Yalçin S
Hacettepe University
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Acta Oncologica | 1997
Yalçin S; Ibrahim Gullu; Gülten Tekuzman; Savaş C
Advances in the diagnosis and treatment of cancer coupled with a better understanding of the pathophysiology, pharmacology and psychology of pain and pain perception have led to improved care of patients suffering from cancer pain (1). Patients with severe cancer pain frequently need repeated doses of potent analgesics. Opioid analgesics are powerful and are widely used in this context, but the associated severe social and medical problems very often prevent them from being satisfactory (2, 3). Ketorolac tromethamine is a non-steroidal anti-inflammatory drug (NSAID) with cyclooxygenase-inhibiting activity (4). It has a potent analgesic, antipyretic and moderate anti-inflammatory activity (4-6). Ketorolac is administered as tromethamine salt orally, intramuscularly, intravenously and as a topical ophthalmic solution (5). The tromethamine salt form enhances its absorption. Clinical studies indicate single dose efficacy greater than that of morphine, pethidine, pentazocine in moderate to severe postoperative pain with evidence of a more favorable adverse effects profile than morphine, pethidine and pentazocine (4). Some studies have also found ketorolac tromethamine to be superior to aspirin, paracetamol and some other non-steroidal anti-inflammatory drugs such as naproxen and indomethacin (4, 7, 8). There are limited data on the use of ketorolac for cancer pain (9, 10). Dipyron, a pyrozolon, is an NSAID with weak anti-inflammatory activity that is widely used in Turkey (11). Dipyron inhibits the prostaglandin biosynthesis, especially in the brain. However, since this inhibition ends when it disappears from the extracellular fluid, antogonism of prostaglandins is also suggested (1 1). In this study we evaluated the efficacy of oral ketorolac in the relief of severe cancer pain in comparison with dipyron. Material and Merhod. A total of 50 patients experiencing severe pain from cancer were enrolled in the study. Twenty-five patients were treated with ketorolac and 25 were treated with dipyron. About half of the patients in both groups had bone metastasis. Mean worst pain scores for the last 24 h were 9.52 in the ketorolac group and 9.76 in the dipyron group. The patients suffered mainly from nociceptive or visceral pain and had not been given regular analgesic treatment. Patients’ characteristics are summarized in Table 1. Patients with significant impairment of brain, liver, kidney, lung and heart function and with gastric or duodenal ulcers were not included. Treatment. Patients were given orally either 10 mg ketorolac tromethamine four times a day or 500 mg dypiron three times a day for two days. Rescue medication was available as paracetamol, if required. No analgesic was allowed within the first two hours of the initial dose. Any patient chronically receiving any kind of analgesics was not included in the study. Clinical assessment. In the beginning of the study pain was evaluated on a 10-point visual analog scale (VAS). All patients completed the study without any withdrawals because of incompliance, adverse effects, severe pain or because of nonresponse to the drugs or rescue medicine. At the end of two days the patients were asked to score their pain on the VAS again and were also asked to answer verbally if they had no pain, (complete relief), felt they had benefited from the drug (incomplete relief), or had derived no benefit (no relief). Statistics. All data analyses were performed using SPSS software. z2-tests, student’s t-tests and Mann-Whitney U-tests were used, as appropriate. A probability of 0.05 was set as the minimum level of significance. Results. The patients in the two treatment groups were comparable in terms of age, sex, severity of pain, and their diagnosis. A summary of the results is presented in Table 2. The decrease in VAS score was statistically significant in both treatment groups (p 0.05). Nevertheless, ketorolac was more successful in promoting complete relief of pain. With ketorolac pain was relieved completely in 13 patients, whereas dypiron
Medical Oncology | 2007
Mustafa Cengiz; Faruk Zorlu; Yalçin S; Murat Gurkaynak; I. Lale Atahan; Ibrahim Gullu
This study is designed to assess the toxicity and therapeutic effectiveness of concurrent gemcitabine and radiotherapy in patients with unresectable pancreatic cancer. Concurrent gemcitabine (400 mg/m2/wk) in six weekly cycles starting on d 1 of radiotherapy (50.4 Gy; 1.8 Gy/fraction/d; 5 d/wk) was prescribed on 22 patients with locally advanced pancreatic cancer. Patients were analyzed with regard to radiological response on computerized tomography, overall survival, and toxicity. Twelve (55%) patients completed the prescription of six gemcitabine cycles and 50.4 Gy radiotherapy; while 10 (45%) received one to five cycles of gemcitabine owing to neutropenia. All patients experienced abdominal discomfort during treatment and three patients required medical intervention. Other toxicities reported were nausea in 13 patients (60%), grade 3 vomiting in 3 (14%). Radiological response evaluations were as follows: complete, 2 (9%); partial, 9 (41%); stable, 7 (32 %); and progressive, 4 (18 %). Median survival was 8.7 mo. Combination of weekly gemcitabine (400 mg/m2) and radiotherapy provided response in 50% of the patients but was associated with severe toxicity resulting in incomplete delivery of the planned chemotherapy.
