Effect of treatment of larynx and hypopharynx carcinomas on serum syndecan-1 concentrations

Anttonen, Anu; Leppä, Sirpa; Heikkilä, Pia; Grénman, Reidar; Joensuu, Heikki

doi:10.1007/s00432-006-0090-z

Cited by 13 publications

(9 citation statements)

References 27 publications

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“…Soluble Sdc-1 is present at low levels in the serum of healthy people, but elevated Sdc-1 levels have been reported in cancer patients (Joensuu et al , 2002; Anttonen et al , 2003, 2006; Yang et al , 2007). In our study, we simultaneously examined Sdc-1 and MMP-7 serum levels in colorectal cancer patients and in healthy adults.…”

Section: Discussionmentioning

confidence: 99%

“…Many studies have confirmed that Sdc-1 shedding from the membrane of pancreatic, lung and larynx tumour cells is accelerated in comparison with shedding from the membrane of normal cells (Joensuu et al , 2002; Anttonen et al , 2003, 2006). In addition, high pretreatment Sdc-1 serum levels are associated with poor prognosis in lung cancer (small cell and non-small cell carcinoma) treated with platinum-based chemotherapy (Joensuu et al , 2002; Anttonen et al , 2003).…”

mentioning

confidence: 96%

“…In addition, high pretreatment Sdc-1 serum levels are associated with poor prognosis in lung cancer (small cell and non-small cell carcinoma) treated with platinum-based chemotherapy (Joensuu et al , 2002; Anttonen et al , 2003). Furthermore, low posttreatment Sdc-1 serum levels in larynx and hypopharynx cancer can prognosticate the sensitivity to anticancer therapy, and high posttreatment Sdc-1 serum levels are an indicator of relapse (Anttonen et al , 2006). Nevertheless, whether Sdc-1 influences the effectiveness of cancer chemotherapy remains to be elucidated.…”

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confidence: 99%

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Shed Syndecan-1 is involved in chemotherapy resistance via the EGFR pathway in colorectal cancer

et al. 2014

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Background:Syndecan-1 (Sdc-1) shedding induced by matrix metalloproteinase-7 (MMP-7) and additional proteases has an important role in cancer development. However, the impact of Sdc-1 shedding on chemotherapeutic resistance has not been reported.Methods:We examined Sdc-1 shedding in colorectal cancer by enzyme-linked immunosorbent assay (ELISA), Dot blot, reverse transcription-PCR (RT-PCR), immunohistochemistry and so on, its impact on chemotherapeutic sensitivity by collagen gel droplet embedded culture-drug sensitivity test (CD-DST) and MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide), and potential mechanisms of action by Dot blot, western blot and immunofluorescence.Results:Sdc-1 shedding was increased in colorectal cancer patients, Sdc-1 serum levels in postoperative patients were lower than in preoperative patients, but still higher than those observed in healthy adults. Patients with high preoperative Sdc-1 serum levels were less responsive to 5-Fluorouracil, Oxaliplatin, Irintecan, Cisplatin or Paclitaxel chemotherapy. Moreover, the disease-free survival of patients with high preoperative Sdc-1 serum levels was significantly poorer. The possible mechanism of chemotherapy resistance in colorectal cancer can be attributed to Sdc-1 shedding, which enhances EGFR phosphorylation and downstream signalling.Conclusions:Shed Sdc-1 is involved in chemotherapy resistance via the EGFR pathway in colorectal cancer, and Sdc-1 serum levels could be a new prognostic marker in colorectal cancer.

