Publications by authors named "Bill Helferich"

Article Synopsis
  • Malignant cells can continuously divide and evolve, leading to growth and resistance to treatments, making their control crucial for therapy success.
  • Cellular mechanisms, including senescence, serve as a defense against uncontrolled growth, often triggered by factors like telomere dysfunction and DNA damage, and are regulated by tumor suppressors p53 and p16/pRB.
  • Targeting cancer cell senescence with lower doses of genotoxic drugs or new therapies may enhance patient outcomes and reduce side effects, but challenges like reversibility and increased resistance must be considered.
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The evasion of anti-growth signaling is an important characteristic of cancer cells. In order to continue to proliferate, cancer cells must somehow uncouple themselves from the many signals that exist to slow down cell growth. Here, we define the anti-growth signaling process, and review several important pathways involved in growth signaling: p53, phosphatase and tensin homolog (PTEN), retinoblastoma protein (Rb), Hippo, growth differentiation factor 15 (GDF15), AT-rich interactive domain 1A (ARID1A), Notch, insulin-like growth factor (IGF), and Krüppel-like factor 5 (KLF5) pathways.

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Deregulation of angiogenesis--the growth of new blood vessels from an existing vasculature--is a main driving force in many severe human diseases including cancer. As such, tumor angiogenesis is important for delivering oxygen and nutrients to growing tumors, and therefore considered an essential pathologic feature of cancer, while also playing a key role in enabling other aspects of tumor pathology such as metabolic deregulation and tumor dissemination/metastasis. Recently, inhibition of tumor angiogenesis has become a clinical anti-cancer strategy in line with chemotherapy, radiotherapy and surgery, which underscore the critical importance of the angiogenic switch during early tumor development.

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