Publications by authors named "Pandis N"

Cytogenetic aberrations have until now not been reported in mammary hamartomas. The finding of multiple, karyotypically abnormal clones in short-term cultures from 2 such tumors supports the interpretation that these are genuinely neoplastic lesions. The deletion del (3) (p13p14) and trisomy 18, both known to occur as primary chromosome abnormalities in breast carcinoma, were among the clonal changes in one case each.

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Tissue samples from a malignant melanoma of the anal canal and its local metastasis were short-term cultured and analyzed cytogenetically. Complex chromosome aberrations were found in the primary tumor, yielding the karyotype 49-50,X,-Y,der(1)t(1;13)(q44;q12),+der(2)t(2;8) (q31;q12),der(6)t(5;6)(q13;q21),+del(6)(q12q21),+7, der(8)t(6;8)(p12;p21),del(11)(p11),der(11)t(11;12) (p15;q24),der(15)t(6;15)(p21;p11-13),+der(20)t(1;20) (q12;q13),der(22)t(11;22)(p11;p11)[34]/88-100,idemx2[3]. In the local metastasis, the same near-tetraploid abnormal clone was detected, indicating that the cell population was clonally stable during tumor progression.

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Chromosome banding analysis of 97 short-term cultured primary breast carcinomas revealed clonal aberrations in 79 tumors, whereas 18 were karyotypically normal. In 34 of the 79 tumors with abnormalities, two to eight clones per case were detected; unrelated clones were present in 27 (34%) cases, whereas only related clones were found in seven. These findings indicate that a substantial proportion of breast carcinomas are of polyclonal origin.

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Cytogenetic analysis of short-term cultures from 52 primary colorectal adenocarcinomas revealed clonal chromosome aberrations in 45 tumors, whereas the remaining 7 had a normal karyotype. More than 1 abnormal clone was detected in 26 tumors; in 18 of them, the clones were cytogenetically unrelated. The modal chromosome number was near-diploid in 32 tumors and near-triploid to near-tetraploid in 13.

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Cytogenetic analysis of short-term cultures from 15 cases of benign proliferative breast disease (PBD), 10 diffuse PBD and 5 papillomas, and 15 fibroadenomas of the breast revealed clonal chromosome abnormalities in 7 diffuse PBD lesions, 4 papillomas and 5 fibroadenomas. The remaining 14 cases had a normal female chromosome complement. Cytogenetically unrelated abnormal clones were seen in 4 fibroadenomas and 2 PBDs.

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Short-term cultures of 29 samples of fibrocystic breast disease were cytogenetically analyzed. Clonal chromosome aberrations were found in six specimens, whereas the remaining 23 had a normal karyotype. Three of the abnormal samples displayed karyotypic anomalies previously associated with breast cancer, i.

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Cytogenetic analysis of short-term cultures of five phyllodes tumors of the breast-classified as benign (one tumor), borderline malignant (two tumors removed from the same breast in 1991 and 1993), and malignant (two tumors)--revealed clonal changes with simple structural abnormalities in the benign tumor, the borderline malignant tumors, and one malignant tumor in which benign areas and areas of borderline malignancy were also present. In contrast, the malignant tumor without admixed borderline malignant or benign areas had a complex karyotype. The karyotype of the benign phyllodes tumor was 46,XX,del(12)(p11p12)/46,XX,t(8;18)(p11;p11)/46,XX.

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Cytogenetic analysis was performed on short-term cell cultures of two foci (A and B) from each of three multifocal breast carcinomas. In case I, four clones (three related and one unrelated) were detected in sample A. In sample B, two of the three related clones and the unrelated clone seen in A were found, as was also a third subclone showing a pattern of clonal evolution slightly different from that detected in A.

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A girl who had been treated, apparently successfully, with surgery and chemotherapy for a hepatoblastoma, fell ill two years later with what was diagnosed as an AMF M(4). A cell line was established from her peripheral blood. This cell line had epithelial morphology and grew both in suspension culture and as a monolayer.

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Scientific methods and models are interdependent. That the techniques one uses determine which findings one gets, is evident. But equally important is the influence of our a priori expectations; they may cause us to choose inadvertently those methods that are most likely to yield results that appear to confirm an already preconceived picture of reality.

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A cell line was established from a liver metastasis of a periampullary pancreatic carcinoma in a patient with Gardner's syndrome. The primary tumor, the liver metastasis, and passages 6 and 15 of the cell line were characterized cytogenetically. The only aberration common to all samples was a der(15)t(8;15); this was probably the primary chromosomal abnormality.

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Short-term cultures from three carcinomas of the gallbladder were cytogenetically analyzed. All three had an abnormal karyotype. The modal chromosome number was near- or hypertriploid in two tumors and near diploid in the third.

