This chapter discusses the relevance of the concept of 'precarity', understood as work conditioned by a lack of security and predictability, in a Nordic context, and links precariousness to both formal work arrangements and to experiences of insecurity. How is precarization of employment expressed in Norway and Denmark? Is the Nordic model resilient to precarization? Framing the discussion in a global perspective, comparable international statistics on frequently used measures of precariousness confirm the image of the Nordic countries as top of the class. The Nordic model of cooperation between the state, strong employers' associations and relatively strong employee unions is often credited as the reason. However, we argue that the Nordic model is continuously subject to renegotiation. Decreasing union density, increasing individualization, increasing inequality and the consequent polarization of working life pose real possibilities of precarization of work also in the Nordic countries.
e22096 Background: The epidermal growth factor receptor (EGFR) is an established target for therapy in colorectal cancer. The extracellular domain of the receptor is shed into circulation and detectable by ELISA. We investigated the changes in sEGFR levels during preoperative chemoradiation (CRT) in rectal cancer patients and third-line treatment with cetuximab and irinotecan (CETIRI) in advanced disease, to elucidate the predictive or prognostic value in these settings. Methods: We included 126 healthy controls and 118 patients with chemorefractory mCRC treated with cetuximab (initial 400/m2 mg followed by weekly 250mg/m2) and irinotecan (350 mg/m2 q3w). Response was evaluated according to RECIST. Furthermore, 114 patients with locally advanced rectal tumours were treated with CRT (60 Gy/30 fractions and concomitant uftoral (300 mg/m2)/leukovorin (22.5 mg) on treatment days, followed by surgery 8 weeks post-treatment and pathological tumour regression evaluation. Pre-treatment and consecutive samples were drawn at each visit. sEGFR was measured by ELISA. Median statistics and Kaplain-Mayer curves with log-rank testing for comparison of survival rates were performed. Results: There were significant differences between the median pre-treatment sEGFR levels in controls, rectal cancer and mCRC (58 ng/ml(56–59 95% C-I), 53 ng/ml(51–55 95% C-I) and 51 ng/ml(49–53 95% C-I), respectively, p<0.000). We detected a rapid increase in sEGFR by the first on- treatment values during CETIRI (p<0.001), and a correlation between the magnitude of increase and a higher degree of skin toxicity, a well known indicator of clinical benefit to EGFR inhibitors. sEGFR in rectal cancer patients displayed a decreasing tendency during CRT (p<0.001), but no correlation to local tumour response. Patients with baseline pre-treatment level > 43.4 ng/ml (mean sEGFR of control group-2xSD) had a significantly higher OS rate than patients with low baseline levels (93% and 59% respectively, HR 0.15, P=0.002). Conclusions: We report a rapid increase in sEGFR by the onset of CETIRI, which may indicate development of skin toxicity and thereby a better change of response. Furthermore, we suggest a potential prognostic value of sEGFR measurement during CRT in locally advanced rectal cancer. No significant financial relationships to disclose.
The backbone of current oncologic treatment of metastatic colorectal cancer (mCRC) consists of fluoropyrimidine together with either oxaliplatin (XELOX/FOLFOX) or irinotecan (XELIRI/FOLFIRI). With an overall objective response rate of approximately 50% for either treatment combination, a major unsolved problem is that no predictors of response to these treatments currently are available. To address this issue, we profiled 742 microRNAs in laser-capture microdissected cancer cells from responding and non-responding patients receiving XELOX/FOLFOX as first-line treatment for mCRC, and identified, among others, high expression of miR-625-3p, miR-181b and miR-27b to be associated with poor clinical response. In a validation cohort of 98 mCRC patients treated first-line with XELOX, high expression of miR-625-3p was confirmed to be associated with poor response (OR 6.25, 95%CIOR [1.8; 21.0]). Independent analyses showed that miR-625-3p was not dysregulated between normal and cancer samples, nor was its expression associated with recurrence of stage II or III disease, indicating that miR-625-3p solely is a response marker. Finally, we also found that these miRNAs are up-regulated in oxaliplatin resistant HCT116/oxPt (miR-625-3p, miR-181b and miR-27b) and LoVo/oxPt (miR-181b) CRC cell lines as compared with their isogenic parental cells. Altogether, our results suggest an association between miR-625-3p and response to first-line oxaliplatin based chemotherapy of mCRC. Citation Format: Mads H. Rasmussen, Niels F. Jensen, Line S. Tarpgaard, Camilla Qvortrup, Maria U. Rømer, Jan Stenvang, Tine P. Hansen, Lise-Lotte Christensen, Jan Lindebjerg, Flemming Hansen, Benny V. Jensen, Torben F. Hansen, Anders M. Jakobsen, Per Pfeiffer, Nils Brünner, Torben F. Ørntoft, Claus L. Andersen. MicroRNA-625-3p is associated with response to first-line oxaliplatin-based treatment of metastatic colorectal cancer. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 1157. doi:10.1158/1538-7445.AM2013-1157
Background: Cell-free DNA (cfDNA) holds promise as a tumor marker of clinical importance. We aimed to investigate the prognostic value of baseline cfDNA in non small-cell lung cancer (NSCLC). Material and Methods: During a three-year period, patients with newly diagnosed, previously untreated advanced NSCLC were included in a consecutive, prospective marker-trial. Plasma was isolated from a pre-treatment peripheral blood sample and the level of total cfDNA was measured by an in-house assay qPCR-method. The treatment comprised carboplatin (AUC 5) intravenously day 1), and vinorelbine (30 mg/m 2 intravenously day 1 and 60 mg/m 2 perorally day 8) q3w for a maximum of six cycles. The primary end-point was overall survival (OS). Secondary end-points were progression free survival (PFS) and overall response rate (ORR). Results: 245 patients were included and received a minimum of 1 cycle of chemotherapy (median 4). The median OS was 8.9 months, the median PFS by intention to treat 5.4 months and the ORR was 25%. The patients were divided into four groups based on quartiles of cfDNA and subsequently dichotomized by the 75th percentile revealing a significantly worse prognosis for patients in the upper 75th percentile (median OS 4.9 months) compared to patients with lower levels (10.0 months) (HR 2.1, 95%CI 1.4 -3.1, p < 0.0001). A multivariate analysis confirmed the independent prognostic value of cfDNA. A subgroup analysis of patients with high cfDNA and poor performance status (PS = 2) identified a group of patients with even worse prognosis (median OS 2.0 versus 9.1 months, HR 3.6, 95%CI 1.4 -9.2, p < 0.0001). Similar and significant results were found when comparing level of cfDNA and PFS. Conclusions: High pre-treatment level of cfDNA seems to have a strong prognostic impact in patients with newly diagnosed advanced NSCLC. Combined with PS it identifies a patient group with minimal or no benefit of chemotherapy.
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