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No phosphorylation of VEGFR2, PDGFRα/β, or KIT was observed on the arrays.
Consensus between CADMA and the TheraScreen kit was observed in 96% of the colorectal cancer samples.
On the other hand, a strong expression of KIT was observed in a partially keratinised epithelial component of teratoma.
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Consequently, preferred binding of masitinib by KIT is observed.
Following ischemia, expression of c-KIT was observed for tubular epithelial cells expressing CD10, identifying this population as of proximal tubular epithelium origin (figure 1O).
A statistically significant association between CD3+ T-lymphocytes and c-kit was observed (P = 0.039).
In contrast, partial co-localization of K5 and c-kit was observed as c-kit began partitioning into the ducts later in development (E18).
A higher prevalence of the variant KIT L541 was observed in patients with metastatic status at diagnosis (KIT L541 correlated nine of 22 versus 15 of 87, p = 0.02).
After litter standardization at birth, no difference in the number of kits weaned was observed between genetic type or environmental constraint (on average 9.5 kits per parturition; Figure 2C).
On the other hand, Asn655Thr mutation at exon 13 of the c-kit gene was observed as a secondary mutation in case 2 with secondary resistance to nilotinib.
In adnexal nontumoral mammary gland c-kit expression was observed in alveolar and ductal mammary epithelium in smaller proportions relative to the tumor.
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Justyna Jupowicz-Kozak
CEO of Professional Science Editing for Scientists @ prosciediting.com