Alterations of PTEN/MMAC1, a candidate tumor suppressor gene, and its homologue, PTH2, in small cell lung cancer cell lines

Kim, Se K.; Su, Lijuan; Oh, Yun; Kemp, Bonnie L.; Hong, Waun Ki; Mao, Li

doi:10.1038/sj.onc.1201512

Cited by 57 publications

(37 citation statements)

References 16 publications

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“…an expressed PTEN pseudogene on chromosome 9 has been identified (Kim et al 1998: Teng et al 1998). Crosshybridization to RNA derived from this pseudogene may therefore account for some of the PTEN transcript profile.…”

Section: )mentioning

confidence: 99%

Mutation and expression analysis of the putative prostate tumour-suppressor gene PTEN

Gray

Stewart²,

Phillips³

et al. 1998

Br J Cancer

149

126

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Section: )mentioning

confidence: 99%

Mutation and expression analysis of the putative prostate tumour-suppressor gene PTEN

Gray

Stewart²,

Phillips³

et al. 1998

Br J Cancer

149

126

View full text Add to dashboard Cite

“…4B), 12 developed PNEC hyperplasia, and 16 had no obvious morphological defects. Because Pten mutations are also found in a significant number of human SCLCs (19,20), we speculated that mutations in Pten could cooperate with p53/Rb mutations to promote SCLC development. Indeed, loss of Pten, in addition to p53 and Rb, significantly accelerated tumor initiation and progression.…”

Section: Pulmonary Neuroendocrine Cells Have Very Limited Potential Tomentioning

confidence: 99%

Functional characterization of pulmonary neuroendocrine cells in lung development, injury, and tumorigenesis

Song

Yao

Lin

et al. 2012

Proc. Natl. Acad. Sci. U.S.A.

259

247

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Pulmonary neuroendocrine cells (PNECs) are proposed to be the first specialized cell type to appear in the lung, but their ontogeny remains obscure. Although studies of PNECs have suggested their involvement in a number of lung functions, neither their in vivo significance nor the molecular mechanisms underlying them have been elucidated. Importantly, PNECs have long been speculated to constitute the cells of origin of human small-cell lung cancer (SCLC) and recent mouse models support this hypothesis. However, a genetic system that permits tracing the early events of PNEC transformation has not been available. To address these key issues, we developed a genetic tool in mice by introducing a fusion protein of Cre recombinase and estrogen receptor (CreER) into the calcitonin gene-related peptide (CGRP) locus that encodes a major peptide in PNECs. The CGRP CreER mouse line has enabled us to manipulate gene activity in PNECs. Lineage tracing using this tool revealed the plasticity of PNECs. PNECs can be colabeled with alveolar cells during lung development, and following lung injury, PNECs can contribute to Clara cells and ciliated cells. Contrary to the current model, we observed that elimination of PNECs has no apparent consequence on Clara cell recovery. We also created mouse models of SCLC in which CGRP CreER was used to ablate multiple tumor suppressors in PNECs that were simultaneously labeled for following their fate. Our findings suggest that SCLC can originate from differentiated PNECs. Together, these studies provide unique insight into PNEC lineage and function and establish the foundation of investigating how PNECs contribute to lung homeostasis, injury/repair, and tumorigenesis.progenitor | naphthalene | cell of origin | tumor suppressor gene

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“…Our study's most interesting finding was related to the expression of the PI3K class III gene: the expression ratio was 2.5 and 11 times greater than in normal tissue in ECa and Dys, respectively. It has been reported that activation of the PI3K signal pathway is closely related to the malignancy of human malignant tumors 10,13,16,17,30) , and it is known that this signal Watanabe S et al Fig. 1 Immunohistochemical studies of H&E stain and p-AKT antibody expression in each region of human tongue (original magnification ‫,04ן‬ ‫)002ן‬ A, Normal Tissue (NT).…”

Section: Gene Analysis Using Cdna Microarraymentioning

confidence: 99%

Activation of PI3K-AKT Pathway in Oral Epithelial Dysplasia and Early Cancer of Tongue

Watanabe

Sato

Okazaki

et al. 2009

Bull. Tokyo Dent. Coll.

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Increasingly, cancers are being diagnosed at an early stage. Leukoplakia, a precancerous lesion, progresses to cancer in 5-10% of cases. We performed genetic analysis using cDNA microarray and immunohistochemistry in 6 patients, 3 with precancerous lesions and 3 with early tongue cancer, to evaluate the usefulness of these methods in the diagnosis of precancerous lesions and early cancer. Samples of normal epithelium, epithelial dysplasia, and cancer tissues were collected by laser microdissection, RNA was extracted, and the signals converted to numerical values. Immunohistochemical analysis was performed using antibody against phospho AKT (p-AKT), a component of the phosphoinositide 3-kinase (PI3K) signal pathway. Five genes showed a 2 times or greater level of increase in expression in epithelial tissue in comparison with in normal tissue, while 4 genes showed a 2 times or greater increase in early cancer tissues. In cancer tissues and epithelial dysplasia tissues, PI3K class III was expressed at 2.5 times and 11 times the level of that found in normal tissue, respectively. Histochemistry using p-AKT antibody revealed no positive cells in normal tissue. Positive cells were noted in the basal and parabasal cell layers, and partially in the spinous layer of epithelial dysplasia tissues, and in the spinous layer of early cancer tissues. These findings suggest that activation of the PI3K-AKT signal pathway is associated with oral carcinogenesis.

show abstract

Alterations of PTEN/MMAC1, a candidate tumor suppressor gene, and its homologue, PTH2, in small cell lung cancer cell lines

Cited by 57 publications

References 16 publications

Mutation and expression analysis of the putative prostate tumour-suppressor gene PTEN

Mutation and expression analysis of the putative prostate tumour-suppressor gene PTEN

Functional characterization of pulmonary neuroendocrine cells in lung development, injury, and tumorigenesis

Activation of PI3K-AKT Pathway in Oral Epithelial Dysplasia and Early Cancer of Tongue

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