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M Sakizli

Publications and source records attributed to M Sakizli.

13 recordsLinked to original sources
PubMed2000

BRCA1, C-erbB-2, and H-ras gene expressions in young women with breast cancer. An immunohistochemical study.

Young age does not seem to be directly related to the aggressiveness of the disease among patients with breast cancer. Identification and analysis of the alterations in a susceptibility gene expression in breast cancer occurring in young women may allow identification of those patients in whom tumors will show an aggressive clinical course. The purpose of the present study was to evaluate the association of BRCA1, H-ras, and c-erbB-2 gene expression with clinicopathologic parameters of prognosis in breast cancer. Formalin-fixed, paraffin-embedded tissue from 35 patients with breast cancer younger than 35 years were immunohistochemically stained for BRCA1, H-ras, and c-erbB-2 expression with monoclonal antibodies. For each antibody, immunoreactivity was assessed by a semiquantitative scoring system. Each case was also graded according to the modified Bloom-Richardson criteria and evaluated for Ki-67 labeling index, hormonal status, tumor size, distant metastasis, and axillary lymph node involvement. Strong expression of c-erbB-2 and H-ras were observed in 9 cases (25.7%) and 13 cases (37.2%), respectively. Loss of BRCA1 expression was found in five cases (14.3%). Statistical analysis showed that loss of BRCA1 expression was significantly associated with higher Ki-67 labeling index and greater tumor size. In addition, stronger H-ras expression was significantly associated with lymph node involvement and distant metastasis. However, c-erbB-2 immunoreactivity did not show statistical significance with any prognostic parameters. We conclude that, although care must be taken not to overstate the importance of our results in view of the lack of information on clinical outcome, alterations in BRCA1 and H-ras gene expression might be of prognostic importance because of the role of H-ras protein on metastatic behavior and the role of BRCA1 protein on tumor growth. However, c-erbB-2 expression seems to be of no importance in the prognosis of breast cancer occurring in young women.

Adult↗
PubMed2000

Consistent loss of heterozygosity at 14Q32 in lymphoid blast crisis of chronic myeloid leukemia.

Little is understood about the basic biological mechanisms that underlie the reasons for acute transformation in chronic myeloid leukemia (CML). Progression of disease may include inactivation of one or more tumor suppressor genes (TSGs). A widely used methodology for indirectly detecting somatic inactivation of TSGs is searching loss of heterozygosity (LOH) for polymorphic loci located in or near the gene(s) of interest. We aimed to analyze DNA of chronic phase and blastic phase archive material of 15 CML patients for LOH using D1S430, D2S123, D3S1611, D11S29, D14S65, D17S520, BAT 40 markers, the dinucleotide repeat located in the ABL gene and the trinucleotide repeat located in the BCR gene (amplification of the trinucleotide in the BCR gene could not be succeeded). LOH was identified by a %50 lost of one of the alleles intensity. LOH was detected with the ABL dinucleotide repeat and D2S123 marker in two patients and with the D14S65 marker in three patients. The three patients exhibiting LOH at the D14S65 locus, all proceeded through lymphoid blast crisis. The D14S65 marker is located at the 14q32 locus which contains the immunoglobulin heavy chain gene and the TCL1 oncogene. 14q32 abnormalities at the molecular level, may be predictive for lymphoid blast crisis, whether or not they are detectable cytogenetically.

Adult↗
PubMed1999

Development of acute promyelocytic leukemia with isochromosome 17q after BCR/ABL positive chronic myeloid leukemia.

We describe a pediatric case of acute promyelocytic leukemia with an i(17q) after treatment of BCR/ABL positive chronic myeloid leukemia (CML) for 3.5 years. The patient was treated with Busulphan, alpha-2a interferon, hydroxyurea, and cytosine arabinoside at various times in the course of the chronic phase of CML, because he had no HLA-identical donor for bone marrow transplantation. Hematologic remission was achieved for a short time, but cytogenetic remission was never possible. When promyelocytic blast crisis was diagnosed according to the French-American-British classification, cytogenetic studies revealed an i(17q) as a new feature in our patient. The promyelocytic transformation was associated with the appearance of an i(17q) preceding CML are discussed in the light of recent literature.

Bone Marrow↗
PubMed1994

SCE frequency of herpes simplex virus type I infected cells.

