Successful host invasion by parasitic helminths involves detection and appropriate response to a range of host-derived signals. Insulin signal response pathways are ancient and highly-conserved throughout the metazoans. However, very little is known about helminth insulin signalling and the potential role it may play in host-parasite interactions. The response of Mesocestoides vogae (Cestoda: Cyclophyllidea) larvae to human insulin was investigated, focusing on tyrosine-phosphorylation status, glucose content, survival and asexual reproduction rate. Parasite larvae were challenged with different levels of insulin for variable periods. The parameters tested were influenced by human insulin, and suggested a host-parasite molecular dialogue.†

Carcinoma of the stomach is one of the most prevalent cancer types in the world today. Only a limited number of biomarkers are available for detection and prognostic evaluation of gastric cancer. New advances in identifying molecular biomarkers are essential. Two major forms of gastric cancer are distinguished according to their morphological and clinicopathological classifications (well-differentiated/intestinal type and poorly differentiated/diffuse type) – characteristics that can also be attributed to different oncogene activations. Many genes related to cell cycle regulation and signal transduction have been implicated in gastric cancer progression. In particular, there is convincing evidence that protein tyrosine kinases (PTKs) are involved in oncogenesis and disease progression. To learn more about the biological significance of all expressed PTKs in human cancers, an improved and more-comprehensive PTK profiling approach has been developed to discover additional PTKs activated in cancer cells. With the completion of the human genome project and the availability of cDNA microarrays or DNA chips, the entire human transcriptome can be used for elucidating genes responsible for human gastric cancer oncogenesis and progression.

The abnormal haemopoietic precursor cells of chronic myeloid leukaemia (CML) carry the cytogenetic abnormality [t(9;22)(q34;q11)] – a reciprocal translocation that results in the expression of a chimaeric protein derived from the fused BCR and ABL genes. This Bcr–Abl protein tyrosine kinase mediates an array of effects on signal transduction pathways affecting cell survival, proliferation, adhesion and genetic stability. The end-result of these abnormal signalling processes is a bi- or triphasic clinical disease. Initially, CML is characterised by the presence of an excess of myeloid progenitor cells and their mature progeny. This chronic phase of CML is followed, either directly or with an intervening ‘accelerated phase’, by a stage where primitive blast cells predominate (acute transformation). This review discusses the role of Bcr–Abl-mediated signalling events in cellular transformation, genetic instability and disease progression in CML, and describes current developments in CML treatment using a Bcr–Abl inhibitor.

The role of mitogen-activated protein (MAP) kinase in mouse egg activation induced by protein kinase inhibitors and a protein tyrosine kinase (PTK) inhibitor was investigated. Separated egg proteins were first probed with anti-Active MAP kinase antibody and then re-probed with anti-ERK2 antibody. Staurosporine and Ro-31-8220, at concentrations that normally inhibit protein kinase C, did not affect egg activation or MAP kinase activity, while higher dosages caused egg activation. Staurosporine at 2 μM induced the metaphase–interphase transition without emission of the second polar body (PB2), while Ro-31-8220 at 40 μM induced PB2 emission, first cleavage, and then the transition to interphase. Half the eggs were also activated by the PTK inhibitor genistein. In each treatment, the proportion of eggs that entered interphase was well correlated with the degree of MAP kinase inactivation. Artificial activation of this kinase by okadaic acid overcame the interphase transition. These data suggest that protein kinase inhibitors and a protein tyrosine kinase inhibitor induce the interphase transition by inactivating MAP kinase in mouse eggs.