The Role of a Secondary Constriction of a Tumour Chromosome

Melander, Yngve

doi:10.1111/j.1601-5223.1963.tb01878.x

Cited by 13 publications

(2 citation statements)

References 21 publications

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“…The chromosomes of various ELD strains have been studied on many occasions by members of the Cancer Chromosome Laboratory at Lund ( LEVAN 1954;TJIO and LEVAN 1954;HANSEN-MELANDER 1958;ISING 1958;LEVAN 1959;MELANDER 1963;NIELSEN 1967NIELSEN ,1969NIELSEN ,1971NIELSEN , I972,1973NIELSEN ,1974aNIELSEN , b, 1975NIELSEN , 1976a. With conventional staining techniques it was possible only to distinguish the above-mentioned markers from the large mass of telocentric chromosomes of different length.…”

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confidence: 99%

Chromosomal evolution in the Ehrlich-Lettré complex of hyperdiploid mouse ascites tumors: Results from seven laboratory strains

Nielsén

2009

Hereditas

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NIELS~N, K. 1976. Chromosomal evolution in the Ehrlich-Lettre complex of hyperdiploid mouse ascites tumors: Results from seven laboratory strains. -Heredim 84: 77-108. Lund, Sweden,The chromosomes of 7 strains of the hyperdiploid Ehrlich-Lettre mouse ascites tumor (ELD) were analyzed by conventional stainings and by Gand C-bandings. A tendency to slow decrease in chromosome number during a 20-year period was revealed in the 7 strains and in the ELD complex in general. A G-band idiogram of the normal mouse chromosomes was elaborated with numbering of regions and bands. By G-band analysis the following average composition of the ELD karyotypes was indicated: unchanged mouse chromosomes (30",), marA, marB, minutes ( I I " o ) , marl -marl2, telocentric markers ( IOU<), anonymous telocentric markers, often strongly rearranged (50%). Great differences were revealed among normal chromosomes and markers in their capacity to persist in the tumor stemline as structurally stable units. The presence of some unchanged chromosomes in most cells of all 7 strains indicated that they involved selective advantage. Evidently chromosomal evolution has operated by preferably maintaining certain elements unchanged and by submitting other elements to heavy rearrangement. The C-band analysis showed that, in addition to the centromeric C-heterochromatin present in all chromosomes, some had interstitial C-bands, as marA in all strains, mar5 and mar7 in specific single strains, and others in numbers varying among the strains.

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Chromosomal evolution in the Ehrlich-Lettré complex of hyperdiploid mouse ascites tumors: Results from seven laboratory strains

Nielsén

2009

Hereditas

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“…The G-and C-band patterns of marA of the present ascites cells were identical with those of the seven sublines just mentioned. The number of marA per cell was proportionate to the total number of chromosomes per cell and marA showed no signs of decrease, which sometimes has been noticed after polyploidization and environmental changes (MELANDER 1963;BOONE et al 1965;STEPHENSON and STEPHEN-SON 1973;NIELSEN 1976b). Biarmed markers.…”

Section: Chromosome Numbers and Morphologymentioning

confidence: 93%

Chromosome band patterns of near tetraploid Ehrlich-Lettré mouse ascites cells (ELT Bonn) in vivo and in vitro

Nielsén

Granzow

2008

Hereditas

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Chromosomes in burkitt lymphomas. I. Serial studies in a case with bilateral tumors showing different chromosomal stemlines

Gripenberg¹,

Levan²,

Clifford³

1969

Intl Journal of Cancer

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The chromosornes of a Burkitt lymphoma case were j X o w e r l through a pwiod of three months, including stages before treatment and during trcatment and progression. The patient had bilateral facial tuniors with nietastascs to lymph nodes on either side of the neck. The chromosomal stemlines wore diffiwnt on the left and the right side. Both were diploid, the left side representing the normal karyotype, the right side exhibiting a number of marker chromosomes. This difliwnce characterized both the facial tumors and the neck metastases. During early stages of the right-side tumor, the marker chrornowmcs M 2 and MC predominated. Both were derived from C group chromosomes and had a constriction on their longer arm, separating a distal segment froni thij rest of the chromosome. M 2 had the uppearance of a small No. 2 chromosome, MC thut of a large C chroniosorne. Lutrr on, M 2 was replaced by M I through ircmslocation of the distal segnient to a No. I chroniosome. Two other marker chromosomes M B and M D resembled B and D chromosomes, respectively, with elongated long arms. A t terminal stages of the diseasc, whcn chetnotherapeutic treatments had been administered repeatedly, highly d i s t u r b d chromosome conditions put vailed with numerous signs of chromosome breakage and errors of spiralization. Also u c u l t u r d cell line established at an early stage from the right-side tiimor showed a high incidence oj' similar aberrations. AN the marker chrotnosonies, except M I , were rcwvered in the culture. IN VlVO I N VITRO J MZMC J M2MCMD M 2MCMD I M B f--Xirradiated cells MB t Orthomerphalan MBDiagram showing the evolution of the markers in the right-side tumor.

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The Role of a Secondary Constriction of a Tumour Chromosome

Cited by 13 publications

References 21 publications

Chromosomal evolution in the Ehrlich-Lettré complex of hyperdiploid mouse ascites tumors: Results from seven laboratory strains

Chromosomal evolution in the Ehrlich-Lettré complex of hyperdiploid mouse ascites tumors: Results from seven laboratory strains

Chromosome band patterns of near tetraploid Ehrlich-Lettré mouse ascites cells (ELT Bonn) in vivo and in vitro

Chromosomes in burkitt lymphomas. I. Serial studies in a case with bilateral tumors showing different chromosomal stemlines

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