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Section: Discussionmentioning

confidence: 99%

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confidence: 96%

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confidence: 99%

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Shed Syndecan-1 is involved in chemotherapy resistance via the EGFR pathway in colorectal cancer

et al. 2014

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“…Furthermore, low serum syndecan-1 level can predict sensitivity to anticancer therapy in larynx and hypopharynx cancer, whereas high posttreatment level is an indicator of relapse [61]. …”

Section: Discussionmentioning

confidence: 99%

Diagnostic and Prognostic Value of Soluble Syndecan-1 in Pleural Malignancies

Mundt

Heidari-Hamedani

Nilsonne

et al. 2014

BioMed Research International

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Background. The distinction between malignant and benign pleural effusions is a diagnostic challenge today and measuring soluble biomarkers could add to the diagnostic accuracy. Syndecan-1 is a proteoglycan involved in various cellular functions and is cleaved from the cell surface in a regulated manner. The shed fragment, which can be recovered in effusion supernatant and in serum, retains its binding capacities, but often with different functions and signalling properties than the cell-bound form. Aim. This study aimed to investigate the diagnostic and prognostic value of soluble syndecan-1 in pleural effusions and sera from patients with pleural malignancies. Study Design. Using two cohorts of patients, we assessed the diagnostic and prognostic value of soluble syndecan-1 in pleural effusions and sera, using enzyme-linked immunosorbent assays. Results. In pleural effusions, syndecan-1 distinguished malignant and benign diseases, with an odds ratio of 8.59 (95% CI 3.67 to 20.09). Furthermore, syndecan-1 in pleural effusions predicted a survival difference for patients with pleural metastatic disease and malignant mesothelioma of 11.2 and 9.2 months, respectively. However, no such effects were seen when syndecan-1 was measured in serum. Conclusion. Soluble syndecan-1 is a promising candidate biomarker for the cytopathological diagnosis and prognostication of malignant pleural effusions.

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“…Furthermore, since both these tissues are highly vascularized, cancers here are usually secondary metastases [99]. For lung cancer patients, serum Sdc-1 (S-Sdc-1) levels decline following tumor resection; whereas recurrent lung cancers demonstrate elevated S-Sdc-1 levels [100]. High S-Sdc-1 levels probably indicate high Hpa activity and extensive paracrine growth and proliferation signals.…”

Section: Roles Of Hs and Important Hs-protein Interactions In Cancermentioning

confidence: 99%

Chemical Tumor Biology of Heparan Sulfate Proteoglycans

Raman¹,

Kuberan²

2010

CCB

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Heparan sulfate proteoglycans (HSPGs) play vital roles in every step of tumor progression allowing cancer cells to proliferate, escape from immune response, invade neighboring tissues, and metastasize to distal sites away from the primary site. Several cancers including breast, lung, brain, pancreatic, skin, and colorectal cancers show aberrant modulation of several key HS biosynthetic enzymes such as 3-O Sulfotransferase and 6-O Sulfotransferase, and also catabolic enzymes such as HSulf-1, HSulf-2 and heparanase. The resulting tumor specific HS fine structures assist cancer cells to breakdown ECM to spread, misregulate signaling pathways to facilitate their proliferation, promote angiogenesis to receive nutrients, and protect themselves against natural killer cells. This review focuses on the changes in the expression of HS biosynthetic and catabolic enzymes in several cancers, the resulting changes in HS fine structures, and the effects of these tumor specific HS signatures on promoting invasion, proliferation, and metastasis. It is possible to retard tumor progression by modulating the deregulated biosynthetic and catabolic pathways of HS chains through novel chemical biology approaches.

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Effect of treatment of larynx and hypopharynx carcinomas on serum syndecan-1 concentrations

Abstract: These findings suggest that a part of S-syndecan-1 originates from the cancerous tissue, and that S-syndecan-1 levels generally decrease following successful cancer treatment.

Cited by 13 publications

References 27 publications

Shed Syndecan-1 is involved in chemotherapy resistance via the EGFR pathway in colorectal cancer

Shed Syndecan-1 is involved in chemotherapy resistance via the EGFR pathway in colorectal cancer

Diagnostic and Prognostic Value of Soluble Syndecan-1 in Pleural Malignancies

Chemical Tumor Biology of Heparan Sulfate Proteoglycans

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