Abstract
We report the case of a young patient with left breast cancer with stage IIB (T2N1M0), negative hormone receptors, HER2-positive and no particular medical history. The patient was particularly sensitive to the neurological and allergic-type toxicity of the adjuvant treatment she received and it required the stopping and successive change of the various prescribed protocols.
Highlights
Pancreatic cancer, including Pancreatic Adenocarcinoma and PNET (Pancreatic Neuroendocrine Tumor), is known to be one of the most common and deadly cancers [1] in our society
Acting as a molecular on/off switch in guanosine triphosphate (GTP) activity, KRAS binds to GTP until deactivation caused by the conversion of GTP into guanosine diphosphate (GDP)
The study found the various effects of co-occurring genomic alterations on survival in patients with KRAS-Mutant
Summary
Pancreatic cancer, including Pancreatic Adenocarcinoma and PNET (Pancreatic Neuroendocrine Tumor), is known to be one of the most common and deadly cancers [1] in our society. Numerous studies [2] have shown a strong relationship between mutations in the KRAS gene, a gene that codes for a protein that regulates the propagation of growth factors and cell signaling molecules, and the development of pancreatic cancer (Figure 1). Mutant forms of the KRAS gene induces an uninterrupted activation of the protein despite the lack of extracellular signals; the excessive activation of KRAS causes the formation of tumor in the pancreas. While the significance of KRAS and its mutant form in promoting pancreatic cancer is heavily studied, there have been few studies analyzing the role of genes that co-occur with mutant-KRAS. The following study analyzes the relationship between mutations in the co-occurring genes and the development of pancreatic cancer. We explore the effects of co-mutations on patient survivability and on various other pathways
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