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Highly functional and added-value cellulose based polymer and textiles have a considerable number of advantages and attractiveness from a technological point of view. The demand for tailored surface modifications for water repellence, long-term hydrophilicity, enhanced adhesion, antibacterial properties, is under mounting investigation. Modification is used to induce deliberate change in nanoscale composition or structure of textile surfaces and to improve different properties. Nevertheless, the considerable structural and chemical complexity, and their properties must be taken into account for the implementation of surface modification, for improving the properties of cellulose based materials as new applications of cellulose based materials emerge, especially in the fields of biotechnology, bioengineering, and most recently in nanotechnology. Different approaches can be classified by two principal routes, namely chemical and physical functionalization methods to improve wettability, adhesion and other material properties.' Different methods have been used for the introduction of new functional groups or compounds onto synthetic and natural textiles, i.e. plasma treatment, sol-gel process, dip-coating, spray coating, pad-batch and layer by layer method. The challenge is, however, an ideal modification that eliminates all the negative properties and preserves all the positive properties of the fibres. In this chapter considerable attention will be given to the advances made in surface treatment to alter chemical and physical properties of cellulose based surfaces without affecting bulk properties. This chapter also cover treatments for water and oil repellency of textiles, engineering of biomedical textiles and finishing techniques.

Aim: The lack of sensitivity of chronic myeloid leukemia (CML) stem cells to imatinib mesylate (IM) commonly leads to drug dose escalation or early disease relapses when therapy is stopped. Here, we report that packaging of IM into a biodegradable carrier based on polyelectrolyte microcapsules increases drug retention and antitumor activity in CML stem cells, also improving the ex vivo purging of malignant progenitors from patient autografts. Materials & methods: Microparticles/capsules were obtained by layer-by-layer (LbL) self-assembly of oppositely charged polyelectrolyte multilayers on removable calcium carbonate (CaCO3) templates and loaded with or without IM. A leukemic cell line (KU812) and CD34+ cells freshly isolated from healthy donors or CML patients were tested. Results & discussion: Polyelectrolyte microcapsules (PMCs) with an average diameter of 3 µm, fluorescently labelled multilayers sensitive to the action of intracellular proteases and 95–99% encapsulation efficiency of IM, were prepared. Cell uptake efficiency of such biodegradable carriers was quantified in KU812, leukemic and normal CD34+ stem cells (range: 70–85%), and empty PMCs did not impact cell viability. IM-loaded PMCs selectively targeted CML cells, by promoting apoptosis at doses that exert only cytostatic effects by IM alone. More importantly, residual CML cells from patient leukapheresis products were reduced or eliminated more efficiently by using IM-loaded PMCs compared with freely soluble IM, with a purging efficiency of several logs. No adverse effects on normal CD34+ stem-cell survival and their clonogenic potential was noticed in long-term cultures of hematopoietic progenitors in vitro. Conclusion: This pilot study provides the proof-of-principle for the clinical application of biodegradable IM-loaded PMC as feasible, safe and effective ex vivo purging agents to target CML stem cells, in order to improve transplant outcome of resistant/relapsed patients or reduce IM dose escalation.

The targeting of BCR-ABL, a hybrid oncogenic tyrosine (Y) kinase, does not eradicate chronic myeloid leukemia (CML)-initiating cells. Activation of beta-catenin was linked to CML leukemogenesis and drug resistance through its BCR-ABL-dependent Y phosphorylation and impaired binding to GSK3 beta (glycogen synthase kinase 3 beta). Herein, we show that GSK3 beta is constitutively Y-216 phospho-activated and predominantly relocated to the cytoplasm in primary CML stem/progenitor cells compared with its balanced active/inactive levels and cytosolic/nuclear distribution in normal cells. Under cytokine support, persistent GSK3 beta activity and its altered subcellular localization were correlated with BCR-ABL-dependent and -independent activation of MAPK and p60-SRC/GSK3 beta complex formation. Specifically, GSK3 beta activity and nuclear import were increased by imatinib mesylate (IM), a selective ABL inhibitor, but prevented by dasatinib that targets both BCR-ABL- and cytokine-dependent MAPK/p60-SRC activity. SB216763, a specific GSK3 inhibitor, promoted an almost complete suppression of primary CML stem/progenitor cells when combined with IM, but not dasatinib, while sparing bcr-abl-negative cells. Our data indicate that GSK3 inhibition acts to prime a pro-differentiative/apoptotic transcription program in the nucleus of IM-treated CML cells by affecting the beta-catenin, cyclinD1, C-EBP alpha, ATF5, mTOR, and p27 levels. In conclusion, our data gain new insight in CML biology, indicating that GSK3 inhibitors may be of therapeutic value in selectively targeting leukemia-initiating cells in combination with IM but not dasatinib. (Blood. 2012;119(10):2335-2345)