Author/Authors :
Stoecklein، نويسنده , , Nikolas H. and Hosch، نويسنده , , Stefan B. and Bezler، نويسنده , , Martin L. Stern، نويسنده , , Franziska and Hartmann، نويسنده , , Claudia H. and Vay، نويسنده , , Christian J. Siegmund، نويسنده , , Annika and Scheunemann، نويسنده , , Peter and Schurr، نويسنده , , Paulus and Knoefel، نويسنده , , Wolfram T. and Verde، نويسنده , , Pablo E. and Reichelt، نويسنده , , Uta and Erbersdobler، نويسنده , , Andreas and Grau، نويسنده , , Roger and Ullrich، نويسنده , , Axel and Izbicki، نويسنده , , Jakob R. and Klein، نويسنده , , Christoph A.، نويسنده ,
Abstract :
Summary
creasing use of primary tumors as surrogate markers for prognosis and therapeutic decisions neglects evolutionary aspects of cancer progression. To address this problem, we studied the precursor cells of metastases directly for the identification of prognostic and therapeutic markers and prospectively analyzed single disseminated cancer cells from lymph nodes and bone marrow of 107 consecutive esophageal cancer patients. Whole-genome screening revealed that primary tumors and lymphatically and hematogenously disseminated cancer cells diverged for most genetic aberrations. However, we identified chromosome 17q12–21, the region comprising HER2, as the most frequent gain in disseminated tumor cells that were isolated from both ectopic sites. Survival analysis demonstrated that HER2 gain in a single disseminated tumor cell but not in primary tumors conferred high risk for early death.
