Increased Epithelial Cell Proliferation in Nasal Polyps

Coste, A.; Rateau, J. G.; Roudot‐Thoraval, Françoise; Chapelin, Catherine; Gilain, L.; Poron, Françoise; Peynègre, R; Bernaudin, Jean-François; Escudier, Estelle

doi:10.1001/archotol.1996.01890160072013

Cited by 68 publications

(55 citation statements)

References 27 publications

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“…Significantly increased epithelial cell proliferation was noted in nasal polyps compared to sinonasal mucosa [9]. The same findings were reported by different authors [1,10]. Although suitable surgical and medical treatments were performed, the recurrence of the polyps could not be prevented.…”

Section: Discussionmentioning

confidence: 57%

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Could Cellular Proliferation Be a Predictive Index for the Relapse of Nasal Polyposis and Down-Regulated by Nasal Steroid Treatment?

Tezer¹,

Erdivanlı

Şanlı

et al. 2012

Indian J Otolaryngol Head Neck Surg

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The aim of this article is to identify the cellular mitotic activity using Ki-67 monoclonal antibody for predicting relapses of nasal polyposis after surgery. A prospective study was conducted at Kartal Training and Research Hospital Otolaryngology Department between January 2006 and September 2008. Nasal polyps were obtained from all patients and pathological materials were analyzed for the Ki-67 staining using immunohistochemistry. Patients were followed after surgery for 12 months for relapse. There was no statistically significant difference between recurrent and nonrecurrent polyps. Polyp recurrence has a multifactorial origin. Ki-67 index alone does not provide sufficient information about polyp recurrence before the operation.

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Section: Discussionmentioning

confidence: 57%

“…Secretory hyperplasia and squamous metaplasia are also observed in nasal polyps. These findings suggest a dysregulation of epithelial morphological changes [1].…”

Section: Introductionmentioning

confidence: 82%

Could Cellular Proliferation Be a Predictive Index for the Relapse of Nasal Polyposis and Down-Regulated by Nasal Steroid Treatment?

Tezer¹,

Erdivanlı

Şanlı

et al. 2012

Indian J Otolaryngol Head Neck Surg

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“…A single-cell suspension was prepared from each tumour sample by mechanical disaggregation, as described previously (Coste et al, 1996). Cellular DNA content was analysed on an Epics Elite flow cytometer (Coulter Electronics, Hialeah, FL, USA).…”

Section: Flow Cytometry Proceduresmentioning

confidence: 99%

Comparative evaluation by semiquantitative reverse transcriptase polymerase chain reaction of MDR1, MRP and GSTp gene expression in breast carcinomas

Lacave

Coulet²,

Ricci³

et al. 1998

Br J Cancer

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Summary Identification and quantitative evaluation of drug resistance markers are essential to assess the impact of multidrug resistance (MDR) in clinical oncology. The MDR1 gene confers pleiotropic drug resistance in tumour cells, but other molecular mechanisms are also involved in drug resistance. In particular, the clinical pattern of expression of the other MDR-related genes is unclear and their interrelationships are still unknown. Here, we report standardization of the procedures used to determine a reliable method of semiquantitative reverse transcriptase polymerase chain reaction (RT-PCR) using a standard series of drug-sensitive and increasingly resistant cell lines to evaluate the expression of three MDR-related genes, i.e. MDR1 (multidrug resistance gene 1), MRP (multidrug resistance related protein) and GSTp (glutathione-S-transferase p), reported to be endogenous standard genes for normalization of mRNAs. A total of 74 breast cancer surgical biopsies, obtained before any treatment, were evaluated by this method. When compared with classical clinical and laboratory findings, GSTp mRNA level was higher in diploid tumours. However, the main finding of our study suggests a clear relationship between two of these MDR-related gene expressions, namely GSTp and MRP. This finding provides new insight into human breast tumours, which may possibly be linked to the glutathione conjugate carrier function of MRP. Well defined semiquantitative RT-PCR procedures can therefore constitute a powerful tool to investigate MDR phenotype at mRNA levels of different related genes in small and precious tumour biopsy specimens.

