Atl

Cortecchia, Stefania; Galanti, Giuseppe; Sgadari, Cecilia; Costa, Silvano; Lillo, Margherita De; Caprara, L; Barillari, Giovanni; Monini, Paolo; Nannini, R; Ensoli, Barbara; Bucchi, Lauro

doi:10.1097/igc.0b013e3182a80b14

Cited by 21 publications

(6 citation statements)

References 25 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Some of these studies do not include hrHPV testing, 4,16 have a short follow-up, 21 or include a very limited number of patients with LSIL/CIN1. 25,26 Other studies analyze specific groups, which were retrospectively selected based on the outcome.…”

Section: Discussionmentioning

confidence: 99%

“…In the last decade, a number of studies have addressed this issue and have suggested that p16-positive LSIL/CIN1 lesions are at higher risk of showing a HSIL/CIN2-3 outcome diagnosis. 4,5,16,17 However, the number of cases included in these series was very small and consequently, the true value of p16 as a marker of 'progression' in these women remains uncertain. Thus, prospective, longitudinal studies focused on the prognostic value of p16 immunostaining in patients with biopsies showing LSIL/CIN1 are needed before definitive conclusions can be drawn.…”

mentioning

confidence: 99%

“…3 In contrast, about 80% of low-grade SIL/CIN1 (LSIL/CIN1) are transient lesions that generally spontaneously regress in 1-2 years. 1,[4][5][6][7] Accordingly, the management of HSIL/CIN2-3 generally involves the excision of the lesion and the transformation zone to prevent the development of cervical cancer, whereas the management of LSIL/CIN1 is conservative, being based on clinical follow-up. 8,9 However, 10 to 15% of LSIL/CIN1 lesions progress to HSIL/CIN2-3.…”

mentioning

confidence: 99%

See 2 more Smart Citations

p16 staining has limited value in predicting the outcome of histological low-grade squamous intraepithelial lesions of the cervix

et al. 2016

View full text Add to dashboard Cite

In order to evaluate the usefulness of p16 staining in predicting the outcome of histological low-grade squamous intraepithelial lesion/cervical intraepithelial neoplasia grade 1 (LSIL/CIN1) we prospectively recruited all the patients referred to colposcopy from 2003 to 2011 due to abnormal screening test results and diagnosed with LSIL/CIN1 at biopsy (n = 507). All biopsies were stained for p16 and re-evaluated after three years by the same gynecological pathologist using the LAST criteria. Follow-up was conducted every 6 months and included a Pap test (liquid-based cytology), high-risk human papillomavirus testing (Hybrid Capture 2 test), and colposcopy. The mean follow-up was 28 months. An outcome diagnosis of HSIL was defined as a histological diagnosis of highgrade SIL/CIN (HSIL/CIN2-3). The diagnosis of LSIL/CIN1 was confirmed in 416 out of 507 biopsies (82%), whereas 58 (11%) were reclassified as negative and 33 (6%) as HSIL/CIN2-3. During follow-up, 86/507 women initially diagnosed with LSIL/CIN1 (17%) showed an outcome diagnosis of HSIL/CIN2-3, with the rate of HSIL final diagnosis of 3% (2/58) in the women with biopsies reclassified as negative, 17% (70/416) in the group with confirmed LSIL and 42% (14/33) in the women with biopsies reclassified as HSIL (Po 0.001). p16 was positive in 245/507 patients (48%) and in 210/416 patients (50%) with confirmed LSIL/CIN1 at re-evaluation. Although positive p16 immunostaining was associated with risk of HSIL/CIN2-3 outcome in the multivariate analysis (Hazard ratio (HR) 1.9; 95% confidence interval (CI): 1.2-3.1; P = 0.009) in the overall group of patients with LSIL/CIN1, this association was not verified in the subset of patients with confirmed LSIL/CIN1 after re-evaluation (HR: 1.6; 95% CI: 0.9-2.6; P = 0.095). In conclusion, in LSIL/CIN1 lesions p16 should be limited to equivocal cases in which HSIL/CIN2 is included in the differential diagnosis since it has low value in clinical practice as a marker of progression of LSIL/CIN1.

show abstract

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

mentioning

confidence: 99%

See 1 more Smart Citation

p16 staining has limited value in predicting the outcome of histological low-grade squamous intraepithelial lesions of the cervix

et al. 2016

View full text Add to dashboard Cite

show abstract

“…Additional analyses are employed to monitor cellular (host) proteins whose synthesis in cervical lesions is de-regulated upon p53 and pRb functional inactivation. These include the cyclin-dependent kinase inhibitor p16INK4a and the proliferation antigen Ki-67 ( Figure 1 ) [ 47 , 48 , 49 ]. In particular, the progression of CIN lesions can be predicted by the combination of low pRb/p53 and high Ki-67/p16INK4a expression in the basal layers of the cervical epithelium [ 47 , 48 , 49 ].…”

Section: Role Of the Hpv-e5 E6 And E7 Proteins In The Developmentmentioning

confidence: 99%

“…These include the cyclin-dependent kinase inhibitor p16INK4a and the proliferation antigen Ki-67 ( Figure 1 ) [ 47 , 48 , 49 ]. In particular, the progression of CIN lesions can be predicted by the combination of low pRb/p53 and high Ki-67/p16INK4a expression in the basal layers of the cervical epithelium [ 47 , 48 , 49 ]. Recent data suggest evaluating the profile of specific cellular micro-RNAs that have an important role in cervical carcinogenesis and are modulated by the E5, E6 or E7 proteins of HR-HPV [ 50 ].…”

Section: Role Of the Hpv-e5 E6 And E7 Proteins In The Developmentmentioning

confidence: 99%

The Impact of Human Papilloma Viruses, Matrix Metallo-Proteinases and HIV Protease Inhibitors on the Onset and Progression of Uterine Cervix Epithelial Tumors: A Review of Preclinical and Clinical Studies

Barillari

Monini

Sgadari

et al. 2018

IJMS

Self Cite

View full text Add to dashboard Cite

Infection of uterine cervix epithelial cells by the Human Papilloma Viruses (HPV) is associated with the development of dysplastic/hyperplastic lesions, termed cervical intraepithelial neoplasia (CIN). CIN lesions may regress, persist or progress to invasive cervical carcinoma (CC), a leading cause of death worldwide. CIN is particularly frequent and aggressive in women infected by both HPV and the Human Immunodeficiency Virus (HIV), as compared to the general female population. In these individuals, however, therapeutic regimens employing HIV protease inhibitors (HIV-PI) have reduced CIN incidence and/or clinical progression, shedding light on the mechanism(s) of its development. This article reviews published work concerning: (i) the role of HPV proteins (including HPV-E5, E6 and E7) and of matrix-metalloproteinases (MMPs) in CIN evolution into invasive CC; and (ii) the effect of HIV-PI on events leading to CIN progression such as basement membrane and extracellular matrix invasion by HPV-positive CIN cells and the formation of new blood vessels. Results from the reviewed literature indicate that CIN clinical progression can be monitored by evaluating the expression of MMPs and HPV proteins and they suggest the use of HIV-PI or their derivatives for the block of CIN evolution into CC in both HIV-infected and uninfected women.

show abstract