Thus, it is of interest to study the relevance of Fusarium fungus to allergic sensitization. Chang et al. tested a list of 54 air-borne allergens in 66 bronchial asthma patients in the Taipei area, and 20 of the patients showed positive skin reaction to Fusarium extracts. O��Neil et al. found that among 69 atopic individuals tested in United States, 17 of the patients had positive skin reactions to an extract of F. solani. Stroud et al. reported that reactivity to fungi was found in 65% of chronic rhinitis patients and reactions to Fusarium, Alternaria and Pullularia were particularly common. Using in-house extracts for EAST and immunoblot experiments, Hoff et al. detected F. culmorum specific IgE antibodies in 23 of 52 subjects with suspected mould allergy in Europe. In India, skin prick tests with 60 allergens were performed on 48 patients with naso-bronchial allergy and results indicated that Aspergillus fumigatus, A. flavus, Alternaria teneis and F. solani were common fungal allergens. In Greece, Gonianakis et al. found that among 571 patients, 42% showed dermal positivity to allergens derived from Alternaria, Cladosporium, Fusarium, Aspergillus, and Mucor. Thus, there is a worldwide indication that Fusarium fungus may play a role in clinical allergy. However, our knowledge about allergens of this airborne Fusarium fungus is still quite limited and standardized Fusarium extracts for clinical diagnostics are lacking. IgE cross-reactivity is an important component of fungal sensitization and could contribute significantly to allergy manifestation. Thus, in addition to the identification and characterization of fungal allergens, it is important to delineate IgE crossreactivity between allergens from different fungal species and even more importantly, between fungal allergens and their human analogues. Previously, we have identified important IgE crossreactive pan-serine protease fungal allergens from prevalent Penicillium and Aspergillus species. Somatic mutations in most cancers represent molecular signatures that are valuable for prognosis predication and treatment management. For example, the KRAS mutations in codons 12 and 13 are predictive NFPS markers of nonresponse to antiepidermal growth factor receptor antibodies like cetuximab and panitumumab. Mutations in EGFR can confer sensitivity or resistance to EGFR tyrosine kinase inhibitors such as gefitinib and erlotinib in patients with advanced non-small-cell lung cancer. However, NQ 301 detection of somatic mutations poses a technical challenge owing to the presence of large excess of wild-type DNA in tumor samples.