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Purpose Multidicplinary tumor board(MTBs) are an an important component of cancer patient care. The participation of patients or caregivers in MTBs is an contentious issue and is uncommon in Turkey. This study aimed to determine what Turkish medical oncologists think about the participation of patients and caregivers in MTBs. Method The study was conducted during 8th Turkish Congress Of Medical Oncology in Antalya İn November 2021. The medical oncologists that participated completed a 9-item questionnaire. The relationships between the participants’ sociodemographic characteristics and their questionnaire responses concerning MTBs were analyzed using Pearson’s chi-square test or the Fisher-Freeman-Halton test. Results No statistically significant correlation was found between the socio-demographic characteristics of the participants and the opinions of cancer patients or their relatives about their participation in multidisciplinary tumor boards. 75% of the participants do not approve participation of patient or caregivers in MTBs. 12% of participants approve the participation of both in the MTBs. 3% of participants approve only the participation of caregivers where as only the 6% of medical oncologist approve only the participation of patients in tumor board. Conclusion Among 109 Turkish medical oncologists, most didn’t approve of the participation of patients or caregivers in MTBs. The 2 major reasons for this lack of approval are fear that patients and caregivers will not understand medical terminology, and the emotional stress their participation can cause MTB members.

BACKGROUND This study aimed to compare preoperative chemoradiotherapy (CRT) with postoperative CRT regarding survival, local control, disease control, sphincter preservation, toxicity and also prognostic factors for the treatment of locally advanced rectal cancer. METHODS Records of 140 patients with locally advanced rectal cancer who received preoperative or postoperative CRT were analyzed retrospectively. We compared the treatment groups (preoperative vs postoperative) according to baseline characteristics (demographic and rectal cancer disease characteristics), and also carried out the survival analyses. RESULTS From January 2010 to December 2019, 140 patients were included in the analysis, 65 received preoperative treatment and 75 postoperative treatment. There was no difference in survival, recurrence or distant metastasis rate in both treatment groups. The ratios of the failure to complete adjuvant chemotherapy (32% vs 4.6%) and acute grade 3-4 toxicity (32% vs 6.2%) were higher in the postoperative group (p

Gastric cancer is still one of the cancers with highest mortality. Most patients present with advanced-stage disease. Palliative chemotherapy is usually the only treatment option for patients with advanced gastric cancer (AGC). Maintenance chemotherapy is an evolving concept in medical oncology. Maintenance chemotherapy can be administered with the same drug(s) in the initial regimen or with an alternative agent. In this article, we report our experience with capecitabine as a maintenance agent for patients with AGC. No treatment-related death was observed due to use of capecitabine. Median progression-free survival was 10.4 months, and median overall survival was 19.7 months. Activity and toxicity profile of capecitabine seems favorable as a maintenance agent in AGC. We believe that capecitabine deserves further trials as a maintenance agent for patients with AGC.

Vitamin B12 (Cbl) deficiency may cause hematologic and neurologic dysfunction. Replacement therapy is effective in correcting hematologic abnormalities and improving neurologic symptoms. Cbl is known to have antioxidant activity. This antioxidant activity may antagonize the effects of chemotherapeutics (i.e. genotoxic effects of paclitaxel) on tumor DNA. We claim that Cbl replacement should be done more cautiously in patients receiving cytotoxic chemotherapy.

Epithelial-mesenchymal transition (EMT) is a process during which cancer cells become more invasive and chemo resistant. EMT may also be associated with tumor dormancy which prevents the cure of cancer with adjuvant treatment. Chemo resistance and dormancy may also decrease response to cytotoxic agents during treatment of metastatic disease. Voltage gated sodium channels (VGSCs) are overexpressed in many cancer types, particularly in those with more aggressive and metastatic potential. VGSCs are thought to be associated with increased invasive and migratory capacity of cancer cells. Inhibition of VGSCs may inhibit EMT and angiogenesis through interaction with intracellular calcium activity and endothelial cells respectively. Blockage of these channels combined with other anticancer therapies may be effective in both adjuvant and palliative setting. Colonization at secondary site may be decelerated by VGSCs inhibition through impeding angiogenesis. This may lead to a temporary palliation of symptoms related to tumor burden in patients with metastatic disease.

