Background: The molecular pathways involved in the onset and progression of idiopathic 60 pulmonary fibrosis (IPF) still need to be fully clarified, being some shared with lung cancer development. HOXB7, a member of homeobox (HOX) gene family, has been found involved in various cancers. Methods: Immunohistochemical (IHC) analysis was run on lung tissue samples from surgical lung biopsy (SLB) of 19 patients with IPF retrospectively selected from the IPF database of the 64 University Hospital of Modena. HOXB7 expression was quantified analyzed and compared it with that of 5 patients with no evidence of pulmonary fibrosis as controls. Results: IHC quantificationthe semi-quantitative analysis of IHC showed that HOXB7 signal intensityprotein expression was higher in IPF patients as compared to controls (difference between means = 15.906.2±6.02.37, p=0.0157). Further, HOXB7 expression resulted higher in IPF patients with a higher extent of fibrosis (50-75%) at high resolution computer tomography compared to those with lower extent (0-25%) (difference between means = 25.74 ± 6.72, p=0.004). Conclusions: The expression of HOXB7 is higher in the lung of IPF patients as compared to controls, being represented in different cellular compartments within the lung niche. Further investigations are needed to clarify its role in the pathogenesis and progression of IPF.
Expression of HOXB7 in the lung of patients with idiopathic pulmonary fibrosis: a proof of concept study / Samarelli, ANNA VALERIA; Tonelli, Roberto; Raineri, Giulia; Mastrolia, Ilenia; Costantini, Matteo; Fabbiani, Luca; Catani, Virginia; Petrachi, Tiziana; Bruzzi, Giulia; Andrisani, Dario; Gozzi, Filippo; Marchioni, Alessandro; Masciale, Valentina; Aramini, Beatrice; Ruggieri, Valentina; Grisendi, Giulia; Dominici, Massimo; Cerri, Stefania; Clini, Enrico. - In: BIOMEDICINES. - ISSN 2227-9059. - 12:6(2024), pp. 1-12. [10.3390/biomedicines12061321]
Expression of HOXB7 in the lung of patients with idiopathic pulmonary fibrosis: a proof of concept study.
Anna Valeria Samarelli;Roberto Tonelli;Giulia Raineri;Ilenia Mastrolia;Matteo Costantini;Luca Fabbiani;Virginia Catani;Tiziana Petrachi;Giulia Bruzzi;Dario Andrisani;Filippo Gozzi;Valentina Masciale;Giulia Grisendi;Massimo Dominici;Stefania Cerri;Enrico Clini
2024
Abstract
Background: The molecular pathways involved in the onset and progression of idiopathic 60 pulmonary fibrosis (IPF) still need to be fully clarified, being some shared with lung cancer development. HOXB7, a member of homeobox (HOX) gene family, has been found involved in various cancers. Methods: Immunohistochemical (IHC) analysis was run on lung tissue samples from surgical lung biopsy (SLB) of 19 patients with IPF retrospectively selected from the IPF database of the 64 University Hospital of Modena. HOXB7 expression was quantified analyzed and compared it with that of 5 patients with no evidence of pulmonary fibrosis as controls. Results: IHC quantificationthe semi-quantitative analysis of IHC showed that HOXB7 signal intensityprotein expression was higher in IPF patients as compared to controls (difference between means = 15.906.2±6.02.37, p=0.0157). Further, HOXB7 expression resulted higher in IPF patients with a higher extent of fibrosis (50-75%) at high resolution computer tomography compared to those with lower extent (0-25%) (difference between means = 25.74 ± 6.72, p=0.004). Conclusions: The expression of HOXB7 is higher in the lung of IPF patients as compared to controls, being represented in different cellular compartments within the lung niche. Further investigations are needed to clarify its role in the pathogenesis and progression of IPF.File | Dimensione | Formato | |
---|---|---|---|
Samarelli (HOXB7-gene expression in IPF- 2024) .pdf
Open access
Tipologia:
Versione pubblicata dall'editore
Dimensione
3.49 MB
Formato
Adobe PDF
|
3.49 MB | Adobe PDF | Visualizza/Apri |
Pubblicazioni consigliate
I metadati presenti in IRIS UNIMORE sono rilasciati con licenza Creative Commons CC0 1.0 Universal, mentre i file delle pubblicazioni sono rilasciati con licenza Attribuzione 4.0 Internazionale (CC BY 4.0), salvo diversa indicazione.
In caso di violazione di copyright, contattare Supporto Iris