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The relationship between cytogenetic findings and clinicohistopathological parameters was assessed in 29 patients with pancreatic adenocarcinoma. Karyotypic analysis revealed normal karyotypes (N) in 8 carcinomas and abnormal karyotypes (A) in 21. Within the A group, 8 cases had simple chromosome abnormalities (As), i.

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Short-term cultures from a primary carcinoma of the Fallopian tube, a tumor type not characterized before by chromosome banding, were examined cytogenetically. Complex chromosome aberrations were found in all mitoses, yielding the karyotype 41,XX,del(1)(p34),del(2)(q31),i(8)(q10),-9, + dic(9;19)(p13;p13), der(12)t(9;12)(p13;q22),-13,-16,-17,-18,-19,-22, +r [61]/84-86,idemx2[15]. Several of the aberrations in the present case are similar to changes found in adenocarcinomas of other organs, including carcinomas of the ovaries and uterus, indicating pathogenetic similarities between Fallopian tube malignancies and the more common gynecologic cancers.

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Cytogenetic analysis of short-term cultures from colorectal adenomas revealed acquired clonal chromosome aberrations in 14 of 17 tumors. In 4 adenomas, only numerical changes were found, whereas 10 had structural rearrangements. Trisomy 7 was found as the sole change in one of the tumors and together with other numerical changes in another.

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Cytogenetic analysis of adenolipomas of the breast, a tumor type that has not been chromosomally characterized before, revealed the karyotypes 47,XX, +del(1)(p22) in one tumor and 46,XX, t(12;16)(q15;q24) in the other. Breast adenolipomas thus seem to be karyotypically identical to sporadic lipomas in other locations: rearrangements of 12q13-15 are the most common cytogenetic aberrations in lipomas, and also breaks in and around 1p22 have been reported in such tumors. The similarity with lipoma could be documented further in case 2, in which epithelial and mesenchymal cells were cultured separately; the t(12;16) was present in the latter but not in the former.

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Cytogenetic analysis of short-term cultures from 52 colorectal carcinomas revealed a normal karyotype in 13 and clonal chromosome aberrations in 39 tumors. In the abnormal group, 13 tumors had simple numerical changes only, whereas 26 had at least one structural rearrangement with or without concomitant numerical changes. The most common numerical abnormalities were, in order of decreasing frequency, +7, -18, -Y, +8, +13 and -14.

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Cytogenetic analysis of short-term cultures of one non-secreting and one prolactin-producing pituitary adenoma revealed simple clonal numerical abnormalities in both tumors. The karyotype of the non-secreting adenoma was 48,XX, +4, +9[42]/49,XX, +4, +9, +20[2]/46,XX[6]. In the prolactin-secreting adenoma, three aberrant clones were detected, giving the karyotype 45,X, -Y[20]/47,XY, +Y[6]/45,XY, -21[3]/46,XY[21].

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Short-term cultures from 20 pancreatic tumours, three endocrine and 17 exocrine, were cytogenetically analysed. All three endocrine tumours had a normal chromosome complement. Clonal chromosome aberrations were detected in 13 of the 17 exocrine tumours: simple karyotypic changes were found in five carcinomas and numerous numerical and/or structural changes in eight.

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Cytogenetic analysis of short-term cultures from benign intestinal tumors revealed clonal chromosome aberrations in five colorectal adenomas, one adenoma of the papilla Vateri, and one hyperplastic polyp of the rectum. One adenoma had numerical aberrations only, but in all other tumors structural rearrangements were found that led to loss of genetic material from 1p. In three of the cases, the deletion was restricted to the 1p36 band; the rest had lost larger 1p segments.

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Interstitial deletions of the short arm of chromosome 3 were found in short-term cultures of five breast carcinomas (of 41 breast cancers with clonal aberrations analyzed by us during the same period). They were the only clonal structural change in three tumors; in the remaining two, the clone with 3p-coexisted with seemingly unrelated clones that had other structural and numerical aberrations. The deletions were identical, del(3)(p12p14), in four cases.

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Background: Little is known about the karyotypes of colorectal carcinomas and, in particular, about how the cytogenetic findings correlate with clinicopathologic features.

Methods: Short-term cultures from 49 colorectal adenocarcinomas were analyzed cytogenetically. The karyotypes were correlated with grade, stage, lymphocytic infiltration, and site (using the chi-square test), with patient age and tumor size (using the Student t test), and with survival (using the log-rank or Mantel-Haenszel test).

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Short-term cultures from 20 breast carcinomas were analyzed cytogenetically. A normal female chromosome complement was found in 4 cases. Clonal chromosome aberrations were detected in 16 tumors.

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Cytogenetic analysis of short-term cultures of a nonneoplastic focal steatosis of the liver showed trisomy 7 as the sole chromosomal change. This finding, especially when viewed in light of previous reports describing +7 in nonneoplastic tissues, strongly suggests that trisomy 7 cannot be considered a tumor-specific abnormality when it occurs as the only change. The cell type in which +7 is present is not yet known.

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