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R Ankathil

Publications and source records attributed to R Ankathil.

At least 19 recordsLinked to original sources
PubMed2002

Expression of folate sensitive and aphidicolin induced chromosomal fragile sites in familial neuroblastoma.

The expression of folate sensitive and aphidicolin induced fragile sites in the blood lymphocyte chromosomes of affected and unaffected members from 2 neuroblastoma families were studied. The subjects included 4 neuroblastoma patients, and 9 of their clinically healthy first degree relatives and corresponding number of age and sex matched controls. Lymphocytes cultured in folate deprived culture medium showed rare fragile sites at band p13.1 of chromosome 1, in a frequency of 3%-5% in all the 4 neuroblastoma patients. In aphidicolin treated cultures, the patients and unaffected members in neuroblastoma families, showed hypersensitivity to aphidicolin, as evidenced by the significant increase in percentage of aberration/cell (ab/c) and damaged cells (dc), over that of controls (P < 0.01). Aphidicolin induced fragile sites were more pronounced in chromosomes 1 and 2. A larger number of subjects have to be studied to prove whether altered fragile site expression may be a cytogenetic evidence for an individual or familial cancer predisposing genetic constitution.

Aphidicolin↗
PubMed1999

Deficient DNA repair capacity: a predisposing factor and high risk predictive marker in familial colorectal cancer.

Even though colorectal cancer tends to aggregate in families, there is paucity of information on the genetic determinism for familial colorectal cancer (FCRC) predisposition. Therefore, we investigated constitutional chromosome abnormalities and bleomycin induced chromosome sensitivity of 26 familial and 30 sporadic colorectal cancer (SCRC) patients, 60 unaffected family members (first/second degree relatives) and 30 normal healthy controls to determine whether these parameters could give any clues on genetic predisposing factors by which high risk members in CRC families could be identified. The test assay used bleomycin-induced chromatid breaks in short term microcultures of peripheral blood lymphocytes of the subjects. The CRC patients, the unaffected family members and the controls did not show any constitutional chromosomal abnormalities. However, with regard to bleomycin sensitivity, there was significant difference between the CRC patients, unaffected relatives and controls. The mean b/c values of 1.64+/-0.42 for the FCRC patients and 1.08+/-0.34 for the SCRC patients were significantly higher than the mean b/c values of 0.62+/-0.18 for the unaffected relatives and 0.52+/-0.12 for the controls (P<0.001). A noteworthy observation was that 6 unaffected members from 6 CRC families also showed bleomycin hypersensitivity, at the initiation of the study. Since they expressed mean b/c values greater than 1.0, which was as high a value as those of the patients, they were regularly followed up. Out of these 6 members, 2 developed CRC later. This clearly demonstrates that mutagen hypersensitivity among unaffected relatives in CRC families may be related to cancer predisposition. Hence, this cytogenetic assay could be utilised to identify the genetically high risk individuals in CRC families.

Adult↗
PubMed1998

DNA repair proficiency: a potential marker for identification of high risk members in breast cancer families.

Breast cancer is the single largest cancer and causes the high rate of cancer mortality among women. A positive family history of breast cancer is recognized as one of the major risk factors for this disease. The present study evaluates bleomycin (BLM)-induced chromosome sensitivity analysis in breast cancer families which provides indirectly a measure of the DNA repair defect of each person. BLM sensitivity assay on cultured lymphocytes of 36 familial breast cancer patients, their 85 first or second degree female relatives, 36 sporadic breast cancer patients and 40 age- and sex-matched controls (without any family history of cancer) were carried out to measure interindividual variation in their DNA repair capacity through mutagen-induced chromosome sensitivity analysis. Fifty percent of familial breast cancer patients and seven unaffected relatives showed hypersensitivity. Compared to hyposensitive relatives these seven subjects may be considered as high risk individuals.

Adolescent↗
PubMed1997

Increased levels of mutagen-induced chromosome breakage in Down syndrome children with malignancy.

Even though an association between Down syndrome (DS) and malignancies has been established, the mechanism behind this is still unclear. We therefore investigated constitutional chromosomal abnormalities and bleomycin-induced chromosome sensitivity in 12 DS children, 8 DS children with malignancies, and 10 normal controls to explore whether these factors play any role in cancer predisposition. Trisomy 21 was the only constitutional cytogenetic abnormality observed in all the DS children. But there was significant variation between the patients and controls with regard to bleomycin sensitivity. Compared to the normal controls, all the DS patients expressed significantly higher chromosomal breaks per cell (b/c) values indicating sensitivity to bleomycin. Furthermore, DS children with malignancies demonstrated significantly higher b/c values than DS children with malignancies. These results permit us to assume that DS children showing mutagen hypersensitivity may be having defective DNA repair competence and hence may be predisposed to malignancies.

Child, Preschool↗
PubMed1997

The cytogenetic identification of high risk members in colorectal cancer families.

