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1 H MRS markers of tumour growth in intrasplenic tumours and liver metastasis induced by injection of HT‐29 cells in nude mice spleen
Author(s) -
Moreno Angel,
López Lluis A.,
Fabra Angels,
Arús* Carles
Publication year - 1998
Publication title -
nmr in biomedicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.278
H-Index - 114
eISSN - 1099-1492
pISSN - 0952-3480
DOI - 10.1002/(sici)1099-1492(199805)11:3<93::aid-nbm520>3.0.co;2-h
Subject(s) - spleen , pathology , metastasis , cancer research , chemistry , biology , medicine , cancer
Abstract We have characterized, by in vitro magnetic resonance spectroscopy (MRS), the metabolite pattern of perchloric acid (PCA) extracts of intrasplenic tumours and hepatic metastasis, produced by intra‐spleen injection of the human colorectal carcinoma cell line HT‐29 and its metastatic variant HT‐29 MMM into nude mice. Our aim was to gain further understanding of colorectal tumour metabolism as a basis for future in vivo studies of human colon cancer by 1 H MRS. Metabolite PCA extract analysis showed a good reproduction of the spectral pattern observed in human primary colon tumours, while they were very different from the spectral pattern of the host tissues (spleen and liver). The main differences between host and tumour tissues involved taurine, phosphocholine (PC), phosphoethanolamine (PE), creatine, glycogen and glucose. Creatine is the most promising marker to follow tumour growth because of its practical absence in the nude mice host tissues. Detection of variable levels of this compound and of taurine in hepatic foci in man, are suggested as possible diagnostic markers. No correlation could be found between spectral pattern differences and the different ability to metastasize of the two HT‐29 cell lines used. Furthemore, indirect evidence for a functional link between taurine and myo‐inositol in colon tumour cells is presented. In summary, our data suggest that the nude mice model may be a suitable system for the MRS study of the changes taking place in host tissues upon tumour progression. © 1998 John Wiley & Sons, Ltd.