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Alteration of blood vessel maturation in the fibrous cap of the tumor rim

  1. Top of page
  2. Alteration of blood vessel maturation in the fibrous cap of the tumor rim
  3. Reprogramming of gastrointestinal cancer cells
  4. Predicting cetuximab accumulation in KRAS wild-type and KRAS mutant colorectal cancer using 64Cu-labeled cetuximab PET
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Page 433–38

Tumor growth commonly depends on the development of new blood vessels, and enhanced tumor suppression has been reported with treatments combining anticancer drugs and angiogenesis inhibitors. However, recent reports suggest that anti-angiogenesis treatment may lead to increased invasive potential of cancer cells at the edge of the tumor. Naito and colleagues investigated the effect of angiogenesis inhibitors on tumor blood vessels, focusing on the vasculature in the fibrous cap of the tumor rim. The researchers report that most blood vessels in the fibrous cap formed at the tumor rim were immature. Treatment with angiogenesis inhibitors destroyed the immature blood vessels, leaving mature vessels covered with mural cells. Mature blood vessels are sheathed with an ECM, and ECM collagen fibers serve as tracks for cancer cell migration. The authors emphasize the importance of destroying maturing blood vessels in the tumor rim for more effective cancer treatment.

doi: 10.1111/j.1349-7006.2011.02157.x

Reprogramming of gastrointestinal cancer cells

  1. Top of page
  2. Alteration of blood vessel maturation in the fibrous cap of the tumor rim
  3. Reprogramming of gastrointestinal cancer cells
  4. Predicting cetuximab accumulation in KRAS wild-type and KRAS mutant colorectal cancer using 64Cu-labeled cetuximab PET
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Page 393–99

In this issue, Dewi and colleagues present the current knowledge of the potential applications of cell reprogramming for reducing aggressive phenotype expression in gastrointestinal cancer, which would minimize relapse following surgical resection. Cell reprogramming reverts mature cells to an immature, undifferentiated state through the loss and re-establishment of epigenetic markers such as DNA methylation. There is some evidence that epigenetic modifications and processes similar to cell reprogramming are important for the development of malignant cancer phenotypes. Reversible and transient epigenetic modifications are the primary regulators of key events in cancer relapse and metastasis, including epithelial–mesenchymal transition. A better understanding of cell reprogramming is necessary for advancing regenerative medicine and cancer therapy. The authors discuss the potential for adapting reprogramming-like processes in normal cells for use in novel cancer treatments.

doi: 10.1111/j.1349-7006.2011.02184.x

Predicting cetuximab accumulation in KRAS wild-type and KRAS mutant colorectal cancer using 64Cu-labeled cetuximab PET

  1. Top of page
  2. Alteration of blood vessel maturation in the fibrous cap of the tumor rim
  3. Reprogramming of gastrointestinal cancer cells
  4. Predicting cetuximab accumulation in KRAS wild-type and KRAS mutant colorectal cancer using 64Cu-labeled cetuximab PET
Thumbnail image of

Page 600–05

Cetuximab, a drug specialized for targeting the extracellular domain of epidermal growth factor receptor (EGFR), is used as a targeted therapy for advanced or metastatic colorectal cancer. However, clinical trials show that cetuximab benefits only a fraction of patients. Some studies show that cetuximab is only effective for patients with wild-type KRAS and wild-type B-type Raf kinase gene tumors, however, other studies suggest that KRAS mutation status has limited use as a predictor for patient response to cetuximab. In their investigation of this issue, Achmad and colleagues found a strong linear correlation between EGFR expression levels and cetuximab accumulation in colorectal tumors with varying EGFR expression levels and KRAS mutation status. The researchers also successfully used PET imaging with 64Cu-DOTA-cetuximab to visualize cetuximab accumulation in colorectal tumors. The authors suggest that 64Cu-DOTA-cetuximab could serve as a tool for the non-invasive assessment of cetuximab accumulation in tumors before the initiation of cetuximab therapy.

doi: 10.1111/j.1349-7006.2011.02166.x