Family history of colorectal cancer is recognized as a risk factor for the disease and the development of colorectal cancer represents a suitable model for illustrating multistep tumor development. Bleomycin induced chromosome sensitivity studies were done in 7 colorectal cancer families consisting of 12 colorectal cancer patients and their 34 first degree relatives and 12 sporadic colorectal patients for comparison and identification of high risk family members with genetic instability. All patients and 4 unaffected relatives showed increased bleomycin sensitivity, which might be due to defective DNA repair system. These four relatives may be classified as high risk (without cancer at present) individuals. The study is being continued in more number of familial colorectal cancer patients and their relatives to arrive at definite conclusions.

Adult↗
PubMed1996

Mutagen sensitivity as a predisposing factor in familial oral cancer.

Pedigree analysis of the oral cancer (OC) patients registered at our Centre had disclosed familial aggregation of oral cancer which hitherto has not been largely reported. There is a paucity of information on the genetic determinism for familial oral cancer predisposition. Therefore, we investigated constitutional chromosome abnormalities and bleomycin-induced chromosome sensitivity of 7 familial and 10 sporadic oral cancer patients and 14 unaffected family members (first-degree relatives) to determine whether these factors could give any clues regarding cancer-predisposing factors. Neither the oral cancer patients nor the unaffected family members showed any constitutional chromosomal abnormalities. However, with regard to bleomycin sensitivity, there was significant difference between the oral-cancer patients and unaffected relatives. The mean b/c value was 1.68 +/- 0.48 for familial OC patients, 1.12 +/- 0.36 for sporadic OC patients and 0.52 +/- 0.18 for the unaffected family members (p < 0.001). A noteworthy observation was that one unaffected family member also showed bleomycin hypersensitivity and expressed a mean b/c value of 1.32, at the initiation of the study. That patient later developed oral carcinoma. This clearly demonstrates that mutagen hypersensitivity among unaffected relatives in OC families may be related to cancer predisposition. The mutagen sensitivity study is being continued in a larger series of subjects, for the development of a cytogenetic marker for prediction of cancer susceptibility.

Adolescent↗
PubMed1996

Clinical implications of cytogenetic classification in adult acute lymphoblastic leukaemia patients.

Cytogenetic analysis performed on pretreated unstimulated, bone marrow/peripheral blood samples of 46 adult patients with acute lymphoblastic leukaemia (ALL) showed sufficient metaphases in 39 patients and insufficient metaphases in 7 patients. G-banded karyotype analysis of these 39 patients revealed non-random clonal chromosome abnormalities in 31 patients and apparently normal karyotypes in 8 patients. Numerical abnormalities involving chromosome trisomies and structural abnormalities involving different types of chromosomal translocations and deletions were encountered in varying percentages. These patients were grouped into various cytogenetic subsets on the basis of their karyotype pattern and followed-up to evaluate their prognosis. Patients with apparently normal karyotypes showed good prognosis and those with 6q- showed intermediate prognosis. But all other patients with hyperdiploid, pseudodiploid and hypodiploid karyotypes were associated with poor prognosis. Cytogenetic classification of ALL patients is thus of clinical importance, as it helps the early identification of clinically important prognostic groups.

Adolescent↗
PubMed1996

Is oral cancer susceptibility inherited? Report of five oral cancer families.

All the oral cancer patients registered at the Regional Cancer Centre, Trivandrum, during January to July 1995 were subjected to detailed pedigree analysis. This revealed that oral cancer tends to aggregate in families. Like other familial cancers, a family history of oral cancer was associated mostly with an early age of onset of the disease. Family members without habits such as tobacco chewing, smoking or alcohol consumption were also affected. These observations prompt us to suggest the probable inheritance of an oral cancer susceptibility gene in these families. The familial aggregation, mostly site-specific, with an autosomal dominant mode of inheritance, was observed in 0.94% of the total oral cancers. This necessitates the need to undertake studies to elucidate the molecular lesions responsible for oral cancer susceptibility in families.

Adult↗
PubMed1995

Nonrandom karyotype abnormalities in 36 multiple myeloma patients.

G-banded analysis performed on pretreated bone marrow samples of 36 multiple myeloma patients allowed the identification of clonal chromosome abnormalities. Abnormalities consisting of trisomies, monosomies, translocations, deletions, and marker chromosomes apparently followed a nonrandom pattern. The chromosomes involved in the production of abnormal karyotypes were numbers 1,2,3,11,12,14,17, and 18. Even though no specific chromosome pattern has been identified, the involvement of chromosomes 1, 3, and 14 was found to be more frequent. Many of the chromosomes and chromosomal breakpoints involved in these abnormalities correspond to the location of identified oncogenes or tumor suppressor genes. Hence, it is presumed that these chromosome abnormalities may be playing an important role in the genesis of multiple myeloma by altering the structure or function of oncogenes or tumor suppressor genes.

Adult↗
PubMed1995

Mandibulofacial dysostosis. Case report.

