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Related Concept Videos

Tumor Progression02:07

Tumor Progression

Tumor progression is a phenomenon where the pre-formed tumor acquires successive mutations to become clinically more aggressive and malignant. In the 1950s, Foulds first described the stepwise progression of cancer cells through successive stages.
Colon cancer is one of the best-documented examples of tumor progression. Early mutation in the APC gene in colon cells causes a small growth on the colon wall called a polyp. With time, this polyp grows into a benign, pre-cancerous tumor. Further...
Tumor Progression02:07

Tumor Progression

Tumor progression is a phenomenon where the pre-formed tumor acquires successive mutations to become clinically more aggressive and malignant. In the 1950s, Foulds first described the stepwise progression of cancer cells through successive stages.
Colon cancer is one of the best-documented examples of tumor progression. Early mutation in the APC gene in colon cells causes a small growth on the colon wall called a polyp. With time, this polyp grows into a benign, pre-cancerous tumor. Further...

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In Vivo Model for Testing Effect of Hypoxia on Tumor Metastasis
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AKT1(E17K) in human solid tumours.

F E Bleeker1, L Felicioni, F Buttitta

  • 1Laboratory of Molecular Genetics, The Oncogenomics Center, Institute for Cancer Research and Treatment, University of Torino Medical School, Candiolo, Italy.

Oncogene
|May 28, 2008
PubMed
Summary
This summary is machine-generated.

The AKT1(E17K) mutation, a driver of cancer, is found in specific tissues like breast, lung, and colorectal cancers. This discovery has implications for targeted cancer therapies.

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Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • The serine-threonine kinase AKT1 is a key component of the PI3K pathway, crucial in cancer development.
  • A specific AKT1 mutation, E17K, leads to constant activation and has been observed in various cancers.

Purpose of the Study:

  • To investigate the frequency and tissue-specific occurrence of the AKT1(E17K) variant in a diverse range of human tumors.
  • To understand the implications of AKT1(E17K) mutations in cancer development and potential therapeutic strategies.

Main Methods:

  • Genomic DNA was extracted from 764 tumor samples, including breast, lung, ovarian, colorectal, pancreatic carcinomas, melanomas, and glioblastomas.
  • The presence of the AKT1(E17K) variant was determined using molecular analysis techniques.
  • Co-occurrence and mutual exclusivity with other PI3K pathway mutations (PIK3CA) were analyzed in breast cancer samples.

Main Results:

  • The AKT1(E17K) mutation was detected in breast (16/273), colorectal (1/88), and lung (1/155) cancers, but not in ovarian, pancreatic, melanoma, or glioblastoma samples.
  • In breast cancers, the AKT1(E17K) variant was mutually exclusive with PIK3CA mutations (E454K, H1047R) and found in ductal and lobular histotypes.
  • The study indicates a tissue-specific pattern for AKT1 mutations within the PI3K signaling pathway.

Conclusions:

  • AKT1(E17K) mutations occur in a tissue-specific manner, suggesting that their oncogenic activity is influenced by the cellular and tissue environment.
  • The findings support the development of targeted therapies specifically for the AKT1(E17K) variant, potentially effective in particular cancer types.