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S Pathak

Publications and source records attributed to S Pathak.

265 records · Page 15Linked to original sources
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Chromosome alterations in cancer development and apoptosis.

Normal somatic cells are programmed to die (or undergo apoptosis) whereas cancer cells program themselves to survive. Some of the cytogenetic alterations that might be involved in apoptosis and continuous cell proliferation of normal and cancer cells such as shortening of telomeres, formation of dicentric chromosomes, transfer of telomeric DNA to the homologous chromosomes, malfunction (inactivation) of the centromeres, endoreduplication of chromosomes and other structural and numerical chromosome abnormalities are discussed here.

Aneuploidy↗
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Multiple specific chromosomal alterations in a rat ascitic histiocytoma 'AK-5'.

In the rat ascitic histiocytoma, AK-5, chromosome numbers vary between 33 and 41 with a peak at 40 chromosomes. None of the metaphase spreads showed double minute chromosomes. The karyotype of this tumor was characterized by hypodiploid chromosome constitution. Giemsa banding analysis revealed 12 clonal marker chromosomes (M1-M12). Tentative identification of these markers were: M1 = ins(1q); M2 = t(5;?); M3 = t(8;10); M4 = t(8;?); M5 = t(10;X); M6 - t(15;?); M7 = t(5;6); M8 = del(13p); M9-M12 = unidentified. M3 being a large near metacentric chromosome serves as a characteristic marker for this tumor. All marker chromosomes except M2 and M4 were present in single copy per cell. In some metaphases M2 was present in 2 copies while M4 was present in 2 or 3 copies per cell. The total cell cycle duration of AK-5 cells was 15.5 h and the different phases, G1, S, G2 + M were estimated as 1.2, 12.2, and 2 h, respectively.

Aneuploidy↗
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Chromosomal markers associated with metastasis in two colon cancer cell lines established from the same patient.

The purpose of this study was to identify specific chromosomal abnormalities that might be involved in colon cancer metastasis. For this reason, we performed extensive karyotypic analysis on two colon cancer cell lines (SW480 and SW620) established from two surgical biopsies taken at different intervals and representing different stages of the disease from the same patient. Despite the karyotypic heterogeneity, several marker chromosomes were shared between the two cell lines, indicating their common origin. We hypothesized that these shared chromosomal aberrations might be critical for the continuous growth of the tumor cells and, therefore, were retained through progression of the disease. Duplication of 16q and new or additional structural chromosomal abnormalities involving breakpoints 3p21, 8p11, 10q25, 13q14, 14q11 and 15q15 were observed as the characteristic anomalies only in the SW620 cell line. As SW620 was established from the abdominal metastatic lesion of the patient, we postulated that the acquisition of these new markers in the progression steps of the primary tumor might represent "hot-spots" that possibly contain genes crucial for metastatic potential in colon cancer.

Abdominal Muscles↗
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High frequency of telomeric association in a family with multiple congenital neoplasia.

Chromosomal analysis of the peripheral blood cultures of a married couple whose second pregnancy gave birth to twin daughters with multiple congenital malignancies revealed normal karyotypes of 46,XX and 46,XY, respectively. However, in the father's blood, 23.3% of metaphases showed telomere-telomere associations involving single-single and double-double chromatids. Such associations were not observed in the metaphases of the mother. We speculate from these observations that the father's genotype may somehow be responsible for the congenital malignancies in their twin daughters.

Adult↗
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Nonrandom chromosomal abnormalities in lymphocyte cultures of individuals with colorectal polyps and of asymptomatic relatives of patients with colorectal cancer or polyps.

We studied chromosomal alterations in the peripheral blood lymphocytes of 10 individuals with colorectal polyps and 10 asymptomatic first-degree relatives of patients with colon cancer or colorectal polyps. The analysis was performed on T-lymphocytes using short term blood cultures and on B-lymphocytes by establishing lymphoblastoid cell lines by Epstein-Barr virus transformation. Chromosomal changes were not common in T- and B-lymphocytes. Chromosomes 1 and 5 were most frequently involved in numerical or structural changes in the patients with polyps as well as in the asymptomatic relatives. These alterations were observed in either the T-lymphocytes or the B-lymphocytes but rarely in both, thus accentuating the importance of studying both the cultures concurrently. Chromosome 5, which is known to play an important role in the development of adenomatous polyps, was found to be involved in 6 (60%) of 10 patients with polyps and 4 (40%) of 10 asymptomatic relatives. These findings show that lymphocytic chromosomal analysis can aid in identifying individuals who are genetically susceptible and are at a higher risk of developing colorectal cancer. Because lymphocytic chromosomal analysis is relatively simple and inexpensive, we expect that it will be very useful in screening asymptomatic individuals who are at a higher risk due to inherited or environmental factors.

