• Lobna Bouzidi, Saadia Makni, Jihen Feki, Rim Kallel, Soumaya Graja, Naourez Gouiaa, Tahya Sellami-Boudawara, and Manel Mellouli.
• Department of Pathology and Research laboratory LR18SP10, University Hospital Habib Bourguiba, Sfax, Tunisia.
• Arch Iran Med. 2022 Apr 1; 25 (4): 250-256.

BackgroundBreast cancer represents the most frequent cancer and cause of death in women worldwide and in Tunisia. Cyclin D1 is a gene of cell cycle regulation. It represents a potential oncogene in invasive breast cancer; however; the results are conflicting. We performed a retrospective study aiming to analyze the prognostic impact of cyclin D1 expression in patients with invasive breast carcinoma of no special type and its relation with clinical-pathological features.MethodsOne hundred cases of invasive breast carcinoma of no special type diagnosed between 2009 and 2011 were included in this study. Immunohistochemical (IHC) staining was performed for cyclin D1 in all cases. Results were analyzed statistically.ResultsCyclin D1 positivity was seen in 74 cases (74%), of which 32 cases (32%) showed strong immunoreactivity. Cyclin D1 staining was statistically significantly associated with estrogen receptor (ER) and progesterone receptor (PR) positivity (P<0.0001) and with low grade SBR (P=0.007). None of the clinical data and other pathological features had any association with cyclin D1 expression (P>0.05). Univariate analysis revealed that expression of cyclin D1 was not statistically associated with overall survival (OS) and disease-free survival (DFS) (P=0.459 and P=0.564, respectively).ConclusionThese results confirm that cyclin D1 overexpression can be employed as a beneficial prognostic marker and suggest that anti-cyclin D1 therapy may be efficient, especially for ER positive tumors.2022 The Author(s). This is an open-access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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