJSdS_Jjom-rXouuyvyJqUDY0woMbwmV1yxQTWt2JE_N9RAQhocTU8rzGFN1OA0ld9o_BJm2EZ5j3SPYCksli5ojvQxBrsW4IE-RFjWKZhTxsqEKSwnmrKf1wnyNnZgcoj02ec9nSEe0dIJ1-PGh-TTW_LKwZTw3eW9Jr--fvl5-726__Ht7vbmvjJCtbmS_Tgax_velRLWWVSyGxsYsRfKAG9HaQW4tm-kQhBgrBoGJyRzSnLeMBDX5OM5txz-tGLKevZpKwoLls5aMSmY5KKA_AyaGFKK6PRj9OXwk-ZMb9b1QRfrerOumdLFetn5cAlfxxntv42L5gJ8PgNYKv72GHUyHheD1kc0Wdvg_xP_F5_VlZU</recordid><startdate>20070601</startdate><enddate>20070601</enddate><creator>Toyoda, Minoru</creator><creator>Chikamatsu, Kazuaki</creator><creator>Sakakura, Koichi</creator><creator>Fukuda, Yoichiro</creator><creator>Takahashi, Katsumasa</creator><creator>Miyashita, Motoaki</creator><creator>Shimamura, Kazuo</creator><creator>Furuya, Nobuhiko</creator><general>Elsevier Ireland Ltd</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><scope>8BM</scope></search><sort><creationdate>20070601</creationdate><title>A case of squamous cell carcinoma of the head and neck producing granulocyte-colony stimulating factor with marked leukocytosis</title><author>Toyoda, Minoru ; 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These tumor-derived factors might be responsible for promoting malignancy. Here, we describe a SCCHN patient with tumor produced G-CSF and characterized by marked leukocytosis. In this 45-year-old man, severe leukocytosis developed in parallel with aggressive tumor growth. G-CSF production by the tumor was confirmed by immunohistochemistry (IHC). Serum G-CSF levels were elevated. The leukocyte counts and the blood G-CSF level decreased following a course of radiotherapy. Tumor cells were also positive for G-CSF receptor, suggesting autocrine growth regulation by G-CSF. Moreover, the tumor cells were also investigated by IHC with anti-p53, anti-P-glycoprotein (P-gp), anti-thymidylate synthase (TS), and anti-dihydropyrimidine dehydrogenase (DPD), which molecules are thought to contribute the acquisition of therapeutic resistance. The tumor cells were positively stained for TS and DPD, but neither p53 nor P-gp. 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| ispartof | Auris, nasus, larynx, 2007-06, Vol.34 (2), p.267-271 |
| issn | 0385-8146 1879-1476 |
| language | eng |
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| source | MEDLINE; Elsevier ScienceDirect Journals |
| subjects | Abscess - pathology Biopsy Carcinoma, Squamous Cell - pathology Carcinoma, Squamous Cell - radiotherapy Diagnosis, Differential Dihydrouracil Dehydrogenase (NADP) - metabolism Disease Progression Follow-Up Studies G-CSF receptor Granulocyte Colony-Stimulating Factor - metabolism Granulocyte-colony stimulating factor (G-CSF) Head and Neck Neoplasms - pathology Head and Neck Neoplasms - radiotherapy Humans Leukocytosis Leukocytosis - pathology Male Malignant phenotype Middle Aged Neck - pathology Palliative Care Radiotherapy Dosage Squamous cell carcinoma of the head and neck (SCCHN) Submandibular Gland - pathology Submandibular Gland Neoplasms - pathology Submandibular Gland Neoplasms - radiotherapy Thymidylate Synthase - metabolism Tomography, X-Ray Computed |
| title | A case of squamous cell carcinoma of the head and neck producing granulocyte-colony stimulating factor with marked leukocytosis |
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