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Biomedical subjects

N Wake

Publications and source records attributed to N Wake.

At least 91 records · Page 5Linked to original sources
PubMed1984

Serial cytogenetic analysis of a recurrent malignant melanoma.

A metastatic malignant melanoma in a 54-yr-old white female was examined cytogenetically on three different occasions. We found two different clones, one hypodiploid and another hypertriploid; however, both clones had the same markers [i.e., der(6),t(6;17), and der(17),t(1;17)]. Detailed analysis of the histopathology and clinical course suggests that these two different clones reflected different morphology and results of therapy.

Chromosome Aberrations↗
PubMed1984

Malignant potential of homozygous and heterozygous complete moles.

There are two main mechanisms of origin for complete hydatidiform mole: (a) fertilization of an empty egg by a haploid sperm followed by duplication (monospermic mole); and (b) fertilization of such an egg by two haploid spermatozoa (dispermic mole). The former is inevitably homozygous (homozygous mole), whereas the latter may be heterozygous for a given genetic marker (heterozygous mole). A recent cytogenetic study showed that three cases of choriocarcinoma were undoubtedly heterozygous, which prompted us to compare the incidence of postmolar sequelae between patients with homozygous moles and those with heterozygous moles. Making use of chromosomal heteromorphisms and human lymphocyte antigen and phosphoglucuromutase 1 polymorphisms, we established the androgenetic origin of a complete mole in 49 of 56 cases. Homozygosity was confirmed in 21 moles, and heterozygosity was confirmed in five. Three of five patients with heterozygous moles developed postmolar trophoblastic disease, whereas none of the 21 patients with homozygous moles suffered postmolar trophoblastic disease except one who showed signs of degenerating residual trophoblasts. Consistent with this observation is the fact that all of the four destructive moles studied here were of dispermic origin. Thus, heterozygous moles seem to have a higher malignant potential than do homozygous moles.

Chromosome Aberrations↗
PubMed1984

Chromosome changes in soft tissue sarcomas.

An analysis of chromosome aberrations in human tumors was performed in 29 cases of soft tissue sarcoma. The tumor tissues were disaggregated with collagenase and the cells cultured for 2-3 days. Analyzable metaphases were obtained in 15 cases, 4 of which showed only normal karyotypes. The remaining 11 tumors showed various numerical and structural abnormalities in their karyotypes: 8 tumors were near-diploid and the remaining 3 were near-triploid. G- and Q-banding analyses revealed clonal abnormalities in the 11 cases with the presence of marker chromosomes; 15 different chromosomes were involved in chromosome rearrangements, chromosomes 1 and 2 being the most frequently affected. Because of the heterogeneity of the tumor group investigated (neurogenic sarcoma, 2 liposarcomas, neurofibrosarcoma, synovial cell sarcoma, fibrosarcoma, mesothelioma, leiomyosarcoma, rhabdomyosarcoma, Ewing's sarcoma, and hemangiopericytoma), it was impossible to reach any conclusion on the specificity of the cytogenetic abnormalities for a particular tumor type.

Adult↗
PubMed1984

[A study for the genesis of trophoblastic tumor, with reference to its androgenetic origin].

Complete mole is an abnormal human pregnancy which is characterized by grossly swollen villi in the absence of a fetus. It has been widely accepted that of all forms of pregnancy that leads to choriocarcinoma, the risk associated with moles is by far the highest, being 2000 to 4000 times greater than that of normal pregnancy or abortion (1). However there has been no direct proof that choriocarcinoma indeed derives from complete mole. In the present study, to shed some light on the genesis of trophoblastic tumor, chromosome, HLA and PGM1 polymorphisms were examined for complete moles and choriocarcinomas. As a result, it has been ascertained that complete mole was androgenetic in origin; the entire genome of the molar conceptus was paternally derived. More than ninety percent of cases were resulted from fertilization of an empty egg (i.e. the nucleus was either eliminated or inactivated) by a haploid sperm. The paternally derived haploid set then duplicated without cytokinesis and restored diploidy. This class of moles had invariably a 46, XX karyotype and was completely homozygous for any genetic markers. Fertilization of an empty egg by two spermatozoa could elucidate remaining cases. The androgenetic origin of complete mole has provided us with a means to directly evaluate the relationship between choriocarcinomas and their putative forerunners; complete homozygosity and exclusive inheritance of a paternal genome would be expected if the tumor arose from complete mole derived from the former mechanism. However, the heterozygosity observed in choriocarcinoma cells suggested that the tumor did not arise from moles which originated from the fertilization of an empty egg by a haploid sperm.(ABSTRACT TRUNCATED AT 250 WORDS)

Choriocarcinoma↗
PubMed1983

[Studies on non-surgical therapy of tubal pregnancy].

