Gastrointestinal stromal tumors with KIT mutations exhibit a remarkably homogeneous gene expression profile

Forskningsoutput: TidskriftsbidragArtikel i vetenskaplig tidskrift

Standard

Gastrointestinal stromal tumors with KIT mutations exhibit a remarkably homogeneous gene expression profile. / Allander, S V; Nupponen, N N; Ringnér, Markus; Hostetter, G; Maher, G W; Goldberger, N; Chen, Y; Carpten, J; Elkahloun, A G; Meltzer, P S.

I: Cancer Research, Vol. 61, Nr. 24, 2001, s. 8624-8628.

Forskningsoutput: TidskriftsbidragArtikel i vetenskaplig tidskrift

Harvard

Allander, SV, Nupponen, NN, Ringnér, M, Hostetter, G, Maher, GW, Goldberger, N, Chen, Y, Carpten, J, Elkahloun, AG & Meltzer, PS 2001, 'Gastrointestinal stromal tumors with KIT mutations exhibit a remarkably homogeneous gene expression profile', Cancer Research, vol. 61, nr. 24, s. 8624-8628.

APA

Allander, S. V., Nupponen, N. N., Ringnér, M., Hostetter, G., Maher, G. W., Goldberger, N., ... Meltzer, P. S. (2001). Gastrointestinal stromal tumors with KIT mutations exhibit a remarkably homogeneous gene expression profile. Cancer Research, 61(24), 8624-8628.

CBE

Allander SV, Nupponen NN, Ringnér M, Hostetter G, Maher GW, Goldberger N, Chen Y, Carpten J, Elkahloun AG, Meltzer PS. 2001. Gastrointestinal stromal tumors with KIT mutations exhibit a remarkably homogeneous gene expression profile. Cancer Research. 61(24):8624-8628.

MLA

Vancouver

Allander SV, Nupponen NN, Ringnér M, Hostetter G, Maher GW, Goldberger N et al. Gastrointestinal stromal tumors with KIT mutations exhibit a remarkably homogeneous gene expression profile. Cancer Research. 2001;61(24):8624-8628.

Author

Allander, S V ; Nupponen, N N ; Ringnér, Markus ; Hostetter, G ; Maher, G W ; Goldberger, N ; Chen, Y ; Carpten, J ; Elkahloun, A G ; Meltzer, P S. / Gastrointestinal stromal tumors with KIT mutations exhibit a remarkably homogeneous gene expression profile. I: Cancer Research. 2001 ; Vol. 61, Nr. 24. s. 8624-8628.

RIS

TY - JOUR

T1 - Gastrointestinal stromal tumors with KIT mutations exhibit a remarkably homogeneous gene expression profile

AU - Allander, S V

AU - Nupponen, N N

AU - Ringnér, Markus

AU - Hostetter, G

AU - Maher, G W

AU - Goldberger, N

AU - Chen, Y

AU - Carpten, J

AU - Elkahloun, A G

AU - Meltzer, P S

PY - 2001

Y1 - 2001

N2 - Gastrointestinal stromal tumors (GISTs), the most common mesenchymal tumors of the digestive tract, are believed to arise from the interstitial cells of Cajal. GISTs are characterized by mutations in the proto-oncogene KIT that lead to constitutive activation of its tyrosine kinase activity. The tyrosine kinase inhibitor STI571, active against the BCR-ABL fusion protein in chronic myeloid leukemia, was recently shown to be highly effective in GISTs. We used 13,826-element cDNA microarrays to define the expression patterns of 13 KIT mutation-positive GISTs and compared them with the expression profiles of a group of spindle cell tumors from locations outside the gastrointestinal tract. Our results showed a remarkably distinct and uniform expression profile for all of the GISTs. In particular, hierarchical clustering of a subset of 113 cDNAs placed all of the GIST samples into one branch, with a Pearson correlation >0.91. This homogeneity suggests that the molecular pathogenesis of a GIST results from expansion of a clone that has acquired an activating mutation in KIT without the extreme genetic instability found in the common epithelial cancers. The results provide insight into the histogenesis of GIST and the clinical behavior of this therapeutically responsive tumor.

AB - Gastrointestinal stromal tumors (GISTs), the most common mesenchymal tumors of the digestive tract, are believed to arise from the interstitial cells of Cajal. GISTs are characterized by mutations in the proto-oncogene KIT that lead to constitutive activation of its tyrosine kinase activity. The tyrosine kinase inhibitor STI571, active against the BCR-ABL fusion protein in chronic myeloid leukemia, was recently shown to be highly effective in GISTs. We used 13,826-element cDNA microarrays to define the expression patterns of 13 KIT mutation-positive GISTs and compared them with the expression profiles of a group of spindle cell tumors from locations outside the gastrointestinal tract. Our results showed a remarkably distinct and uniform expression profile for all of the GISTs. In particular, hierarchical clustering of a subset of 113 cDNAs placed all of the GIST samples into one branch, with a Pearson correlation >0.91. This homogeneity suggests that the molecular pathogenesis of a GIST results from expansion of a clone that has acquired an activating mutation in KIT without the extreme genetic instability found in the common epithelial cancers. The results provide insight into the histogenesis of GIST and the clinical behavior of this therapeutically responsive tumor.

M3 - Article

VL - 61

SP - 8624

EP - 8628

JO - Cancer research. Supplement

JF - Cancer research. Supplement

SN - 1538-7445

IS - 24

ER -