The reaction of rabbits to Rous sarcoma virus.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to J Mark.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
The cytogenetical findings in two cases of cultured salivary polymorphous low-grade adenocarcinoma (PLGA) are reported. The first PLGA was a carcinoma ex pleomorphic adenoma of the parotid gland. This had a pseudodiploid stemline characterized by extensive and complicated structural rearrangements. The chromosomal findings showed many similarities to those in the only previously studied case of PLGA (also a carcinoma ex pleomorphic adenoma of the parotid). The results in both could fit with abnormalities superimposed on those typical of mixed tumors. The second PLGA reported derived from a minor salivary gland. It showed a completely different picture, distinguished by a hypodiploid, almost exclusively numerical, variation and the occurrence of a stemline characterized by only monosomy 22. Etiological differences were proposed as one possible explanation for the cytogenetical differences between the two types of PLGA.
This report concerns the first cytogenetical study of a benign salivary gland oncocytoma. The cultured tumor was studied in five consecutive preparations. The first three were dominated by cells with a normal karyotype. In the two subsequent preparations a hyperdiploid stemline characterized by trisomy 7 had taken over. Trisomy 7 has previously been observed in a number of different, benign, premalignant and malignant conditions. We interpreted trisomy 7 in the salivary gland oncocytoma, as in these other conditions, to be a neoplasia-related, probably primary, gross chromosomal change and not an expression of aging or comparable events in normal cells.
Using banding techniques the chromosomes were studied in 15 leiomyomas. The material comprised nine uterine myomas from one patient, one parametrial leiomyoma from a second patient and five tumors from a third patient with disseminated peritoneal leiomyomatosis. The results were considered together with pooled data from the literature. From this it could be concluded that: (1) each leiomyoma was the product of a separate clonal development; (2) different leiomyomas from the same patient sometimes showed an identical abnormal stemline (possibly because of etiological influences); (3) uterine and extra-uterine leiomyomas seemed to follow similar evolutionary pathways in their chromosomal progression.
A clearly benign parotid tumor, an adenolymphoma, was studied cytogenetically using short-term cultured material. The first preparation showed only a normal stemline. The two subsequent preparations were both characterized by a pseudodiploid stemline with the karyotype 46,XY,del(7) (p12p14-15), t(11;19) (q21;p12-13). The 11;19 translocation was identical to that characterizing the abnormal stemline of the only previously studied case. These suggestive observations give rise to several questions, in particular whether or not all adenolymphomas contain cells with this specific reciprocal translocation and, in cases with the translocation, its implications at the molecular level.
Two malignant mesotheliomas were studied by banding techniques. Both neoplasms had a hypodiploid stemline. Five and eight marker chromosomes, respectively, were included in the stemline karyotypes. Monosomy 14, monosomy 22 and a No. 13 with an interstitial long-arm deletion were deviations found in both neoplasms. In addition, closely located regions in No. 1 and No. 3 were involved in both tumors in the formation of other marker types with dissimilar morphology.
Detailed observations by banding technique in 21 cultured human benign uterine leiomyomas are reported. More than half of the tumors (51%) had a primary or secondary abnormal stemline. The abnormal stemlines were usually characterized only by structural changes, in particular reciprocal translocations. These translocations, as well as instances of inversions, predominantly affected the chromosome types Nos. 1,2 and 12 and preferentially the regions 1p36, 2p24 and 12q14-15. Available data concerning cytogenetical deviations in benign human tumor types indicate that, in contrast to most malignant neoplasms, they are characterized by comparatively few and simple, either numerical or, more frequently, structural changes. The biological implications of these deviations are rapidly emerging as one of the most urgent areas for future studies with molecular techniques.
The chromosomal banding patterns in 20 human malignant salivary gland tumors are reported. Abnormal stem-and/or sidelines were observed in 14 cases, and abnormal clones and variant cells in the remaining 6 cases. No less than 8 tumors showed clonal rearrangements involving the long arm of chromosome 6, i.e. terminal deletions with breakpoints in the 6q22-25 region. The possible involvement of c-myb or a putative tumor suppressor gene in the 6q deletions is considered. Other recurrent deviations were loss of the Y chromosome, trisomy 8 and 11q- markers. The combined data from this and previous studies show that most of the rearrangements are not restricted to a certain type of malignant salivary gland tumor, but are seen in several tumor types, indicating a close evolutionary relationship between different malignant salivary gland tumors.
Using short-term cultures, the chromosomes in 19 human benign pleomorphic adenomas were studied by banding methods. The results were considered together with 81 previously reported adenomas. This survey showed that 53% of the 100 adenomas had a normal stemline. However, almost all cases with a normal stemline contained variant cells. Those with trisomy 7, trisomy 8, or loss of an X chromosome had progressional importance, as well as those variant cells containing markers composed of certain specific chromosome segments. In 47 adenomas a total of 50 abnormal stemlines were seen. They could be divided into four groups: (a) A large group with chromosome 8 involvement, usually translocation of the segment distal to 8q12; (b) A small group with chromosome 12 involvement, mostly translocation of the segment distal to 12q13-15; (c) A small group with translocations and/or deletions affecting a distal segment of either the short or the long arm of No. 3; (d) A small and heterogenous group with abnormalities which were related to those seen in variant cells from cases with a normal stemline. Comparisons between sites of localized oncogenes and deduced break points for markers in stemlines with only structural changes revealed accordance in 75% of the cases (33/44). It is noteworthy that almost 50% of the abnormal stemlines showed a proximal long-arm rearrangement of No. 8 that could fit with activation of the oncogene c-mos.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Using G-banding technique, the chromosomes were studied in four consecutive preparations from cultured material from a human adenoid cystic carcinoma of the submandibular gland. The results indicated that the carcinoma had originated with a normal diploid stemline, and that reciprocal translocations played a predominant role in development of an abnormal stemline. The propensity of developing variant cells, as well as an abnormal stemline, characterized by various types of reciprocal translocations, was found to be a property shared by two other types of salivary gland neoplasms studied by banding techniques, namely the pleomorphic adenoma and the acinic cell tumour. The tissue of origin is suggested to be the crucial determinant responsible for this important cytogenetical similarity between different types of salivary gland tumours.
The cytogenetical observations in the first double-minute (DM)-positive benign neoplasm, a human pleomorphic adenoma, are described. It is suggested that in the present adenoma the first DM was formed from a structurally and/or functionally specialized segment of the long arm of a chromosome No 12. If so, the results also indicate a close relation between chromosome regions preferentially involved in structural rearrangements in a certain tumour type and chromosome regions with the potential capacity to become released and behave and function as DMs.