Adult↗
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Cytogenetic abnormalities in colon cancer patients: a comparison of T- and B-lymphocytes.

Cytogenetic analysis of peripheral blood lymphocytes of 19 colorectal cancer patients was carried out in short term blood cultures (T-cells) as well as in Epstein-Barr virus transformed B-cell lymphoblastoid cell lines. One hundred Giemsa-banded metaphases from the T lymphocytes and 50 metaphases from the B lymphocytes of each patient were evaluated for cytogenetic abnormalities. Clonality was not observed in every paired sample. Structural and/or numerical aberrations were most frequent in chromosomes #1, #2, #5, #7, #9, #12, #14, #17, #18 and #21. Aberrations among these chromosomes could be observed individually in either of the cultures, which proves that the analysis of both cultures (T and B cells) is complementary to each other. In some cases involving multiple primary cancers it was interesting that the specific chromosomal change, crucial for a particular malignancy, was identified only in the lymphoblastoid cell line analysis. This supports the notion that B-cell analysis can serve as a useful adjunct to the study of short-term blood cultures and also poses a question as to whether the specific chromosomal changes observed in the analysis are confined to the B-cell lineage.

Adenocarcinoma↗
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Genetic susceptibility to lung cancer as determined by lymphocytic chromosome analysis.

Chromosomal anomalies were analyzed in the lymphocyte cultures among 96 untreated lung cancer patients and 74 clinically normal comparison subjects. The analysis revealed that >15% of the lung cancer patients showed structural or numerical rearrangements in chromosomes 1,3,5,7,9,12,14, and 21. A case control comparison showed that these aberrations were significantly higher in chromosome 7 [odds ratio (OR) = 2.32; 95% confidence interval (CI), 1.14 and 4.82], chromosome 9 (OR = 2.61; 95% CI, 1.27 and 5.48), chromosome 12 (OR = 4.10; 95% CI, 1.40 and 14.54), and chromosome 21 (OR = 7.75; 95% CI, 1.73 and 70.80) of the patients than in the controls. However, only chromosome 9 (OR = 3.57; 95% CI, 1.33 and 9.46) and chromosome 21 (OR = 6.94; 95% CI, 3.15 and 9.98) retained significance after stratifying on smoking status. Among the lung cancer patients, the breakpoints cluster in specific regions of some of these chromosomes. These regions are 1p13-q21, 3q21-q13, 7p12-q12, 7q12-q12,7q22, 7q32, 9p13-q13, 12p13, 14q11, and 14q32. The distribution of lung cancer patients, according to histological types, showed that aberrations in chromosomes 1,7, and 9 dominated the scenario of chromosomal changes in non-small cell lung carcinomas. Thus, the data on lymphocytic chromosomal rearrangements in lung cancer patients not only indicate the importance of specific genetic changes in the etiology of lung cancer but also emphasizes the putative role of such analysis in determining primary genetic abnormalities in the large heterogeneous group of lung cancers.

Case-Control Studies↗
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Fluorescent in situ hybridization analysis in blood lymphocytes of lung cancer patients.

Genetic predisposition to lung cancer was determined by observing nonrandom chromosomal alterations in peripheral blood lymphocytes (PBLs) of lung cancer patients. The histological distribution of the cases showed that chromosomes 7 and 9 were frequently altered in squamous cell lung carcinoma (SCLC) patients. We analyzed PBLs of 26 SCLC patients and 5 controls using fluorescent in situ hybridization (FISH) with whole chromosome painting probes of chromosomes 7 and 9 to further investigate the frequency of rearrangements in these chromosomes. Our results suggested that seeking nonrandom aberrations in larger numbers of cells using FISH strengthened our previous observation of mosaicism and involvement of specific chromosomes in lung cancer patients. On combining our previous data, aberrations in chromosome 7 (16 of 26 patients), chromosome 9 (14 of 26), and the present study, we could actually pinpoint more individuals with abnormalities of chromosome 7 (23 of 26) and chromosome 9 (21 of 26). Thus, analyzing more cells in PBLs and adding FISH analysis serve as useful adjuncts to our studies of nonrandom chromosomal aberrations and genetic mosaicicm.