The effects of herpes simplex virus type I (HSV-I) on SCE frequencies in human lymphocytes in vitro were investigated. SCE frequencies in controls (mean +/- 1SD 5.2 +/- 1.6) and in cells exposed to the virus for 3 and 6 h (mean +/- 1SD 5.3 +/- 1.6 and 5.8 +/- 1.6 respectively) were about the same. However, cells infected for 9 to 24 h showed a significant increase of SCE frequencies (p < 0.05).

Cells, Cultured↗
PubMed1981

Herpes simplex type 2 neutralization antibodies in patients with cancers of urinary bladder, prostate, and cervix.

In the blood samples obtained from a total of 68 patients with cancers of the urinary bladder, prostate, and cervix, who applied to the Departments of Urology, Obstetrics, and Gynecology of Hacettepe Medical Faculty, neutralizing antibodies were sought for against herpes simplex type 2 by neutralization test. The same test was applied to 35 control patients with no known malignancies. In contrast to the presence of the antibody in 62.86% of the control subjects, this ratio was 90.70% in patients with cancer of the urinary bladder, 87.50% in those with prostatic carcinoma, and 88.89% in those with cancer of the cervix.

Adult↗
PubMedDate not supplied

Sister chromatid exchange in lymphocytes of patients with cancer of the larynx.

The frequency of sister chromatid exchange (SCE) was studied in cultured peripheral lymphocytes from 15 untreated patients with carcinoma of the larynx and 10 healthy control subjects. Bromodeoxyuridine-incorporated chromosomes were treated with Hoechst 33258 and stained according to conventional methods. To measure SCE frequency, at least 15 mitoses per donor were evaluated. The SCE values were found to be higher in cancer cases than in control cases.

Adult↗
PubMedDate not supplied

Two brothers with a 7.0 kb gene deletion associated with isolated growth hormone deficiency type 1A.

Familial growth hormone deficiency type 1A is an autosomal recessive disease, caused by various homogenous deletions of both alleles of growth hormone gene 1 (hGH1). The hGH1 gene deletion is an event occurring between the 5' and the 3' flanking regions by unequal recombination, which causes a deletion in the hGH1 gene, mostly of 6.7 kb and rarely 7.6 or 7.0 kb in size. Two brothers diagnosed with GH deficiency syndrome were sent to our hospital for further evaluation. DNA samples of the probands and controls were amplified by PCR; restriction endonuclease analysis was done with Sma I enzyme and the patterns were evaluated. Gel electrophoresis results showed that the two brothers had a 7.0 kb deletion. These are the third and fourth cases reported with a 7.0 kb deletion. Both patients responded well to replacement therapy and did not develop antibodies against rGH. No other relatives presented with macro deletions in the hGH1 gene.

Child↗
PubMedDate not supplied

A Turkish family with 6.7 Kb deletion associated with isolated growth hormone deficiency type 1A.

Familial growth hormone deficiency type 1A is an autosomal recessive disease caused by homogenous deletions of both alleles of growth hormone gene 1 (hGH1) in various patterns. The hGH1 gene deletion is an event that probably occurs between the 5' and 3' flanking regions by unequal recombination, and results in deletion of the hGH1 gene in different patterns. Deletions are mostly 6.7 kb and rarely 7.0 kb, 7.6 kb and 45 kb in size. A four-year-old girl diagnosed with growth hormone deficiency syndrome was send to us for further evaluation. DNA samples of the patient, her parents and controls were amplified by polymerase chain reaction (PCR); furthermore, restriction endonuclease analysis was done with Sma I enzyme and the patterns were evaluated. Our gel electrophoresis results show that the gene deletion pattern of the patient represents a homogenous 6.7 kb deletion, while her parents had a heterogeneous 6.7 kb deletion pattern.

Child, Preschool↗
PubMedDate not supplied

A case of mixed gonadal dysgenesis with 45 X/46 XY karyotype and aortic coarctation.

We report a case of mixed gonadal dysgenesis with 45 X/46 XY karyotype and aortic coarctation. An eight month-old patient was admitted to our endocrinology department for evaluation of ambiguous genitalia. On physical examination, a wide neck with a low posterior hairline, bifid scrotum, small phallus, testis in the right labioscrotal fold, single orifice and typical findings of aortic coarctation were present. The chromosome karyotype of the patient was 45 X/46 XY. On the laparotomy there was an infantile uterus, fallopian tubes, and a streak gonad on the left. The follow-up of the patient included sex assignment, genital reconstruction and cardiovascular treatment.

Aortic Coarctation↗