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Biomedical subjects

S Kakati

Publications and source records attributed to S Kakati.

At least 19 recordsLinked to original sources
PubMed1991

Constitutional extra chromosomal element in a family with Wilms' tumor.

We report the presence of an extra chromosomal element in a family with Wilms' tumor (WT). This family has three children, two of whom were affected. One son, the proband, had bilateral and one daughter had unilateral WT. The first child, the father, and the mother did not have WT. The son with bilateral WT had a ring chromosome (R) both in the lymphocytes as well as in the kidney tissue. The size of the ring varied considerably from cell to cell. The daughter with unilateral WT had an abnormal clone containing a small chromosomal ring (r) in phytohemagglutinin (PHA)-stimulated and Epstein-Barr virus (EBV)-transformed lymphocytes. The mother had a karyotype similar to that of the daughter with WT. We hypothesize that the proband's ring chromosome could be the amplified form of the r inherited from the mother. Chromosome 11 was cytogenetically normal in all the cells examined of the affected children and the unaffected mother. In situ hybridization with a centromere-specific DNA cocktail indicated dispersed centromeric DNA both in r and R.

Adult↗
PubMed1988

Comparison of radiation-induced chromosomal damage between normal individuals and patients with familial polyposis coli.

Cultured leukocytes of peripheral blood obtained from normal, healthy individuals and from patients with familial polyposis coli (FP) were exposed to 0 rads or 300 rads of 137Cs gamma radiation at G0 to compare damage in these two groups. Only cells in the first mitotic division were considered. The average chromosomal damage in the FP patients was not significantly higher than that in the normal group. The induced chromosomal damage at G0 was normally distributed in both the control and the patient groups as well as when they were combined.

Adenomatous Polyposis Coli↗
PubMed1988

Abnormally banded region in a poorly differentiated sarcoma is not correlated with amplification of c-MYC or c-MOS protooncogenes.

A poorly differentiated sarcoma in a 32-year-old female revealed a large, abnormally banded region in one chromosome #8 in all metaphases. The modal karyotype was 46,XX, -8, +mar. Southern blot hybridization was performed with probes for two protooncogenes located in chromosome 8q (c-MYC and c-MOS). No amplification or rearrangement was observed to account for the cytogenetic abnormality.

Adult↗
PubMed1987

Cytogenetic findings in a primary adrenocortical carcinoma.

Cytogenetic analysis of a primary adrenocortical carcinoma revealed clonal rearrangements of several autosomes and sex chromosomes. In all metaphases the following marker chromosomes were present: 4p+,t(3;12)(p14;p13),14q+, t(15;20)(p11;q11), t(5;18) (p13.3;p11.2), psu dic(18)t(18.3)(p11.39;p12), and psu dic(20)t(20;9)(q11.2;p11). The results are discussed in relation to the cytogenetic findings in other solid tumors, especially of the kidney.

Adrenal Cortex Neoplasms↗
PubMed1986

Gardner syndrome in a man with an interstitial deletion of 5q.

Chromosome analysis of blood cells from a 42-year-old white male with mental retardation, colon carcinoma, horseshoe kidney, absence of left lobe of the liver, agenesis of the gallbladder, and possible Gardner syndrome revealed a constitutional marker chromosome due to del(5)(q13q15) or del(5)(q15q22). A polymorphic chromosome #22 with enlarged satellites was inherited from the father, who is phenotypically normal, and was probably unrelated to the congenital malformations. This is the first report of a Gardner syndrome patient with an interstitial deletion of 5q.

Chromosome Banding↗
PubMed1986

A method to generate microcells from human lymphoblasts for use in microcell mediated chromosome transfer.

A method is described to generate microcells from human lymphoblasts for use in microcell-mediated chromosome transfer (MMCT). Micronuclei were induced in cells from a human lymphoblastic cell line by prolonged colcemid treatment, and were separated from these lymphoblasts by: attaching the cells to Concanavalin A coated plastic slides designed for enucleation, and centrifuging the slides in medium containing cytochalasin B. Microcells of less than 3 microns in diameter were fused with thymidine kinase negative mouse fibroblasts (LMTK-). HAT medium (hypoxanthine, aminopterin, and thymidine) was used to select microcell hybrids expressing thymidine kinase activity. Positive clones were isolated and Q-banded for chromosome analysis. Unlike previous methods, this procedure permits microcells to be easily generated from lymphoid cells. The methodology of enucleation of microcells may be extended to a variety of other donor cell types which can be micronucleated but which do not adhere tightly to enucleation slides and do not exhibit extrusion subdivision. This feature makes our methodology particularly useful for constructing a library of hybrid clones containing one or a few human chromosomes.

