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Contrast nephropathy risk has been increasing in cancer patients. Nephrotoxic side effects of anti-vascular endothelial growth factor/receptor (anti-VEGF/R) drugs used in oncologic treatment are also prominent. The purpose of this study was to identify the possible association among anti-VEGF/R drugs use and development of the contrast-induced nephropathy (CIN) in patients with cancers. A total of 92 patients were included in this prospective cross-sectional study. Patients whose glomerular filtration rate (GFR) of

We aimed to assess whether anti-EGFR combined chemotherapy regimens are related with loss of skeletal muscle mass and to compare cetuximab and panitumumab therapies in the aspect of skeletal muscle area change as well as to assess whether skeletal muscle mass loss has prognostic significance in the RAS wild mCRC patients. A total of 56 patients (30 patients in cetuximab arm and 26 patients in panitumumab) who had computed tomography images were retrospectively evaluated at the diagnosis and follow up during the treatment period before progression. During treatment period 24 patients (42.8%) had muscle loss. Of these, 7 (29.2%) patients were treated at first-line and 17 (70.8%) patients were treated at second-line setting. There was no significant difference in the aspect of skeletal muscle loss among cetuximab and panitumumab combined treatment regimens. Median PFS was 9.1 (8.6–9.6) months in muscle loss group and 13.9 (7.2–20.6) months in muscle stable group (p = 0.001). Median OS was 23.4 (95% CI 15.8–31.0) months in muscle stable group and 19.1 (95% CI 17.0–21.3) months in muscle loss group (p = 0.57) at first-line setting. For second-line, median OS was 21.2 (14.7–27.7) months in muscle stable group and 14.4 (6.0-22.4) months in muscle loss group (p = 0.003). Decrease in skeletal muscle mass before progression on CT imaging is an independent indicator for shorter PFS value in RAS WT mCRC patients who received anti-EGFR combined chemotherapy regimens at both the first and second-line settings. Beside that shorter overall survival values also were significantly seen in patients who had muscle loss during anti-EGFR therapy in the second-line setting.

Background: Lung cancer is one of the most lethal cancers. It is mainly classified into 2 groups: non-small cell lung cancer (NSCLC) and small cell lung cancer (SCLC). Extrapulmonary small cell carcinomas (EPSCC) are very rare. The Ras oncogene controls most of the cellular functions in the cell. Overall, 21.6% of human cancers contain a Kirsten Ras (KRAS) mutation. SCLC and EPSCC have several similar features but their clinical course is different. Aims: We investigated the KRAS mutation status in SCLC and EPSCC. Study design: Mutation research. Methods: Thirty-seven SCLC and 15 EPSCC patients were included in the study. The pathological diagnoses were confirmed by a second pathologist. KRAS analysis was performed in our medical genetic department. DNA isolation was performed with primary tumor tissue using the QIAamp DNA FFPE Tissue kit (Qiagen; Hilden, Germany) in all patients. The therascreen KRAS Pyro Kit 24 V1 (Qiagen; Hilden, Germany) was used for KRAS analyses. Results: Thirty-four (91.9%) of the SCLC patients were male, while 11 (73.3%) of the EPSCC l patients were female. SCLC was more common in males, and EPSCC in females (p=0.001). A KRAS mutation was found in 6 (16.2%) if SCLC patients. The most common mutation was Q61R (CAA>CGA). Among the 15 EPSCC patients, 2 had a KRAS mutation (13.3%). When KRAS mutant and wild type patients were compared in the SCLC group, no difference was found for overall survival (p=0.6). Conclusion: In previous studies, the incidence of KRAS mutation in SCLC was 1-3%; however, it was 16.2% in our study. Therefore, there may be ethnic and geographical differences in the KRAS mutations of SCLC. As a result, KRAS mutation should not be excluded in SCLC.

The aim of this study was to retrospectively compare the efficacy and toxicity of the oxaliplatin + 5-fluorouracil (5-FU) + leucovorin (LV) regimen [modified (m)FOLFOX-6] with that of the docetaxel + cisplatin + 5-FU regimen (DCF) in patients with advanced gastric cancer (AGC). A total of 72 patients received DCF (75 mg/m2 docetaxel and 75 mg/m2 cisplatin on day 1 and 750 mg/m2 5-FU on days 1–5) every 21 days, whereas 54 patients received mFOLFOX-6 (85 mg/m2 oxaliplatin and 400 mg/m2 LV as a 2-h infusion, followed by a 5-FU bolus of 400 mg/m2 and 2,400 mg/m2 5-FU as a 46-h continuous infusion) every 14 days. In the DCF arm, 55 (76.4%) of the patients received prophylactic granulocyte colony-stimulating factor (G-CSF), 48–72 h following completion of chemotherapy. The median follow-up of the study was 12.1 months. The overall response rate (ORR) was 37.0% for mFOLFOX-6 and 40.3% for DCF (P=0.72). The median time to progression was 6.5 and 6.2 months in the mFOLFOX-6 and DCF arms, respectively (P=0.70). The median overall survival was 11.4 and 13.5 months in the mFOLFOX-6 and DCF arms, respectively (P=0.72). The rates of hematological toxicity did not differ between the two arms. However, in the subgroup analysis, grade 3–4 neutropenia and febrile neutropenia were significantly more common among patients who had not received G-CSF prophylaxis in the DCF arm. The incidence of grade 3–4 nausea/vomiting and diarrhea were significantly higher in the DCF arm. In conclusion, the present study demonstrated that the efficacy of the mFOLFOX-6 regimen was comparable to that of the DCF regimen in AGC patients. In addition, the benefit of G-CSF prophylaxis in conjunction with the DCF regimen was demonstrated.