Total or subtotal gastrectomy are performed as curative or palliative treatment in patients with gastric cancer. Anemia is a frequent complication of gastrectomy. Patients undergoing total or subtotal gastrectomy should be carefully monitored for the development of anemia and be given appropriate treatment when indicated. This survey-based study aimed to determine the level of knowledge about post-gastrectomy anemia in Turkish medical oncologists.The study included 110 Turkish medical oncologists that agreed voluntarily to participate in the survey and answer an 8-item questionnaire. The survey was distributed as a questionnaire during the 5th Turkish Medical Oncology Congress in March 2014.All participants completed the questionnaire. Most of the participants would not recommend oral iron or cobalamin replacement after gastrectomy.The results of the survey indicate that Turkish medical oncologists have some knowledge about post-gastrectomy anemia, but need to learn more about appropriate follow-up and replacement therapies for post-gastrectomy anemia.

Background: The aim of this study was to explore the prognostic role of metabolic response to chemotherapy, determined by FDG-PET, in patients with metastatic non-small-cell lung cancer (NSCLC). Materials and Methods: Thirty patients with metastatic NSCLC were analyzed for prognostic factors related to overall survival (OS) and progression free survival (PFS). Disease evaluation was conducted with FDG-PET/CT and contrast-enhanced CT prior to and at the end of first-line chemotherapy. Response evaluation of 19 of 30 patients was also performed after 2-3 cycles of chemotherapy. Morphological and metabolic responses were assessed according to RECIST and PERCIST, respectively. Results: The median OS and PFS were 11 months and 6.2 months, respectively. At the end of first-line chemotherapy, 10 patients achieved metabolic and anatomic responses. Of the 19 patients who had an interim response analysis after 2-3 cycles of chemotherapy, 3 achieved an anatomic response, while 9 achieved a metabolic response. In univariate analyses, favorable prognostic factors for OS were number of cycles of first-line chemotherapy, and achieving a response to chemotherapy at completion of therapy according to the PERCIST and RECIST. The OS of patients with a metabolic response after 2-3 cycles of chemotherapy was also significantly extended. Anatomic response at interim analysis did not predict OS, probably due to few patients with anatomic response. In multivariate analyses, metabolic response after completion of therapy was an independent prognostic factor for OS. Conclusions: Metabolic response is at least as effective as anatomic response in predicting survival. Metabolic response may be an earlier predictive factor for treatment response and OS in NSCLC patients.

A 38-year-old woman presented with a mass in the left breast. Biopsy of the lesion revealed invasive ductal carcinoma. Bilateral adrenal metastasis was detected in whole body positron emission tomography scanning. Needle biopsy of the left adrenal lesion proved infiltration of malignant cells from breast carcinoma. After eight cycles of neoadjuvant (preoperative) chemotherapy, mastectomy, bilateral adrenalectomy, and bilateral oopherectomy were performed. No further hormonal treatment was recommended due to the resection of both adrenal glands and ovaries. The patient is still followed without any sign of progression. To our knowledge, this is the first case representing multimodality approach to breast cancer with bilateral synchronous adrenal metastasis. Patients with oligometastatic disease may benefit from aggressive treatment including local therapies.

[No abstract available]

e15003 Background: Chemotherapy improves the survival of patients with advanced gastric cancer, but patient survival remains less than 12 months despite optimal treatment. Maintenance therapy after...