Animals↗
PubMed1986

Use of radiation induced chromosomal damage in human lymphocytes as a biological dosimeter is questionable.

Using dicentric chromosomes and acentric fragments as indicators of radiation sensitivity, a study has been performed on human lymphocyte chromosomes by irradiating peripheral blood cells at G0. Donor-to-donor variation has been noticed regarding radiation sensitivity even when metaphase spreads were scored at the first cell cycle. Thus, it appears that, at the present state, use of chromosomal damage in peripheral blood cell cultures as an effective biological dosimeter for effects of radiation is questionable.

Biological Assay↗
PubMed1985

Chromosome changes in a secondary lymphoma.

A case of probable secondary lymphoma, poorly differentiated lymphocytic lymphoma (PDLL), is described in which two chromosomal translocations were observed, i.e., t(10;19)(q11;q13) and t(1;6)(q21;p11.1-2). A consistent numerical aberration was monosomy of chromosome #21. Accumulation of more data on secondary lymphomas is necessary in order to reach a general conclusion as to whether or not there are any nonrandom chromosomal aberrations that differentiate primary from secondary lymphomas.

Adenocarcinoma↗
PubMed1979

Chromosomes and causation of human cancer and leukemia: XXXVI. The 14q+ anomaly in an American Burkitt lymphoma and its value in the definition of lymphoproliferative disorders.

A case of a 10-year-old boy with American Burkitt lymphoma is presented in whom a 14q+ due to t(8;14)(q23;q32) was shown to exist in the ascitic lymphoma cells. This appears to be the first demonstration of such a translocation in uncultured material. In addition, another translocation involving the X chromosome, hitherto not observed in Burkitt tumors, was demonstrated. The karyotypic findings have been related to the cytogenetic experience in Burkitt and other lymphomas, with emphasis being put on the importance of the 14q+ anomaly in lymphoproliferative diseases.

Burkitt Lymphoma↗
PubMed1978

Chromosomes in solid tumors.

Systematic chromosomal studies in solid tumors have been scanty (excepting meningiomas), because of the fact that it is difficult to obtain tumor material at desired times and only in about 10--15% of the cases adequate chromosome preparations are suitable with a direct technique or short term culture. A few facts that emerge from the study of various solid tumors are as follows: 1. modal number of chromosomes in parimary tumors tends to be lower that of metastatic; 2. certain chromosomes and chromosome regions are more susceptible for breakage to oncogenic conditions, hence, there is non-random involvement of certain chromosomes in human neoplasia and 3. certain chromosome changes are more often associated with metastatic spread than others.

Chromosome Banding↗
PubMed1978

Sister chromatid exchange in Philadelphia chromosome (Ph1)-positive leukemia.

The sister chromatid exchange (SCE) frequency was studied in the leukemic cells of 12 patients, 10 with Philadelphia chromosome (Ph1)-positive chronic myelocytic leukemia (CML), 1 with Ph1-negative CML, and 1 with acute myeloblastic leukemia. Except for two patients in the blastic phase of CML, the SCE values were within the normal range [3.8 +/- 6.4 (S.D.) SCE/cell; normal is 3.3 +/- 2.2 SCE/cell]. In the two cases with the blastic phase of CML, the values were 7.6 +/- 3.2 and 8.9 +/- 4.7 SCE/cell, a statistically significant difference from the control values. However, in the patient with acute myeoblastic leukemia, the SCE incidence increased from 3.6 to 24.4 SCE per cell when therapy was changed to daunorubicin and vincristine and the disease became progressive. Further studies on SCE and leukemia may prove the usefulness of this determination for therapeutic and clinical purposes.

Adolescent↗
PubMed1977

Chromosomes and causation of human cancer and leukemia. XXII. Karyotypic changes in malignant melanoma.