The aim of this study was to define the factors that -affect response and post-progression survival of metastatic gastric cancer (MGC) and gastroesophageal junction cancer (GEJ) -patients treated with second-line chemotherapy.We retrospectively reviewed the data of 59 patients with MGC or GEJ adenocarcinoma who received second-line treatment.The median age was 54 years old (26-77). Response to second-line treatment was strongly associated with disease control with first-line treatment (p 0.01). Median progression-free survival (PFS), overall survival (OS) and post-progression survival (PPS) were 3.2 (95% CI : 2.63-3.80), 6.5 (95% CI : 3.78-9.35) and 2.7 months (95% CI : 1.89-3.68), respectively. PFS (r = 0.55, p 0.01) and PPS (r = 0.89, p 0.01) were correlated with OS. Response to second-line treatment was independently related to PFS (HR : 0.12 95%CI : 0.53-0.26, p 0.001). Having an ECOG 0 performance status (HR : 0.42 ; 95%CI : 0.21-0.86, p = 0.02) and response to second-line therapy (HR : 0.47 ; 95%CI : 0.25-0.85, p = 0.01) were independently associated with OS.PPS and PFS were correlated with OS after second-line treatment of MGC. Response to second-line treatment prolonged OS by increasing PFS, and having an ECOG 0 PS prolonged OS by increasing PPS.

BACKGROUND. The study was conducted with the aim of reviewing the clinical features, therapy, and natural course of patients with extrapulmonary small-cell carcinoma (EPSCC) and small-cell lung carcinoma (SCLC) to better define current concepts regarding EPSCCs. METHODS. The medical records of patients with proven diagnosis of small-cell carcinoma (SmCC) between January 1999 and May 2006 were retrospectively reviewed. A total of 65 SmCC cases were included in the study (11 [17%] cases of EPSCC and 54 [83%] cases of SCLC). RESULTS. Progression-free survival of all patients with EPSCC and patients with extensive EPSCC disease was 7 months (95% confidence interval [CI], 0.58–13.42) and 7 months (95% CI, 4.71–13.29), respectively. Overall survival of all patients with EPSCC and patients with extensive EPSSC disease was 32 months (95% CI, 18.74–45.26) and 28 months (95% CI, 12.24–43.76), respectively. Progression-free survival and overall survival for all patients with SCLC were 5 months (95% CI, 2.26–7.74) and 10 months (95% CI, 5.95–14.05), respectively. Progression-free survival and overall survival for patients with extensive disease were 3 months (95% CI, 4.71–13.29) and 5 months (95% CI, 3.33–6.67), respectively. Overall survival was significantly better in all patients with EPSCC and in patients with extensive EPSCC disease compared with all patients with SCLC and patients with extensive SCLC disease (P = .014, P = .004, respectively). Early death and brain metastasis were observed in a higher number of patients with SCLC compared with EPSCC; however, these results were not statistically significant (P = .33 and P = .076, respectively). Smoking history was significantly less in the EPSCC group (P < .0001). CONCLUSIONS. EPSCC is usually treated similarly to SCLC. However, this study suggests some differences such as etiology, clinic course, survival, frequency of brain metastases, and early death between these entities. These possible differences may influence the choice of therapeutic approach. Cancer 2007. © 2007 American Cancer Society.

Spontaneous intracranial hypotension (SICH) is an entity, which is secondary to iatrogenic manipulation and breaching of dura. Postural headache in patients should be suspected, cranial magnetic resonance imaging (MRI) is essential for precise diagnosis. Hallmark of MRI is regular shape of pachymeningeal gadolinium enhancement and subdural effusion. It may mimic central nervous system (CNS) metastasis. Prevention of such cases from receiving cranial radiotherapy by misinterpretation of the gadolinium enhancement as CNS metastasis is an important issue. Capecitabine is an antineoplastic agent, of which metabolites can cross blood-brain barrier in CNS via epithelial tissue. It may cause decrease in CSF production. SICH might be the clinical reflection of this decrease in CSF production. Review of the English literature revealed limited data because of the very little experience with oncologic patients suffering from intracranial hypotension. We report a case of spontaneous intracranial hypotension during capecitabine treatment. Patient was completely well following drug discontinuation and supportive treatment.

ture cyctic teratoma of the ovary. Pathol Int 1998;48:834-39. [CrossRef] 4. Abbosh PH, Zhang S, Maclennan GT. Germ cell origin of testicular carcinoid tumors. Clin Cancer Res 2008;14:1393-96. [CrossRef]

Although testicular germ cell tumors have become curable neoplasms, a better understanding of the clinicopathologic features is needed for the rare manifestations associated with treatment failure. We report a rare case of metastatic pure choriocarcinoma involving the small intestine arising from a testicular mixed germ cell tumor. In a patient who developed massive upper gastrointestinal hemorrhage during treatment, the intestinal metastases and focus of bleeding could only be determined by laparotomy. We propose an approach for the determination of subclinical intestinal metastases of testicular germ cell tumor; the case is discussed in light of similar reports in literature.