[No abstract available]

To the editor: The use of dexamethasone for cancer-related fatigue (CRF) in patients with advanced cancer is a controversial issue. Beneficial effects of dexamethasone may be counterbalanced by its serious side effects. The exact mechanism of the action of steroids on cancer-related fatigue is unknown. Recently, Yennurajalingam et al. hypothesized that dexamethasone exerts its effects on CRF mainly by interfering with the peripheral effects of proinflammatory cytokines [1]. We believe that this may not be the case for some of patients with CRF. The exact pathogenesis of CRF is unknown. A role of systemic inflammation or imbalance between hypothalamicpituitary-adrenal (HPA) axis and systemic cytokines has been proposed [2, 3]. Advanced stage cancer represents a state of chronic stress. Low levels of endogenous cortisol, which may be associated with symptoms in advanced cancer, had been demonstrated by Lundstrom et al. [4]. Major symptoms of adrenal insufficiency (i.e., fatigue, nausea, loss of appetite) may be misinterpreted as CRF. Indeed, some patients treated for CRF may have unrecognized adrenal insufficiency. High dose of dexamethasone (8–16 mg/day) is commonly used as antiemetic therapy in highly and moderately emetic regimens. Updated ASCO guidelines on antiemetics recommend a 4-day course of dexamethasone (12 mg on day 1 and 8 mg on days 2–4) for highly emetogenic chemotherapy and 1–3-day 8 mg course for moderately emetogenic chemotherapy [5]. Highdose steroids may suppress the hypothalamic pituitary and adrenal axis, even with short-term use [6]. Han et al. published their article on adrenal suppression related to the use of dexamethasone as an antiemetic therapy in patients with cancer in July 2012 [7]. Patients receiving dexamethasone as an antiemetic for at least 3 days per cycle and for more than 3 months were included in this study. Adrenal suppression was demonstrated biochemically in 45 of the 103 patients (43.7 %). Adrenal suppression was more common in patients receiving megestrol acetate concomitantly. Daily replacement therapy with 7.5–10 mg of prednisolone for 1–2 weeks in patients with suppressed HPA axis resulted in the improvement of symptoms associated with adrenal insufficiency. This dose of prednisolone is approximately equivalent to 1 mg of dexamethasone [8]. This is about one eighth of the dose recommended in the study of Yennurajalingam et al. We believe that this lower dose may allow the use of steroid for longer periods and spare some of the patients with CRF from serious side effects of higher doses of steroids. Metabolic (i.e., hyperglycemia, hypokalemia) and muscular side effects (i.e., proximal muscle weakness) of long-term use of steroids may be confused with CRF or even increase the severity of CRF. Lower dexamethasone dose will probably cause less metabolic and muscular side effects. For those patients with continuing symptoms of CRF, steroid dose may be gradually increased. In the current study, no follow up for the quality of life was made after cessation of dexamethasone [1]. As CRF is a chronic problem, symptoms may become worse after cessation of high-dose dexamethasone. Lesser dose of dexamethasone may be used more safely for longer periods of time for some patients with this chronic problem. There are still unanswered questions about CRF: What should be done for patients without biochemical evidence of HPA axis suppression? Should we search for biochemical evidence of inflammation (i.e., C-reactive protein) in this group of patients? Should we start with higher doses of dexamethasone when we have laboratory evidence of both systemic inflammation and HPA axis suppression? Should adrenal insufficiency be in the routine checklist of evaluation O. O. Eren (*) :B. Oyan Medical Oncology Section, Department of Internal Medicine, Yeditepe University Hospital, Devlet yolu, Ankara Caddesi, 102-104 Istanbul, Turkey e-mail: droneren@hotmail.com

Our objective was to determine whether serum leptin levels and obesity-related factors could affect outcome for metastatic breast cancer (MBC) patients treated with aromatase inhibitors (AIs). Sixty MBC patients treated with first line hormonal therapy were enrolled in this study. Median age was 51 years (range 28–75). Median leptin level was 19400 pg/ml (1970–91900) and estradiol level 29.6 pg/ml (4.0–181.9). Factors associated with overall survival in univariate analysis were age and waist-to-hip ratio (WHR), whereas only WHR retained significance in the multivariate analysis. However, no factor was associated with progression-free survival. However, WHR was found to be a significant prognostic marker only if the leptin level was ≥19400 pg/ml (HR = 0.38; 95% CI: 0.16–0.91). This study suggests that serum leptin levels and WHR together may serve as potential prognostic markers in MBC patients treated with AIs.