Acta Oncologica | 1997
Ismail Celik; Başçil N; Yalçin S; Ibrahim Gullu; Ayse Kars; Ibrahim Barista; Gülten Tekuzman
debulking is the mainstay of treatment, and subsequent radiotherapy and/or chemotherapy following total excision may improve relapse-free survival rates compared with surgery alone (3-5). Nevertheless, the vast majority of HPCs are locally aggressive and recurrences after primary surgery are common, as more than two thirds of the cases have a propensity to develop local recurrence prior to distant metastases (2,4). We, herein, present two interesting cases: using ifosfamide as an alternative treatment modality for metastatic and recurrent HPC cases.
Journal of Surgical Oncology | 2000
Ibrahim Barista; Gülten Tekuzman; Yalçin S; Ibrahim Gullu; Nilüfer Güler; Yavuz Ozisik; Ayse Kars; Ismail Celik; Alev Turker; Kadri Altundag; Nurullah Zengin; Aysegul Uner; Esmen Baltali; Firat D
Our objective was to assess the efficacy of a standard dose ifosfamide and doxorubicin containing regimen in the treatment of advanced soft tissue sarcomas. Forty consecutive patients with a median age of 35.5 years were treated. Ifosfamide was administered at a dose of 2.5 g/m2/day as 72‐hour continuous infusion with mesna at the same dosage and schedule. Doxorubicin was given at the dose of 60 mg/m2/day as 2‐hour infusion on day 1. Six patients had a complete response (15%), and 9 (22.5%) had a partial response, fourteen patients (35%) stable disease, and 11 (27.5%) did not respond to chemotherapy. The median duration of response was 13 and 5 months for the complete and partial responders, respectively. The median survival was 37 months. Febrile neutropenia was encountered in 9 cases (22.5%). The present ifosfamide and doxorubicin combination is a moderately effective and well‐tolerable regimen in the treatment of advanced soft tissue sarcomas. J. Surg. Oncol. 2000;73:12–16.
Archive | 1993
Ibrahim Gullu; Yalçin S; Gülten Tekuzman; Ayse Kars; Esmen Baltali; Nilüfer Güler; Ibrahim Barista; Firat D; Coskun F. Bekdik; Zehra Koray
The tumor markers; CEA, CA 19-9, CA 125, CA 15-3 levels in effusions caused by some common malignant tumors, such as breast, gastrointestinal tract and ovarian cancers were compared to the serum levels of the same group of patients. Thirty three patients were included in the study group. Comparison with benign effusions (12 patients) was also carried out. Corresponding tumor markers designated for each tumor type were analyzed besides CEA which was measured in all patients. Although we got more positive results in malign effusions than the sera, this difference was not statistically significant (p>0.05). But mean values of tumor markers were found to be statistically higher in malign effusions when they are compared to the sera of the same patients and to the benign effusions of control group (p < 0.05). As a result, determination of tumor markers in the effusions is more sensitive than in the sera and this method is also useful for differential diagnosis of benign and malign effusions.
Tumori | 2014
Mehmet Artac; N. S. Turhal; Murat Kocer; Bulent Karabulut; Hakan Bozcuk; Yalçin S; Mustafa Karaağaç; Seyda Gunduz; Nalan Isik; Kazim Uygun
BACKGROUND A high-risk group of patients with stage II colon cancer has been identified by the results of studies in Western populations. The aim of this study was to investigate the prognostic factors of adjuvant chemotherapy in Turkish patients with stage II colon cancer. METHODS A total of 554 stage II colon cancer patients were retrospectively enrolled in the study. Three hundred fifty-three patients had received adjuvant chemotherapy (5-FU-LV, FOLFOX or FLOX) and 201 had received no adjuvant chemotherapy. T4 tumor stage, lymphovascular invasion, perineural invasion, bowel obstruction and/or perforation, <12 harvested lymph nodes, and poor differentiation were defined as high-risk factors. RESULTS The median age of the patients was 62 years (range 26-88). The median disease-free survival (DFS) was 58.1 months (95% CI, 47.6 months to 68.5 months) in the non-treatment group and has not been reached in the treatment group (P <0.01). In univariate analysis, patient age >60 years and T4 tumor stage were statistically significant factors that affected DFS as poor prognostic factors. Adjuvant chemotherapy reduced the risk of recurrence with statistical significance (P <0.01). In multivariate analysis, patient age >60 years and T4 tumor stage were independent risk factors affecting DFS. In addition, adjuvant chemotherapy was an independent favorable prognostic factor for DFS (P <0.01). CONCLUSIONS Clinical and pathological risk factors in patients with stage II colon cancer may be different in the Turkish population compared to other populations. Further prospective studies in colon cancer are needed to understand the differences in biology and risk factors between races.
