Cancer Research

Cancer Research

Research Toward a Cure

 

May is... Melanoma/Skin Cancer Awareness Month

  • Melanoma is the most serious cancer of the skin, affecting the cells that produce and transport the pigment melanin
  • If caught in its early stages, and with treatment, more that 75% of patients with melanoma survive at least five years after diagnosis
  • Prevention: Protect your skin by avoiding the sun during the midday hours; using sunscreen with an SPF of at least 15; and avoid sunbathing and tanning salons.
  • Examine your skin regularly and have your doctor check your skin at least once a year, during all health exams

May is Melanoma/Skin Cancer Awareness Month

 

Organization Spotlight: Cancer Treatment Centers of America

cancerCentersLogo

Since 1988, the Cancer Treatment Centers of America (CTCA) has made the commitment to help patients win their fights against cancer using advanced technology and a personalized approach. Each hospital in the CTCA national network is fully accredited and provides state-of-the-art cancer treatment by a dedicated team of oncologists, surgeons, and other health experts. The CTCA is motivated to provide innovative treatments to fight cancer, with a personalized approach. With hospitals in suburban Chicago, Tulsa, Philadelpha, suburban Phoenix, CTCA continues to provide comprehensive, patient-centered cancer care to more patients and families across the United States.

Refrences:

  • Van Veelen, W., et al.
  • β-catenin tyrosine 654 phosphorylation increases Wnt signalling and intestinal tumorigenesis.
  • Gut 60: 9 1204-12 (2011)
  • β-catenin plays an important dual role in cell adhesion and Wnt signaling. Deregulation of Wnt/β-catenin signaling is a key factor in colorectal carcinogenesis. This study examines the role of β-catenin phosphorylation at Tyr654 in Wnt signaling and colorectal tumorigenesis. A conditional knock-in mouse model was generated, with a phospho-mimicking Y654E mutation in the endogenous β-catenin gene. Quantitative, two-color fluorescent Western blotting was used to monitor protein levels, extent of phosphorylation, and formation of cadherin/catenin complexes. The mutant β-catenin E654 protein displayed reduced affinity for cadherins, increased signaling, and greatly increased phosphorylation at Ser675 by protein kinase A (PKA). Expression of the Y654E mimic predisposed animals to intestinal tumor development, but did not trigger a more invasive tumor phenotype. The authors propose that Y654 phosphorylation of β-catenin increases tumor initiation by enhancement of Wnt signaling.

  • Kim, H.D., et al.
  • Signaling network state predicts twist-mediated effects on breast cell migration across diverse growth factor contexts
  • Mol Cell Proteomics 10: 11 M111.008433 (2011)
  • The epithelial-mesenchymal transition (EMT) involves dramatic changes in cell motility, as cells lose adhesion and increase migration. Signals from multiple pathways and growth factor receptors are integrated to produce different migration behaviors. This study presents a quantitative analysis of multipathway signaling networks and cell motility, before and after EMT induction. In human mammary epithelial cells, the transcription factor Twist was ectopically expressed to induce EMT. Quantitative Western blotting and bead-based ELISA were used to assess the early activation kinetics of 14 signaling proteins that function downstream of receptor tyrosine kinases. Migration characteristics were monitored before and after Twist-mediated EMT induction in monolayer and single cell contexts, with stimulation by a panel of growth factors. Phosphorylation of the 14 target proteins was measured. Migration responses to growth factors varied dramatically in pre- and post-induction cells. A partial least-squares regression model was applied to the dataset to correlate signaling activities with phenotypic response. A single model accounted for cell behavior, and accurately predicted motility for a new growth factor context. This study may yield insight into the impact of tumor cell EMT status on response to targeted drugs.


 

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