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Regulation of glioblastoma stem-like cells by Id proteins and Olig transcription factors

  1. Top of page
  2. Regulation of glioblastoma stem-like cells by Id proteins and Olig transcription factors
  3. Reduction of renal uptake of 111In-DOTA- or A700-RAFT-RGD during integrin αvβ3 targeting using single photon emission computed tomography and optical imaging
  4. Expression of a splicing variant of CADM1 specific to small-cell lung cancer
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Page 1028–37

Increasing evidence points to cancer stem cells as playing a critical role in the therapeutic resistance and recurrence of glioblastoma multiforme (GBM), the most common and aggressive primary brain tumor in adults. Recurrent GBM growth is nearly certain following treatment, contributing to a 2-year survival rate of less than 30%. An improved understanding of how molecular signaling regulates the self-renewal and differentiation of cancer stem cells is necessary for the development of more effective treatments. As basic helix–loop–helix (bHLH) transcription factors are critical for the differentiation of normal stem cells, Wu and colleagues examined their role in cancer stem cells. The authors found that the bHLH family members inhibitor of DNA binding protein 2 and 4 (Id2 and Id4) regulate GBM neurosphere differentiation by downregulating other members of the bHLH family, oligodendroglial lineage-associated transcription factor 1 and 2 (Olig1 and Olig2). The researchers suggest that Id proteins and their downstream targets may be potential targets for differentiation therapy in cancer stem cells. doi: 10.1111/j.1349-7006.2012.02260.x

Reduction of renal uptake of 111In-DOTA- or A700-RAFT-RGD during integrin αvβ3 targeting using single photon emission computed tomography and optical imaging

  1. Top of page
  2. Regulation of glioblastoma stem-like cells by Id proteins and Olig transcription factors
  3. Reduction of renal uptake of 111In-DOTA- or A700-RAFT-RGD during integrin αvβ3 targeting using single photon emission computed tomography and optical imaging
  4. Expression of a splicing variant of CADM1 specific to small-cell lung cancer
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Page 1105–10

The tetrameric RGD-based peptide regioselectively addressable functionalized template-(cyclo-[RGD-f-K])4 (RAFT-RGD) has potential as a tumor-targeting agent for cancer diagnosis and therapy. The RAFT-RGD peptide specifically targets integrin αvβ3 in vitro and in vivo. However, approximately 30–50% of the total dose of Indium-111-labeled RAFT-RGD is retained in the kidneys, causing a risk of renal toxicity and limiting the potential use of RAFT-RGD for internal radiotherapy and imaging. Briat and colleagues studied the effect of Gelofusine on RAFT-RGD renal retention in αvβ3-positive tumor-bearing mice. Single photon emission computed tomography and optical imaging 1 and 24 h after tracer injection, as well as confocal microscopy analysis of kidney sections, revealed that Gelofusine significantly induced a >50% reduction in the renal reabsorption of 111In-DOTA-RAFT-RGD and A700-RAFT-RGD with no effect on uptake. The researchers conclude that RAFT-RGD is a promising agent for both αvβ3-positive tumor imaging and vectorization of radionuclides for tumor therapy. doi: 10.1111/j.1349-7006.2012.02286.x

Expression of a splicing variant of CADM1 specific to small-cell lung cancer

  1. Top of page
  2. Regulation of glioblastoma stem-like cells by Id proteins and Olig transcription factors
  3. Reduction of renal uptake of 111In-DOTA- or A700-RAFT-RGD during integrin αvβ3 targeting using single photon emission computed tomography and optical imaging
  4. Expression of a splicing variant of CADM1 specific to small-cell lung cancer
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Page 1051–57

A member of the immunoglobin superfamily of cell adhesion molecules, CADM1 suppresses tumors in a variety of cancers yet confers an invasive phenotype characteristic to adult T-cell leukemia. Kikuchi and colleagues investigated the role of CADM1 in small-cell lung cancer (SCLC), one of the presentative cancers that is refractory to therapeutic approaches. Immunohistochemistry revealed that 10 of 35 primary SCLC tumors expressed CADM1 protein. Further analysis showed a strong correlation between CADM1 and anchorage-independent cell growth. Variant 8/9 of CADM1 was specifically expressed in SCLC and resulted in enhanced tumorigenicity in nude mice when transfected into SCLC cells lacking CADM1. The results suggest that CADM1 acts as an oncoprotein promoting malignant growth in SCLC cells and could be a potential target for diagnosis and treatment of SCLC. doi: 10.1111/j.1349-7006.2012.02277.x