A case of mandibulofacial dysostosis (Treacher Collins syndrome) is presented. Clinical features and skull radiographs revealed typical anomalies associated with the syndrome. Cleft of the soft palate and unerupted multiple supernumerary teeth were present in this case. No haematological, biochemical or immunological abnormalities could be detected in the patient. Pedigree analysis showed an autosomal dominant mode of transmission of the disease. Chromosomal studies did not reveal any structural or numerical discrepancies.

Adolescent↗
PubMed1994

Oral squamous cell carcinoma in a case of dyskeratosis congenita.

Oral manifestations of dyskeratosis congenita (DCG) have received little attention in dental literature. This report is a case of dyskeratosis congenita in a 17-year-old female which was associated with oral lesions such as leukoplakia, superimposed candidal infection, desquamative gingivitis, and severe periodontitis. Histopathologic examination of the granular lesion on the right lateral border of the dorsum of the tongue showed well-differentiated squamous cell carcinoma. Etiopathogenesis, clinical features, and laboratory findings of this disease are discussed.

Adolescent↗
PubMed1994

Lectin cytochemistry in the exfoliative cytology of uterine cervix.

A lectin was isolated from the seeds of jack fruit (Artocarpus integrifolia) and purified using a column of immobilized N-acetyl-D-galactosamine. This jack fruit lectin (JFL) was then conjugated to horse-radish peroxidase (HRP) type VI and used to study the cell surface carbohydrate profile of the cytological smears of the uterine cervix using diaminobenzidine as substrate. Cervical smears from 15 healthy individuals and 65 patients with dysplasia, carcinoma in situ and carcinoma of uterine cervix were used for the study. Normal cells showed weak binding in the membrane as well as cytoplasm, whereas carcinomatous cells showed strong binding towards JFL. Carcinoma in situ cells showed a binding pattern similar to that of carcinoma. Dysplastic cells showed difference in binding in mild, moderate and severe dysplasia. The intensity of binding increased with the severity of the dysplasia. The nature and intensity of binding of jack fruit lectin with cancer tissues suggest that this lectin may be of use as a diagnostic aid in exfoliative cytology.

Carcinoma in Situ↗
PubMed1993

Chromosomal aberrations induced by methyl parathion in human peripheral lymphocytes of alcoholics and smokers.

1 Two different concentrations (0.08 and 0.16 micrograms ml-1) of methyl parathion (MP), a broad-spectrum insecticide, were tested on peripheral lymphocytes of healthy non-smoking non-alcoholics (CN), chronic smokers (SM) and alcoholics with smoking habit (ALSM). 2 SM and ALSM revealed a significant increase in chromosome aberration frequencies in peripheral lymphocytes compared to the CN group. 3 MP did not induce chromosomal aberrations in vitro in the CN group at either of the concentrations tested. 4 In SM and ALSM, MP induced a significant increase in chromosomal aberrations in vitro in peripheral lymphocytes at a concentration of 0.16 micrograms ml-1. 5 The results indicate that the damage induced by MP in peripheral lymphocytes is potentiated by smoking and alcohol intake.

Alcoholism↗
PubMed1992

Chromosomes in Hodgkin's disease--analysis of involved lymph nodes.

Chromosome studies carried out using lymph nodes of 47 patients with Hodgkin's disease gave analyzable metaphases in 22 patients of which 16 (72.7%) showed chromosome abnormalities. The modal chromosome number ranged from near-diploidy to near-tetraploidy. Chromosomes 1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15, 16, 18, 21 and 22 were involved in trisomy and tetrasomy whereas chromosome 17 was involved in monosomy. Structural abnormalities like deletions of chromosomes 1(p13), 6(q24) and addition of chromatin material to chromosomes 11(q13) and 14(q32) were also detected. The involvement of chromosomes 2, 5, 12, 18 and 21 in numerical abnormalities, and chromosome 14(14q+) in structural aberrations was found to be more frequent in Hodgkin's disease. No clinical correlation could be defined between the various chromosome abnormalities and prognosis of these patients.

Adolescent↗
PubMed1990

Circulating immune complexes in localised juvenile periodontitis.

This study determined the quantity and type of circulating immune complexes (CIC) in the sera of 15 patients with localised juvenile periodontitis (LJP). There was a significantly higher level IgG and IgM in LJP patients as compared with the controls. The possible role of CIC in the pathogenesis of juvenile periodontitis is discussed.

Adolescent↗
PubMed1990

Cell-mediated and humoral immune responses in patients with localized juvenile periodontitis.

Cell-mediated and humoral immune responses were assessed in 21 patients with localized juvenile periodontitis (LJP), and in an equal number of control subjects. The cell-mediated immunity, assessed by enumeration of total rosette forming cells [TRFC] and high affinity rosette forming cells [HARFC], was found to be depressed in LJP patients compared to controls. Estimation of serum immunoglobulins G,A,M,D and E levels were done using single radial immunodiffusion. All the immunoglobulins except IgD were found to be elevated significantly in LJP patients. The defective immune response found in LJP patients may be the cause or effect of the disease process. Further investigations are necessary to determine whether these defects are genetically controlled.

Adolescent↗