Correlation of Thymidine Phosphorylase Staining and the Ki-67 Labeling Index to Clinicopathologic Factors and Hepatic Metastasis in Patients with Colorectal Cancer

Kitabatake, Toshiaki; Kojima, Kuniaki; Fukasawa, Masaki; Beppu, Tomoe; Futagawa, Shunji

doi:10.1007/s005950200046

Cited by 13 publications

(9 citation statements)

References 15 publications

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“…Finally, the combination of a lower proliferative activity with a similar AI in metastases relative to primaries is consistent with the clinical observation that liver metastases are sometimes slow growing. Other groups using immunohistochemical methods have come to similar conclusions (Thomas et al, 1998;Agui et al, 2002;Kitabatake et al, 2002;Seong et al, 2004). …”

Section: Discussionsupporting

confidence: 57%

Slow proliferation as a biological feature of colorectal cancer metastasis

et al. 2009

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BACKGROUND: We have recently reported an inverse relationship between colon cancer progression and tumour proliferative activity. Here, we extend our findings by evaluating the proliferative activity of liver metastatic lesions and primary colorectal cancers (CRC) that differ in their metastatic potential. METHODS: Using an earlier established multi-gene proliferation signature (GPS), proliferative levels were analysed in 73 primary CRCs and 27 liver metastases. RESULTS: Compared with primary CRCs, we observed a significantly lower expression of the GPS in liver metastases and confirmed their lower proliferative levels by quantitative RT -PCR and Ki-67 immunostaining. No difference could be detected in apoptotic indices as assessed by M30 immunostaining, indicating that the net growth rate is lower in metastases relative to primary tumours. Notably, relapsed primaries or those with established metastases had significantly lower proliferative activity than CRCs that were non-metastatic and did not relapse. CONCLUSION: Our results suggest that slow proliferation is a biological characteristic of both liver metastases and those primary tumours with the ability to metastasise. The delineation of the mechanisms underlying the inverse association between proliferation and CRC aggressiveness may be important for the development of new therapeutic strategies.

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Section: Discussionsupporting

confidence: 57%

Slow proliferation as a biological feature of colorectal cancer metastasis

et al. 2009

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“…24 Valera et al 25 reported a signifi cant association between Ki-67 and CRC tumor depth, lymph node involvement, and the presence of distant metastasis. Kitabatake et al 26 also reported an association between high-level Ki-67 expression and a higher frequency of metachronous liver metastasis. In contrast, some authors have concluded that CRC patients with low Ki-67 expression have a poor prognosis, [27][28][29] and some studies have found no correlation between Ki-67 expression and liver metastasis.…”

Section: Discussionmentioning

confidence: 92%

Assessment of SMAD4, p53, and Ki-67 alterations as a predictor of liver metastasis in human colorectal cancer

et al. 2010

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“…49 and 83), Mad4, and Pdgfec ("platelet-derived endothelial growth factor/thymidine phosphorylase/gliostatin"; NM_138302). Pdgfec had previ-ously been localized to the peripheral nervous system (20), identified as a protein that has a potential role in development and regeneration of the central nervous system (4), and determined to be highly expressed in invasive colorectal tumors (44); therefore, this gene/protein may regulate the switch between proliferation and differentiation in the process of neurogenesis in the OM. Mad4 is highly induced in differentiated cells (39,43), so we would expect to find this protein localized to one or more nonproliferating cell populations in the OM.…”

Section: Discussionmentioning

confidence: 99%