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LETTER TO THE EDITOR Separate Karyotypic Features in a Local Recurrence and a Metastasis of a Fibrosarcoma Recently we reported multiple chromosome rearrangements in the fifth recurrence of a fibrosarcoma in a 39-year-old man [1]. Thirteen months after that investigation, the patient had developed a 5 x 5 x 2.5 cm local recurrence in the left thoracic wall, and a solitary metastasis, 2 cm in diameter, in the right lung. Both tumors showed similar histologic features: highly cellular spindle cell sarcomatous growth with a herringbone pattern, focal collagen production, and numerous mitotic figures. The histology of both lesions was identical to that of the primary tumor and earlier recurrences. Samples obtained from the sixth local recurrence and the lung metastasis were processed for cytogenetic analysis as previously described [2]. In both tumors, two clones were detected. The major clone of the local recurrence had chromosome aberrations identical to those found in the previously investigated tumor, giving the karyotype 43,Y,t(X;18)(p11;q11),t(2;15)(p23:q26),- 3, + der(3)dic(3:?)(p11:?),- 5, + der(5)ins(5;?)(qllq13;?)t(5;?)(p15:?),t(7;22)(qll:q13),-11,- 18,- 19, 21, + mar. In addition to these changes, the rearrangement t(4;13)(p14;q13) was present in a minor clone: the majority of these cells were hypotetraploid, with 85 and 86 chro- mosomes. Two clones were also detected in the metastatic tumor. In addition to the changes described in the karyotype above, one clone had -10 and 16q+, and the other 10, 14, and 16q+. None of the abnormalities t(4;13)(p14:q13), -10, -14, and 16q+ had been found in the previously analyzed tumor, even as nonclonal changes. It seems rea- sonable to suggest that tumor cells remaining from the fifth local recurrence had expanded clonally to give rise to the present recurrence, and that the subclone with t(4;13)(p14:q13) evolved only relatively late. The finding of 10 and 16q+ in all metaphases from the metastasis but in none from the recurrent tumor indicates that these changes emerged at or shortly after the time when the cells metastasized to the lung. Later loss of one chromosome 14 gave rise to a side-line. Supported by grants from the Swedish Cancer Society, the Swedish Work Environment Fund, the JAP Foundation for Medical Research and the Lund University Medical Faculty. N. MANDAHL S. HElM K. ARHEDEN A. RYDHOLM H. WILLI~N F. MITELMAN Departments of Clinical Genetics, Orthopedics, and Clinical Pathology Lund University Hospital S-221 85 Lurid, Sweden 139

Separate karyotypic features in a local recurrence and a metastasis of a fibrosarcoma

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Page 1: Separate karyotypic features in a local recurrence and a metastasis of a fibrosarcoma

LETTER TO THE EDITOR

Separate Karyotypic Features in a

Local Recurrence and a Metastasis

of a Fibrosarcoma

Recently we reported mult iple chromosome rearrangements in the fifth recurrence of a fibrosarcoma in a 39-year-old man [1]. Thirteen months after that investigation, the patient had developed a 5 x 5 x 2.5 cm local recurrence in the left thoracic wall, and a solitary metastasis, 2 cm in diameter, in the right lung. Both tumors showed similar histologic features: highly cellular spindle cell sarcomatous growth with a herringbone pattern, focal collagen production, and numerous mitotic figures. The histology of both lesions was identical to that of the primary tumor and earlier recurrences.

Samples obtained from the sixth local recurrence and the lung metastasis were processed for cytogenetic analysis as previously described [2]. In both tumors, two clones were detected. The major clone of the local recurrence had chromosome aberrations identical to those found in the previously investigated tumor, giving the karyotype 43,Y,t(X;18)(p11;q11),t(2;15)(p23:q26),- 3, + der(3)dic(3:?)(p11:?),- 5, + der(5)ins(5;?)(qllq13;?)t(5;?)(p15:?),t(7;22)(qll:q13),- 1 1 , - 1 8 , - 19, 21, + mar. In addition to these changes, the rearrangement t(4;13)(p14;q13) was present in a minor clone: the majority of these cells were hypotetraploid, with 85 and 86 chro- mosomes. Two clones were also detected in the metastatic tumor. In addit ion to the changes described in the karyotype above, one clone had - 1 0 and 16q+, and the other 10, 14, and 16q+.

None of the abnormalities t(4;13)(p14:q13), - 1 0 , - 1 4 , and 16q+ had been found in the previously analyzed tumor, even as nonclonal changes. It seems rea- sonable to suggest that tumor cells remaining from the fifth local recurrence had expanded clonally to give rise to the present recurrence, and that the subclone with t(4;13)(p14:q13) evolved only relatively late. The finding of 10 and 16q+ in all metaphases from the metastasis but in none from the recurrent tumor indicates that these changes emerged at or shortly after the time when the cells metastasized to the lung. Later loss of one chromosome 14 gave rise to a side-line.

Supported by grants from the Swedish Cancer Society, the Swedish Work Environment Fund, the JAP Foundation for Medical Research and the Lund University Medical Faculty.

N. MANDAHL S. HElM K. ARHEDEN A. RYDHOLM H. WILLI~N F. MITELMAN

Departments of Clinical Genetics, Orthopedics, and Clinical Pathology Lund University Hospital

S-221 85 Lurid, Sweden

139

Page 2: Separate karyotypic features in a local recurrence and a metastasis of a fibrosarcoma

140 N. M a n d a h l et al.

REFERENCES

1. Mandahl N, Helm S, Arheden K, Rydholm A, Will6n H, Mitelman F {1988): Multiple karyo- typic rearrangements, including t(X;18)(p11;q11), in a fibrosarcoma. Cancer Genet Cytoge- net 30:323-327.

2. Mandahl N, Heim S, Arheden K, Rydholm A, Will6n H, Mitelman F (1988): Three major cytogenetic subgroups can be identified among chromosomally abnormal solitary lipomas. Hum Genet 79:203-208.