Medical Oncology | 1996
Yalçin S; Nilüfer Güler; Söylemezoğlu F
We report a case of medulloblastoma as a secondary malignancy in a patient treated for immature teratoma of the ovary (ITO). ITO is a rare but curable tumor of the ovary using combination chemotherapy. There is a great deal of interest in the long-term effects of chemotherapy in these patients. Once regarded as fatal not many series of patients with ITO have been reported with the long follow up as in the present case. This case may start a debate on the susceptibility of central nervous system tumors following chemotherapy in patients with ITO.
Leukemia | 1997
Ibrahim Barista; Ismail Celik; Ibrahim Gullu; Yalçin S
1392 of mutations in the genomic DNA. PCR Meth Appl 1991; 1: References 34–38. 7 Ogawa S, Hangaishi A, Miyawaki S, Hirosawa S, Miura Y, Takeyama K, Kamada N, Ohtake S, Uike N, Shimazaki C, Toyama K, 1 Tricot G, Boogaerts MA, De Wolf-Peeters C, van den Berghe H, Verwilghen RL. The myelodysplastic syndrome: different evolution Hirano M, Mizoguchi H, Kobayashi Y, Furusawa S, Saito M, Emi N, Yazaki Y, Ueda R, Hirai H. Loss of cyclin-dependent kinase 4patterns based on sequential morphological and cytogenetic investigations. Br J Haematol 1985; 59: 659–670. inhibitor (p16; MTS1) gene is frequently in and highly specific to lymphoid tumors in primary human hematopoietic malignancies. 2 Kaneko H, Horiike S, Taniwaki M, Misawa S. Microsatellite instability is an early genetic event in myelodysplastic syndrome but Blood 1995; 86: 1548–1556. 8 Quesnel B, Preudhomme C, Philippe N, Vanrumbeke M, Dervite is infrequent and not associated with TGF-b receptor type II gene mutation. Leukemia 1996; 10: 1696–1699. I, Lai JL, Bauters F, Wattel E, Fenaux P. p16 gene homozygous deletions in acute lymphoblastic leukemia. Blood 1995; 85: 3 Nobori T, Miura K, Wu DJ, Lois A, Takabayashi K, Carson DA. Deletions of the cyclin-dependent kinase 4-inhibitor gene in mul657–663. 9 Nakai H, Misawa S, Toguchida J, Yandell DW, Ishizaki K. Fretiple human cancers. Nature 1994; 368: 753–756. 4 Kamb A, Gruis NA, Weaver-Feldhous J, Liu Q, Harshman K, Tavquent p53 gene mutations in blast crisis of chronic myelogenous leukemia, especially in myeloid crisis harboring loss of a chromotigian SV, Stockert E, Day RS III, Johnson BE, Skolnick MH. A cell cycle regulator potentially involved in the genesis of many tumor some 17p. Cancer Res 1992; 52: 6588–6593. 10 El-Deiry W, Tokino T, Velculescu VE, Levy DB, Parsons R, Trent types. Science 1994; 264: 436–440. 5 Nakao M, Yokota S, Kaneko H, Seriu T, Koizumi S, Takaue Y, JM, Lin D, Mercer WE, Kinzler KW, Vogelstein B. WAF1, a potential mediator of p53 tumor suppression. Cell 1993; 75: 817–825. Fujimoto T, Misawa S. Alterations of CDKN2 gene structure in childhood acute lymphoblastic leukemia: mutations of CDKN2 are 11 Serrano M, Hannon GJ, Beach D. A new regulatory motif in cellcycle control causing specific inhibition of cyclin D/CDK4. Nature observed preferentially in T lineage. Leukemia 1996; 10: 249–254. 6 Hayashi K. PCR-SSCP: a simple and sensitive method for detection 1993; 366: 704–707.
Cancer Investigation | 1998
Yalçin S; Ibrahim Gullu; Ibrahim Barista; Gülten Tekuzman; Yavuz Ozisik; Ismail Celik; Ayse Kars
Tumori | 1996
Ibrahim Gullu; Ismail Celik; Gülten Tekuzman; Altunbaş M; Nilüfer Güler; Ibrahim Barista; Alkiş N; Yalçin S; Ayse Kars; Esmen Baltali; Kansu E; Firat D