Hepatitis B reactivation due to chemotherapy is a cause of serious morbidity and mortality in some of the patients with cancer. In this study, we retrospectively assessed the prevalence of hepatitis B reactivation among the patients undergoing cytotoxic chemotherapy. We investigated efficacy of lamivudine prophylaxis against hepatitis B reactivation as well.

We read the excellent review article by Davis et al. entitled ‘Targeting EMT in cancer: opportunities for pharmacological intervention’ [1xTargeting EMT in cancer: opportunities for pharmacological intervention. Davis, F.M. et al. Trends Pharmacol. Sci. 2014; 35: 479–488Abstract | Full Text | Full Text PDF | PubMed | Scopus (34)See all References[1] with great interest. The authors listed possible targets for inhibiting epithelial–mesenchymal transition (EMT)-associated metastasis. We think that the concept of blockade of voltage-gated sodium channels (VGSCs) for inhibiting the metastatic process deserves further consideration.It is known that VGSCs, which are normally expressed in excitable cells, are expressed aberrantly in many types of cancer cells [2xVoltage-gated sodium channels and metastatic disease. Brackenbury, W.J. Channels. 2012; 6: 352–361Crossref | PubMed | Scopus (41)See all References[2]. Their expression is associated with the aggressive clinical behavior of cancer cells. VGSCs (as other ion channels) are thought to be associated with many characteristics of cancer [3xIon channels and the hallmarks of cancer. Prevarskaya, N. et al. Trends Mol. Med. 2010; 16: 107–121Abstract | Full Text | Full Text PDF | PubMed | Scopus (123)See all References[3]. VGSCs are known to strengthen the migratory and invasive properties of cancer cells via regulation of pH, gene expression, and intracellular calcium (Ca2+) levels [4xVoltage-gated sodium channel expression and potentiation of human breast cancer metastasis. Fraser, S.P. et al. Clin. Cancer Res. 2005; 11: 5381–5389Crossref | PubMed | Scopus (145)See all References, 5xNav1.5 enhances breast cancer cell invasiveness by increasing NHE1-dependent H+ efflux in caveolae. Brisson, L. et al. Oncogene. 2011; 30: 2070–2076Crossref | PubMed | Scopus (51)See all References, 6xVoltage-gated Na+ channel SCN5A is a key regulator of a gene transcriptional network that controls colon cancer invasion. House, C.D. et al. Cancer Res. 2010; 70: 6957–6967Crossref | PubMed | Scopus (74)See all References, 7xTherapeutic potential for phenytoin: targeting Nav1.5 sodium channels to reduce migration and invasion in metastatic breast cancer. Yang, M. et al. Breast Cancer Res. Treat. 2012; 134: 603–615Crossref | PubMed | Scopus (42)See all References]. Recently, Davis and colleagues [8xInduction of epithelial–mesenchymal transition (EMT) in breast cancer cells is calcium signal dependent. Davis, F.M. et al. Oncogene. 2013; 33: 2307–2316Crossref | PubMed | Scopus (42)See all References[8] reported that attenuation of Ca2+ signaling via intracellular Ca2+ chelation inhibits epidermal growth factor (EGF)- and hypoxia-induced EMT in breast cancer cell lines. In addition, Ca2+ chelation causes downregulation of EGF-induced activation of STAT3 phosphorylation and expression of the EMT marker vimentin [8xInduction of epithelial–mesenchymal transition (EMT) in breast cancer cells is calcium signal dependent. Davis, F.M. et al. Oncogene. 2013; 33: 2307–2316Crossref | PubMed | Scopus (42)See all References[8]. Blockade of VGSCs inhibits metastatic capacity, but not proliferation, of cancer cells, and this has been shown in breast and prostate cancer models [9xVoltage-gated sodium channel expression and potentiation of human breast cancer metastasis. Fraser, S.P. et al. Clin. Cancer Res. 2005; 11: 5381–5389Crossref | PubMed | Scopus (178)See all References, 10xContribution of functional voltage-gated Na+ channel expression to cell behaviors involved in the metastatic cascade in rat prostate cancer. I. Lateral motility. Fraser, S.P. et al. J. Cell. Physiol. 2003; 195: 479–487Crossref | PubMed | Scopus (94)See all References]. The researchers reported that the mechanisms governing primary and secondary tumor growth (i.e., colonization at secondary sites) differ, which might be why proliferation at secondary sites is not affected by VGSCs. Blockade of VGSCs via tetrodotoxin – a potent highly-selective sodium channel blocker – significantly decreased the number, but not the size, of metastatic lesions in an xenograft model of prostate carcinoma [11xVoltage-gated sodium channel activity promotes prostate cancer metastasis in vivo. Yildirim, S. et al. Cancer Lett. 2012; 323: 58–61Abstract | Full Text | Full Text PDF | PubMed | Scopus (30)See all References[11]. The researchers concluded that VGSC blockers were unable to inhibit proliferation at secondary sites. We think this effect of VGSG blockade is due to inhibition of EMT and a consequent reduction in the metastatic capacity of cancer cells. Because inhibition of VGSCs does not appear to have a significant effect on proliferation at secondary sites, the size of the metastatic lesions was not affected. This also indicates that VGSCs do not have strong inhibitory activity on the mesenchymal–epithelial transition (MET). We agree that inhibition of EMT (i.e., strategies to promote MET) might hasten the colonization of cancer cells that have already left the primary site and/or reinforce the viability of metastatic deposits; however, we also know that proliferating cells are more sensitive to the effects of cytotoxic chemotherapy and targeted therapies. In the presence of effective systemic treatment, inhibition of EMT might be of less potential hazard. Inexpensive drugs without serious side effects that have significant sodium channel-blocking activity, such as local anesthetics, anticonvulsants, anti-arrhythmics, and anti-hypertensives, could be tested in future trials on blockade of VGSCs and inhibition of EMT [12xPersistent current blockers of voltage-gated sodium channels: a clinical opportunity for controlling metastatic disease. Djamgoz, M.B. et al. Recent Pat. Anticancer Drug Discov. 2013; 8: 66–84Crossref | PubMedSee all References[12].In conclusion, blockade of VGSCs could be a potential strategy for inhibiting EMT, and might reduce the invasion, migratory capacity, and chemoresistance of cancer cells. Because blockade of VGSCs does not appear to negatively affect MET, we think this treatment strategy could even be combined with cytotoxic chemotherapy or targeted therapies.

