The effect of cigarette smoking on cell proliferation in normal uterine cervix epithelium

Campaner, Adriana Bittencourt; Eras, Aline Estefanes; Paganini, Camila Bianca Lecciolle; Galvão, Maria Antonieta Longo

doi:10.1007/s00404-010-1586-y

Cited by 2 publications

(2 citation statements)

References 25 publications

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“…The absence of this smoking-driven phenomenon in LGSILs may suggest that the degree of inflammation in these cases is insufficient to trigger higher proliferation rates. Our finding of no major differences in normal tissue cell proliferation rates for smokers vs. non-smokers agrees with previous reports [37]. Taken together, our data suggest a strong effect of smoking on cell proliferation that manifests independently of disease stage and most prominently in basal and parabasal epithelial layers.…”

Section: Discussionsupporting

confidence: 93%

Evaluation of HPV Infection and Smoking Status Impacts on Cell Proliferation in Epithelial Layers of Cervical Neoplasia

et al. 2014

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Accurate cervical intra-epithelial neoplasia (CIN) lesion grading is needed for effective patient management. We applied computer-assisted scanning and analytic approaches to immuno-stained CIN lesion sections to more accurately delineate disease states and decipher cell proliferation impacts from HPV and smoking within individual epithelial layers. A patient cohort undergoing cervical screening was identified (n = 196) and biopsies of varying disease grades and with intact basement membranes and epithelial layers were obtained (n = 261). Specimens were sectioned, stained (Mib1), and scanned using a high-resolution imaging system. We achieved semi-automated delineation of proliferation status and epithelial cell layers using Otsu segmentation, manual image review, Voronoi tessellation, and immuno-staining. Data were interrogated against known status for HPV infection, smoking, and disease grade. We observed increased cell proliferation and decreased epithelial thickness with increased disease grade (when analyzing the epithelium at full thickness). Analysis within individual cell layers showed a ≥50% increase in cell proliferation for CIN2 vs. CIN1 lesions in higher epithelial layers (with minimal differences seen in basal/parabasal layers). Higher rates of proliferation for HPV-positive vs. -negative cases were seen in epithelial layers beyond the basal/parabasal layers in normal and CIN1 tissues. Comparing smokers vs. non-smokers, we observed increased cell proliferation in parabasal (low and high grade lesions) and basal layers (high grade only). In sum, we report CIN grade-specific differences in cell proliferation within individual epithelial layers. We also show HPV and smoking impacts on cell layer-specific proliferation. Our findings yield insight into CIN progression biology and demonstrate that rigorous, semi-automated imaging of histopathological specimens may be applied to improve disease grading accuracy.

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Section: Discussionsupporting

confidence: 93%

Evaluation of HPV Infection and Smoking Status Impacts on Cell Proliferation in Epithelial Layers of Cervical Neoplasia

et al. 2014

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“…So, the persistence of HPV infection would be the intermediate stage in carcinogenesis. The recognition and control of this situation and the risk factors could avoid its development .…”

Section: Discussionmentioning

confidence: 99%

Post‐cervical conization outcomes in patients with high‐grade intraepithelial lesions

Simões

Campaner

2013

APMIS

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To investigate the rates of residual, recurrent and invasive disease after cervical conization in patients diagnosed with cervical intraepithelial neoplasia (CIN) grades 2/3. A retrospective study was conducted with 274 patients undergoing cervical conization due to diagnosis of CIN 2/3. Cervical conization was done through the Loop Electrosurgical Excision Procedure (LEEP) and Cold Knife Conization. Data related to personal, familial, gynecological, and obstetric antecedents, as well as surgical specimens margins were collected from medical records. The outcome after conization was evaluated, including the time of follow-up and disease recurrence. The outcome after conization was not associated with age of menarche (p = 0.920), age of the first sexual intercourse (p = 0.533), number of parturition (p = 0.063), number of sexual partners (p = 0.328), immunosuppression (p = 0.225), smoking habit (p = 0.193), and conization type (p = 0.198). However, the outcome presented a significant association with age (p < 0.001), pregnancy numbers (p = 0.009), use of hormonal contraception methods (p = 0.016), menopause (p = 0.007), type of margins (p = 0.011), and cone histological results (p = 0.030). The routine control of all patients who had undergone cervical conization is obligate, independently of surgical margins, due to the risk of disease recurrence; the older patients and those with CIN 3 should have a more rigorous follow-up.

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The effect of cigarette smoking on cell proliferation in normal uterine cervix epithelium

Abstract: The results indicated that there was no significant difference between cell proliferation in smokers and nonsmokers; however, it was shown that in the smokers' group, amount of cigarettes smoked during throughout lifetime can increase cell proliferation in normal cervical epithelium.

Cited by 2 publications

References 25 publications

Evaluation of HPV Infection and Smoking Status Impacts on Cell Proliferation in Epithelial Layers of Cervical Neoplasia

Evaluation of HPV Infection and Smoking Status Impacts on Cell Proliferation in Epithelial Layers of Cervical Neoplasia

Post‐cervical conization outcomes in patients with high‐grade intraepithelial lesions

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