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“…Equal background rates of stem-cell birth and death were assumed, reflecting the assumed, approximately constant value of stem-cell number N over the modeled post-natal rat lifespan (105 weeks). Premalignant cells generating NREA were assumed under normal conditions to proliferate at elevated rates of n b 0 assuming n = 5, consistent with n-fold (hyperplastic) elevation in turnover rates with observed values of n between 5 and 20 in putative premalignant cells that are histologically identifiable (Rotstein et al, 1986;Dragan et al, 1993;Zerban, 1994), as well as in nasal polyps (Coste et al, 1996). It was assumed that n = 1 for premalignant cells generating NRON, consistent with the observation that neuroendocrine cells and associated neuroepithelial bodies in mouse bronchiolar epithelium show very little if any mitotic activity and appear to be relatively resistant to chemically induced cytotoxicity (Ogawa et al, 1993).…”

Section: Biologically Based (Mvk) Modeling To Bound Moa Uncertaintymentioning

confidence: 83%

Mode-of-Action Uncertainty for Dual-Mode Carcinogens: A Bounding Approach for Naphthalene-Induced Nasal Tumors in Rats Based on PBPK and 2-Stage Stochastic Cancer Risk Models

Bogen¹

2007

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A relatively simple, quantitative approach is proposed to address a specific, important gap in the approach recommended by the USEPA Guidelines for Cancer Risk Assessment to address uncertainty in carcinogenic mode of action of certain chemicals when risk is extrapolated from bioassay data. These Guidelines recognize that some chemical carcinogens may have a site-specific mode of action (MOA) that is dual, involving mutation in addition to cell-killing induced hyperplasia. Although genotoxicity may contribute to increased risk at all doses, the Guidelines imply that for dual MOA (DMOA) carcinogens, judgment be used to compare and assess results obtained using separate "linear" (genotoxic) vs. "nonlinear" (nongenotoxic) approaches to low-level risk extrapolation. However, the Guidelines allow the latter approach to be used only when evidence is sufficient to parameterize a biologically based model that reliably extrapolates risk to low levels of concern. The Guidelines thus effectively prevent MOA uncertainty from being characterized and addressed when data are insufficient to parameterize such a model, but otherwise clearly support a DMOA. A bounding factor approach-similar to that used in reference dose procedures for classic toxicity endpoints-can address MOA uncertainty in a way that avoids explicit modeling of low-dose risk as a function of administered or internal dose. Even when a "nonlinear" toxicokinetic model cannot be fully validated, implications of DMOA uncertainty on low-dose risk may be bounded with reasonable confidence when target tumor types happen to be extremely rare. This concept was illustrated for a likely DMOA rodent carcinogen naphthalene, specifically to the issue of risk extrapolation from bioassay data on naphthalene-induced nasal tumors in rats. Bioassay data, supplemental toxicokinetic data, and related physiologically based pharmacokinetic and 2-stage stochastic carcinogenesis modeling results all clearly indicate that naphthalene is a DMOA carcinogen.Plausibility bounds on rat-tumor-type specific DMOA-related uncertainty were obtained using a 2-stage model adapted to reflect the empirical link between genotoxic and cytotoxic effects of the most potent identified genotoxic naphthalene metabolites, 1,2-and 1,4-naphthoquinone.Bound-specific "adjustment" factors were then used to reduce naphthalene risk estimated by linear extrapolation (under the default genotoxic MOA assumption), to account for the DMOA exhibited by this compound.3

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Increased Epithelial Cell Proliferation in Nasal Polyps

Cited by 68 publications

References 27 publications

Could Cellular Proliferation Be a Predictive Index for the Relapse of Nasal Polyposis and Down-Regulated by Nasal Steroid Treatment?

Could Cellular Proliferation Be a Predictive Index for the Relapse of Nasal Polyposis and Down-Regulated by Nasal Steroid Treatment?

Comparative evaluation by semiquantitative reverse transcriptase polymerase chain reaction of MDR1, MRP and GSTp gene expression in breast carcinomas

Mode-of-Action Uncertainty for Dual-Mode Carcinogens: A Bounding Approach for Naphthalene-Induced Nasal Tumors in Rats Based on PBPK and 2-Stage Stochastic Cancer Risk Models

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