8 cases of tubal pregnancy in the pre-abortional stage were detected by B-scope examination. The administration of MTX (total doses: 60-300mg) resulted in complete remission in 7 cases; the other received tubectomy because of the progression of abortion. The dose of MTX used to obtain remission is responsible for the HCG titer of urine before the treatment; 60-150mg of MTX was sufficient in cases which showed a titer below 1,000iu/l, although 75-300mg was necessary in cases over 4,000iu/l. The patency of tubes after the regimen was confirmed in 4 out of 5 cases with hystero-salpingography. Serious side effects were not observed in the present study in spite of the great efficacy; transient suppression of liver has been observed in 2 cases. Two patients had normal intra-uterine pregnancy subsequent to the treatment; one had a matured full-term female neonate and the other received D & C in 9 gestational weeks. These results suggest that the MTX regimen is practical for the treatment of patients with tubal pregnancy. This is characterized by unimpaired fertility following the treatment, although the detection of patients in the pre-abortional stage is absolutely necessary.

Adult↗
PubMed1982

Chromosomes and causation of human cancer and leukemia. XLVIII. T-cell acute leukemia in ataxia telangiectasia.

Cytogenetic and immunologic studies were performed on the cells of an 18-year-old female with ataxia telangiectasia (AT) associated with acute lymphocytic leukemia (ALL). At the onset of the leukemia 15.4% of peripheral blood cells stimulated with phytohemagglutinin (PHA) contained a tandem translocation of the long arm of chromosome #14, i.e., t(14;14). To ascertain if these karyotypically abnormal cells and the leukemic cells had a common lineage, chromosome analyses were performed on bone marrow cells. Examination of the marrow cells on the seven occasions when leukemic cells were present in the marrow, including times when they were predominant, showed only a normal karyotype without the presence of t(14;14). However, an abnormal clone, which had the karyotype 45,XX,-9,t(9;6)(q12;q13), was identified in the marrow cells on the last examination during the terminal phase of the leukemia. Immunologically, the ALL was classified as an atypical type which had characteristics in common with certain T-cell subsets. We suggest that the malignant cells did not originate from the preexisting cells with a tandem duplication of the 14q.

Adolescent↗
PubMed1982

Chromosomes and causation of human cancer and leukemia. XLVII. severe hypodiploidy and chromosome conglomerations in ALL.

A case of acute lymphoblastic leukemia (ALL) of the L1 type with severe hypodiploidy in the marrow cells (modal chromosome number, 36) is described. In addition, most of the metaphases contained chromosome conglomerations which consisted of varying numbers of chromosomes and appeared similar to conglomerations previously observed by us in a case of chronic myelocytic leukemia (CML) in the blastic phase (BP), where some cells contained less than 20 chromosomes. The karyotype of the ALL cells of our case was similar to those of published near-haploid ALL cases, possibly indicative of a common pathway of cytogenetic evolution.

Blood Cell Count↗
PubMed1982

Genetic instability coupled to clonal selection as a mechanism for tumor progression in the Dunning R-3327 rat prostatic adenocarcinoma system.

The androgen-sensitive Dunning R-3327-H prostatic adenocarcinoma has been maintained by continuous serial passage in intact male rats for many years. While it has been possible to maintain the original characteristics of the well-differentiated H tumor over 16 years, there have evolved spontaneously, however, more aberrant sublines from this tumor at several subpassages in intact male rats. Serial passage of these individual sublines has established five additional R-3327 tumors each with distinct phenotypes and each more aberrant than the parent H tumor. In addition, it has been possible by passage of the H tumor in castrated male rats to obtain a well-differentiated slow-growing adrogen-insensitive tumor termed the Hl-S tumor. The continuous serial passage of this Hl-S tumor has likewise resulted in the emergence of three new types of Dunning tumors. The results from the biochemical and chromosomal studies presented demonstrate that there is a consistent association in each of these tumor progressions between the expression of genetic instability, which results in the addition of phenotypically new clones of cells to the tumor population, and the subsequent selection of these newly developed clone. These results suggest that the process of genetic instability coupled to clonal selection is one mechanism for the change in tumor phenotype characteristically associated with tumor progression within this system of prostatic tumors.

Adenocarcinoma↗
PubMed1982

Chromosomal changes associated with progression of the Dunning R-3327 rat prostatic adenocarcinoma system.