Adult↗
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Non-random primary and secondary chromosomal abnormalities in human gastric cancers.

By using Giemsa-banding and fluorescence in situ hybridization techniques, we have been able to identify primary and secondary cytogenetic abnormalities in four gastric tumors at different stages of development. Structural and numerical abnormalities were present in all four gastric tumors in chromosomes 3, 7, 11, and X. Other abnormalities involving chromosomes 1, 5, 6, 8, 13, 15, 17, 18, 19 and 22 were observed, but only in three advanced gastric tumors, suggesting that these were secondary/tertiary genetic defects. Based on these results it was possible for us to decipher primary and secondary genetic abnormalities in these four gastric tumors.

Biopsy↗
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A modified fluorescence in situ hybridization (FISH) technique.

We have modified and shortened the routine fluorescence in situ hybridization (FISH) technique by using microwave or formalin pretreatment for artificially aging and microwave heating only for dehydrating the regular chromosome preparations. The all-human telomere probe (Oncor, Inc., Gaithersburg, MD) was used on murine K-1735 clone X-21 melanoma cells for this purpose. The intensity of signals obtained by our modified technique(s) was comparable to that obtained by the routine procedure. However, pretreatment of slides with hydrogen peroxide (H2O2) completely obliterates the FISH signals.

Animals↗
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A simple bedside manoeuvre to detect ascites.

BACKGROUND: Shifting dullness and fluid wave are two techniques commonly used to detect ascites. However, these may fail to detect moderate or minimal ascites. Ultrasonography is a good non-invasive method to detect ascites but may not be available in distant rural areas of India. We assessed the utility of the puddle sign and auscultatory percussion for detecting ascites. METHODS: Sixty-six patients with suspected ascites were included in the study. Those with a previous history of ascites, or therapeutic paracentesis and in whom ascites was detected by shifting dullness or fluid wave were excluded. The puddle sign and auscultatory percussion were elicited in all the patients. Ultrasonography was used as the gold standard. To eliminate any observer bias the investigators were blinded to each others' findings. RESULTS: Auscultatory percussion had a greater sensitivity (65.7% v. 45%, p < 0.05) but a lower specificity than the puddle sign (48.4% v. 67.7%, p < 0.05). There were no significant differences between positive and negative predictive values and the positive and negative likelihood ratios. CONCLUSION: Auscultatory percussion is a better method than puddle sign for detecting ascites as it has a greater sensitivity.

Adult↗
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Paclitaxel and water-soluble poly (L-glutamic acid)-paclitaxel, induce direct chromosomal abnormalities and cell death in a murine metastatic melanoma cell line.

The purpose of this study was to demonstrate the effects of paclitaxel and water-soluble poly (L-glutamic acid)-paclitaxel (PG-TXL), on chromosome morphology, telomeric associations, and induction of cell death in a murine melanoma cell line (K-1735 clone X-21). Murine melanoma cells were treated with various concentrations (0.1 microgram, 1.0 microgram, 4.0 micrograms, and 8.0 micrograms/ml) of paclitaxel alone, PG alone, or PG-TXL for 2 hr and 4 hr and harvested immediately without recovery. We found that: (1) the frequency of metaphases with telomeric associations increased, (2) metaphases had clumped and distorted chromosome morphology, (3) cells accumulated in metaphase (mitotic arrest), and (4) cell death had been induced. Cells treated with PG-TXL showed more such abnormalities than did cells treated with either paclitaxel or PG alone. Our preliminary results indicate that PG-TXL may be superior to paclitaxel alone in inducing cytotoxic effects, and these effects could be mediated by various chromosomal abnormalities in cancer cells.

Animals↗