Detailed karyotypic analysis with G- and C-banding has been performed on cells of four malignant melanomas. The modal number in two cases was in the hypodiploid range, the chromosome numbers varying from 39 to 43. These two tumors had 5 to 13 marker chromosomes. The other two tumors were in the polyploid range, with modal numbers of 63 to 157 chromosomes. The cells had a minimum of 11 and a maximum of 40 marker chromosomes. Chromosome no. 1 was more frequently involved in aberrations than any other chromosome. The most common breakpoints on this chromosome were 1q21, 1q25 and 1q32. Frequent breakpoints were also noticed in the centromeric region in various chromosomes. In chromosome no. 1, however, the centromeric area does not seem to be involved. The more common breakpoints on the various chromosomes were 1q21, 1q25, 1q32, 5p13, 9q13, 11q23, 12q13. No common markers were noticed among these four cases of melanoma, but are noticed in unrelated tumors.

Aged↗
PubMed1976

Chromosomes and causation of human cancer and leukemia. XIV. Origin of a large number of markers in a cancer.

A cancerous effusion from a patient with cancer of the breast, with a high modal number of chromosomes (81-83) and with 11-13 abnormal chromosomes (markers) of eight different origins, has been examined in detail karyotypically with C-, G-, and Q-banding techniques. Except for a rare chromosome, all the normal chromosomes were identified and, more importantly, the origin of all markers was ascertained. This study indicates the feasibility of identifying all the chromosomes in cancer cells, even in those with highly polyploid and complicated chromosome constitutions.

Adenocarcinoma↗
PubMed1976

Chromosomes and causation of human cancer and leukemia. XVII. Banding studies in acute myeloblastic leukemia (AML).

Chromosomes were studied in the bone marrow and/or blood cells from 38 patients with acute myeloblastic leukemia (AML). The initial analysis with conventional Giemsa staining revealed that 16 of the 38 patients with AML studied had chromosomal abnormalities. The cells of these 38 patients (16 with abnormal karyotypes and 22 with normal karyotypes) were re-examined with Q- and G-banding techniques. Twenty-two patients with conventionally stained normal karyotypes did not show any abnormalities, even with banding techniques. Three cases had a common translocation between the long arm of No. 8 and No. 21, i.e., [t(8;21)(q22;q22)], the so-called prototypic karyotype. Two cases had a 45, XX,-21 karyotype; and three cases had trisomy of the long arm of chromosome No. 1. The banding patterns revealed that in two of the three latter cases, the presence of the trisomy of the long arm of No. 1 apparently occurred late in the disease. Therefore, it is possible that the trisomy of the long arm of No. 1 might bear a relationship to selective growth advantage of the leukemic cells in some cases with AML. The presence of extra No. 8 and No. 9 chromosomes and deletion of the long arm of No. 7, frequently reported in several leukemic disorders, were also found in the present cases, but with other chromosomal abnormalities. Chromosomes No. 6,No. 15,No. 19,No. 20, and X were not involved in any structural and/or numerical changes. The present data suggest that some chromosomal changes are nonrandom in AML and that further chromosomal studies may lead to a division of AML patients into subgroups on the basis of their karyotypes.

Adult↗
PubMed1976

The chromosomes and causation of human cancer and leukemia. XIX. Common markers in various tumors.

Most human cancers are associated with abnormal (marker) chromosomes. In past and present studies banding analysis have uncovered a much larger number of markers in cancer cells than was seen with standard (Giemsa) staining. Furthermore, common markers of identical morphology and origin were found in tumors of related or unrelated tissues or organs, suggesting that in all probability such markers, although present in cancers of diverse nature, may indicate a common etiology, either related to the causation of the cancers, to the progression of the tumors, or to the predilection of certain chromosomes to undergo morphologic changes leading to marker formation. Even though some markers were common to different tumors, the bulk of the markers in the cancers studied could not be identified with certainty and their nature varied from tumor to tumor.

Aged↗
PubMed1976

C- and G-bands of the opossum chromosomes: terminal sequences of DNA replication.

The sex chromosomes of the opossum, Didelphys virginiana, are the only elements that exhibit C-banding. In contrast, the sex chromosomes as well as the autosomes bear specific G-Bands. However, unlike other mammalian species different types of G-banding are observed if the chromosomes are pretreated with trypsin and SSC solution The SSC-pretreated chromosomes show discrete bands only when stained with Giemsa at certain pH values. An asynchronous pattern of terminal DNA replication is observed among the three C-banding regions of the X-chromosome. The inter- and intrapositive G-banding areas of the chromosomes are not always late in DNA replication in comparison to those negatively stained G-banding areas.

Animals↗