A new human prostate carcinoma cell line, 22Rv1

Sramkoski, R. Michael; Pretlow, Thomas G.; Giaconia, Joseph M.; Pretlow, Theresa P.; Schwartz, Stuart; Sy, Man Sun; Marengo, Susan Ruth; Rhim, Johng S.; Stankovic, John A.; Jacobberger, James W.

doi:10.1007/s11626-999-0115-4

Cited by 493 publications

(472 citation statements)

References 29 publications

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“…A lower concentration of gefitinib blocked ligand stimulated EGFR phosphorylation in human keratinocytes, whereas significant inhibition of downstream signaling, that is, MAPK phosphorylation, was achieved only at higher doses of gefitinib. The inhibitory concentrations of gefitinib in NHEK were similar to those observed for blocking pEGFR and pMAPK in 22Rv1 cells (Figure 2B), an androgen-independent prostate cancer cell line (Sramkoski et al, 1999). This confirms previously reported observations of differential inhibition of EGFR and MAPK phosphorylation in glioma cell lines (Li et al, 2003) and shows the effectiveness of gefitinib against EGFR signaling in human keratinocytes.…”

Section: Results Egfr Is the Major Her/erbb Receptor In Primary Humansupporting

confidence: 90%

Epidermal growth factor receptor dimerization status determines skin toxicity to HER-kinase targeted therapies

Laux

Jain

Singh³

et al. 2005

Br J Cancer

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Skin toxicity, a common drug-related adverse event observed in cancer patients treated with epidermal growth factor receptor (EGFR)-directed therapies is rarely seen with therapies targeting HER2. This study reports the significance of the EGFR and HER2 dimerization status in skin with regard to these dermatologic side effects. We demonstrate the differential effect of HER-directed therapies on the ligand driven activation status of EGFR, HER2 and MAPK in normal human epidermal keratinocytes. EGFR-directed therapies, such as gefitinib and cetuximab, inhibited ligand-induced activation of EGFR and MAPK in human keratinocytes. Pertuzumab, an antibody interfering with functional HER2 heterodimerization, failed to block ligand-induced HER signaling in primary keratinocytes. Using a novel proximity-based dimerization assay (eTagt) we show that EGFR homodimers are the predominant HER dimer pair in normal primary kertinocytes and in normal skin tissue from 16 patients with solid malignancies. The presence of [p]EGFR and [p]MAPK, but the absence of [p]HER2, demonstrates productive signaling via EGFR but not HER2 in human skin. These data illustrate the importance of the EGFR dimerization partner in human skin and suggests that inhibition of EGFR homodimer signaling rather than EGFR/HER2 heterodimer signaling maybe the key molecular event determining dermatologic toxicity discrepancies observed between EGFR-targeted versus HER2-targeted therapies.

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Section: Results Egfr Is the Major Her/erbb Receptor In Primary Humansupporting

confidence: 90%

Epidermal growth factor receptor dimerization status determines skin toxicity to HER-kinase targeted therapies

Laux

Jain

Singh³

et al. 2005

Br J Cancer

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“…In the prostate cell lines examined, expression levels in LNCaP and PC3 cells (derived from prostate metastases; Kaighn et al, 1979;Horoszewicz et al, 1983) were approximately one-fifth those in PNT2C2, P4E6 and 22Rv1 cells (derived from normal prostate cells or primary prostate cancer cells; Berthon et al, 1995;Sramkoski et al, 1999;Maitland et al, 2001). Furthermore, in screens of clonogenic activity with a range of chemotherapeutic agents and UV irradiation, we have found that, in general, PNT2C2 and P4E6 cells show high sensitivity, 22Rv1 cells show intermediate sensitivity and PC3 and LNCaP cells show high resistance.…”

Section: Discussionmentioning

confidence: 99%

GAS5, a non-protein-coding RNA, controls apoptosis and is downregulated in breast cancer

et al. 2008

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Effective control of both cell survival and cell proliferation is critical to the prevention of oncogenesis and to successful cancer therapy. Using functional expression cloning, we have identified GAS5 (growth arrest-specific transcript 5) as critical to the control of mammalian apoptosis and cell population growth. GAS5 transcripts are subject to complex post-transcriptional processing and some, but not all, GAS5 transcripts sensitize mammalian cells to apoptosis inducers. We have found that, in some cell lines, GAS5 expression induces growth arrest and apoptosis independently of other stimuli. GAS5 transcript levels were significantly reduced in breast cancer samples relative to adjacent unaffected normal breast epithelial tissues. The GAS5 gene has no significant protein-coding potential but expression encodes small nucleolar RNAs (snoRNAs) in its introns. Taken together with the recent demonstration of tumor suppressor characteristics in the related snoRNA U50, our observations suggest that such snoRNAs form a novel family of genes controlling oncogenesis and sensitivity to therapy in cancer.

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“…The CWR22Rv1 cells were derived from a recurrent tumor, following ADT of a CWR22 xenograft, which was originally established from a human prostate primary tumor [47][48][49]. CWR22Rv1 cells are CK5-negative and CK8/18-positive, and express a mutant 114-kDa AR (an in-frame duplication of exon 3 of AR gene, which results in the insertion of 39 amino acids in the DNA-binding domain) [9,43,47].…”

Section: Cwr22rv1 Cellsmentioning

confidence: 99%

The diverse and contrasting effects of using human prostate cancer cell lines to study androgen receptor roles in prostate cancer

Yu¹,

Lai²,

Xia³

et al. 2008

Asian J Androl

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The androgen receptor (AR) plays an important role in the development and progression of prostate cancer (PCa). Androgen deprivation therapy is initially effective in blocking tumor growth, but it eventually leads to the hormonerefractory state. The detailed mechanisms of the conversion from androgen dependence to androgen independence remain unclear. Several PCa cell lines were established to study the role of AR in PCa, but the results were often inconsistent or contrasting in different cell lines, or in the same cell line grown under different conditions. The cellular and molecular alteration of epithelial cells and their microenvironments are complicated, and it is difficult to use a single cell line to address this important issue and also to study the pathophysiological effects of AR. In this paper, we summarize the different effects of AR on multiple cell lines and show the disadvantages of using a single human PCa cell line to study AR effects on PCa. We also discuss the advantages of widely used epithelium-stroma co-culture systems, xenograft mouse models, and genetically engineered PCa mouse models. The combination of in vitro cell line studies and in vivo mouse models might lead to more credible results and better strategies for the study of AR roles in PCa.

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A new human prostate carcinoma cell line, 22Rv1

Cited by 493 publications

References 29 publications

Epidermal growth factor receptor dimerization status determines skin toxicity to HER-kinase targeted therapies

Epidermal growth factor receptor dimerization status determines skin toxicity to HER-kinase targeted therapies

GAS5, a non-protein-coding RNA, controls apoptosis and is downregulated in breast cancer

The diverse and contrasting effects of using human prostate cancer cell lines to study androgen receptor roles in prostate cancer

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