e17685 Background: Cancer is a stressful situation itself and brings along a number of psychiatric disorders, which are frequently encountered as depression and sleep disorders. The purpose of this...

Peroxisome proliferator-activated receptor gamma (PPARg) is a member of the nuclear receptor superfamily of ligand-dependent transcriptional factors [1]. PPARg plays a role both in colon non-alcoholic fatty liver disease and cancer [2]. It has been shown that PPARg plays an important role in the differentiation of adipocytes and monocytes/macrophages, as well as in cell proliferation, apoptosis and carcinoma cell arrest [1]. PPARg was cloned was a transcription factor involved in fat cell differentiation and is required for the induction of adipocyte differentiation. PPARg induces hepatic steatosis, and liganded PPARg promotes adipocyte differentiation [3]. PPARg is highly expressed in human colon and colorectal cancer. Structurally, diverse PPARg agonists inhibit the growth of multiple cancer cell lines, including colon cancer cells [1]. By the light of these findings, we hypothesize that both non-alcoholic fatty liver disease and colon cancer may result from distorted mechanisms of PPARg regulation. PPARg ligand effects may be governed by specific molecular genetic determinants and identifying these genetic determinants is therefore of considerable importance [3] to understand the pathogenesis of both non-alcoholic fatty liver disease and colon cancer. Hence, the identification of genetic variants of PPARg regulation may not only disclose mechanisms underlying non-alcoholic fatty liver disease development, but may also lead to the discovery of genes that predispose to colorectal malignancy.