Several distinct sublines have developed upon serial passages of the original Dunning R-3327-H rat prostatic tumor. These tumors, each in different progressional stages, have been examined cytogenetically in the present study in order to explore the role of chromosomal changes in tumorigenesis. The original parent H tumor, from which all the other tumors were derived, has a normal karyotype, suggesting that visible alterations in chromosome structure are not essential in the early stages of the tumor. Nonrandom involvement of chromosome 4 in abnormalities observed in the increasingly aberrant tumors derived from the H tumor indicates that chromosomes most often affected may carry genetic material which is important in the regulation of cell proliferation and that this genetic material needs to undergo changes in the process of malignant transformation. Cytogenetic analysis of the Dunning sublines as a group indicated that the karyotypes of the tumors in later progressional stages tend to deviate more from the normal than those found in earlier stages. Comparison of chromosomal changes and phenotypic characteristics observed in this series of tumors suggested that the growth rate, dedifferentiation, and attainment of metastatic ability were related to the chromosome variation. The appearance and clonal development of tumor cells with a typical translocation, i.e. t(4;7), accelerated tumor growth rates of the differentiated tumors. Duplication of chromosomes was associated with a markedly increased growth rate and dedifferentiation of tumor cells in the anaplastic tumors. In addition, chromosomal loss from tetraploidy and development of complex rearrangements were associated with attainment of metastatic ability. These results point to the importance of chromosome changes in the development and biology of tumors.

Adenocarcinoma↗
PubMed1982

[The propensity to malignant changes in heterozygous moles].

There are at least two mechanisms of origin for complete mole, each with different genetic implications; 1) the fertilization of an empty egg by a haploid sperm and its subsequent duplication (homozygous mole), 2) the fertilization of such an egg by two haploid sperms, which produces an heterozygous constitution of allelic genes (heterozygous mole). The present study was undertaken to investigate whether the difference of origin would determine whether the moles underwent malignant transformation or not. By using of chromosomal, enzymatic and HLA polymorphisms, 35 moles were confirmed to be androgenetic in origin. Among them fifteen homozygous and 4 heterozygous moles were identified. The persistency of high HCG titration of the urine in the mother was observed in all 4 cases from the latter (4/4-100%), though the percentage of the development of sequelae in the former was low (1/15-6.7%). The diagnosis of destructive mole was established in the uterine lesion of 2 heterozygous moles by pathological examination. These two patients had lung metastases. A high incidence of sequelae after the expulsion of heterozygous moles suggests that the heterozygous constitution of allelic genes plays an important role in the process of malignant transformation of trophoblasts.

Adult↗
PubMed1981

Chromosomes and causation of human cancer and leukemia. XLIV. A method for chromosome analysis of solid tumors.

Mechanical and enzymatic disaggregation procedures have been utilized for the preparation of materials suitable for chromosome examination of tissues from various kinds of solid tumors. A great number of the cells disaggregated with the latter procedure were observed to attach to the bottom of culture flasks after 2 days in vitro; cells obtained with the former method were not attached. In general, the enzymatic procedure yielded a significantly larger number of viable cells that would undergo mitosis after short term culture and considerably improved the quality of banding as compared to the mechanical method. However, there were no significant differences among the basic karyotypes observed in the cells obtained by the mechanical approach versus those seen following the enzymatic method. This evidence, together with the high success rate of karyotyping in the enzyme-treated preparations, suggest that this should be the procedure of preference for cytogenetic examination of various tumors, particularly where in the past karyotypic examination has been very difficult, e.g., the early stages of tumor development.

Cells, Cultured↗
PubMed1981

Chromosome and cellular origin of choriocarcinoma.

The preferential association of choriocarcinoma with complete moles has long been recognized. In fact, of all forms of pregnancy that lead to choriocarcinoma, the risk associated with hydatidiform moles is 2000 to 4000 times greater than that of normal pregnancy or abortion. In order to corroborate the cell lineage between hydatidiform moles and choriocarcinoma, we investigated the chromosomal constitution and polymorphisms in the latter cells. Three choriocarcinomas from three women with a previous history of hydatidiform moles were examined chromosomally. Two hundred thirteen cells were analyzed for their chromosome number by conventional Giemsa staining; karyotyping of 33 cells with Q- and C-banding revealed 13 kinds of structural abnormalities unequivocally identified as of clonal origin. Two cases exhibited involvement of the long arm of chromosome 1 in rearrangements. Complete homozygosity and exclusive inheritance of a paternal genome would be expected if the tumor arose from a preceding molar pregnancy. However, the heterozygosity observed in choriocarcinoma cells suggests no common cellular lineage with complete moles; the latter originate through fertilization of an "empty egg" by a haploid sperm, followed by duplication of the chromosomes. Several possibilities have to be considered for the origin of choriocarcinomas, since it seems unlikely that alterations in the paracentric areas of the marker chromosomes occurred during tumor development. One possibility is that moles which are characterized by heterozygosity may transform into choriocarcinomas. Another possibility is that such tumors may originate from trophoblasts of the conceptuses rather than from moles.

Adult↗