Multi-tier Loyalty Programs to Stimulate Customer Engagement

Customers differ in their purchase behavior, profitability, attitude toward the firm, and so on. These differences between customers have led to numerous firms introducing multi-tier loyalty programs. A multi-tier loyalty program explicitly distinguishes between customers by means of hierarchical tiers (e.g. Silver, Gold, Platinum) and assigns customers to different tiers based on their past purchase behavior. Next, customers in different tiers are provided varying levels of tangible rewards and intangible benefits, which are potentially powerful instruments to stimulate customer engagement. In this chapter, we focus on the design and effectiveness of such multi-tier loyalty programs. Building on loyalty program and customer prioritization research, we discuss whether, why, and how multi-tier loyalty programs are effective (or not) in influencing customer behavior, thereby enhancing customer engagement and financial performance

In vivo evolution of tumour cells after the generation of double-strand DNA breaks

In vitro, the ratio of single- to double-strand DNA breaks (DSB) and their absolute values determine the cell death pathway. The consequences of the generation of various numbers of DSB generated in vivo in tumour cells have been analysed in two different experimental tumour models. Synchronisation of DSB generation and control of their number have been achieved using different doses of bleomycin (BLM) and tumour cell permeabilisation by means of locally delivered electric pulses. According to BLM dose, different cell death pathways are observed. At a low therapeutic dose, a mitotic cell death pathway is detected. It is characterised by the appearance of 'atypical mitosis', TUNEL and caspase-3 positive, 24 h after the treatment, and later by the presence of typical apoptotic figures, mainly TUNEL positive but caspase-3 negative. Caspase-3 is thus an early marker of apoptosis. Mitotic cell death is also followed by lymphocytic infiltration reaction. At high doses of BLM, pseudoapoptosis is detected within a few minutes after the treatment. These cell death pathways are discussed as a function of the number of DSB generated, by comparison with previous results obtained in vitro using BLM or ionising radiation

Human MUC4 mucin induces ultra-structural changes and tumorigenicity in pancreatic cancer cells

MUC4 is a type-1 transmembrane glycoprotein and is overexpressed in many carcinomas. It is a heterodimeric protein of 930 kDa, composed of a mucin-type subunit, MUC4α, and a membrane-bound growth factor-like subunit, MUC4β. MUC4 mRNA contains unique 5′ and 3′ coding sequences along with a large variable number of tandem repeat (VNTR) domain of 7–19 kb. A direct association of MUC4 overexpression has been established with the degree of invasiveness and poor prognosis of pancreatic cancer. To understand the precise role of MUC4 in pancreatic cancer, we engineered a MUC4 complementary DNA construct, mini-MUC4, whose deduced protein (320 kDa) is comparable with that of wild-type MUC4 (930 kDa) but represents only 10% of VNTR. Stable ectopic expression of mini-MUC4 in two human pancreatic cancer cell lines, Panc1 and MiaPaCa, showed that MUC4 minigene expression follows a biosynthesis and localisation pattern similar to the wild-type MUC4. Expression of MUC4 resulted in increased growth, motility, and invasiveness of the pancreatic cancer cells in vitro. Ultra-structural examination of MUC4-transfected cells showed the presence of increased number and size of mitochondria. The MUC4-expressing cells also demonstrated an enhanced tumorigenicity in an orthotopic xenograft nude mice model, further supporting a direct role of MUC4 in inducing the cancer properties. In conclusion, our results suggest that MUC4 promotes tumorigenicity and is directly involved in growth and survival of the cancer cells