Polish Journal of Pathology最新文献

This study aimed to investigate whether the crosstalk between the osteoprotegerin (OPG)/receptor activator of nuclear factor-kB (RANK)/receptor activator of nuclear factor-kB ligand (RANKL) in bone marrow mesenchymal stem cells (BMSCs) and Wnt/b-catenin pathways in Pca cells regulates bone metastasis of PCa. Our study showed that there was increased OPG/RANKL/RANK and b-catenin expression in the tissue of PCa and its bone metastasis. This study further showed that RANKL knockdown in BMSCs or b-catenin knockdown in PC-3s blocked the proliferation and migration of BMSCs and the proliferation, migration, and invasion of PC-3s in vitro. Conversely, RANKL overexpression in BMSCs and b-catenin overexpression in PC-3s promoted the proliferation and migration of BMSCs and the proliferation, migration, and invasion of PC-3s in vitro. These data indicate that the RANKL pathway in BMSCs promoted the PC-3s invasion and the catenin pathway in PC-3s activated BMSCs with expression of cancer-associated fibroblast markers, which promoted the bone metastasis. This suggests that the interaction and crosstalk between BMSCs in bone microenvironment and PCa play a critical role in the exquisite tropism for Pca bone metastasis. Cancer therapies classically target tumour cells; however, based on this study, targeting BMSCs in bone microenvironment is a reasonable option for PCa therapy strategy.

The use of chemotherapy in breast cancer management has significantly contributed to the decrease in its mortality. Currently, the prognosis is determined by molecular biomarkers, such as oestrogen receptors, and human epidermal growth factor receptor 2. However, the increasing use of advanced molecular technologies, including oncotype DX recurrence score (ODX-RS), has provided the ability to estimate the risk of recurrence. Research has demonstrated that the ODX-RS helps to predict recurrence risk and the potential benefit of chemotherapy in breast cancer. As a result, it can assist clinicians in making decisions regarding using the chemotherapy. The goal of work is to explore the correlation between the ODX-RS and Ki-67 proliferative index (Ki-67-PI). This study included 137 patients with oestrogen positive, human epidermal growth factor receptor 2-negative early breast cancer, and had non- or early axillary disease. Patients with low Ki-67-PI were as follows: low ODX-RS in 17%, intermediate ODX-RS in 80%, and high ODX-RS in 2%. In the high Ki-67-PI group: low ODX-RS in 12%, intermediate ODX-RS in 48%, and high ODX-RS in 40%. In conclusion, the results show no significant correlation between the ODX-RS and Ki-67-PI (r = 0.511, p-value < 0.9).

C1q/TNF-related protein-9 (CTRP9) has been reported to play roles in several types of retinal diseases. However, the role and the potential mechanism of CTRP9 in glaucoma are still incompletely understood. The expression of CTRP9 in OGD/R-induced retinal ganglion cells (RGCs) was detected by quantitative real-time polymerase chain reaction and western blot assay. Cell proliferation was identified by cell counting Kit-8 assay. Flow cytometry, enzyme-linked immunosorbent assay and western blot assay were performed to assess cell apoptosis. Unfolded protein response (UPR), endoplasmic reticulum (ER) stress and the AMPK pathway were evaluated by western blot assay. The data showed that the expression of CTRP9 was significantly downregulated in OGD/R-induced 661W cells. OGD/R treatment reduced cell viability, promoted cell apoptosis and activated the UPR and ER stress. The overexpression of CTRP9 reversed the effects of OGD/R on 661W cell viability, apoptosis, the UPR and ER stress, as well as the AMPK pathway. However, Compound C, an inhibitor of AMPK signaling, reversed the protection of CTRP9 overexpression against injury from OGD/R in 661W cells. In summary, the results revealed that CTRP9 abated the apoptosis and UPR of OGD/R-induced RGCs by regulating the AMPK pathway, which may provide a promising target for the treatment of glaucoma.

Precancerous cervical lesions are metaplastic alterations of epithelial cells of the cervix, eventually developing into cervical cancer. Despite primary and secondary prevention, the burden of cervical cancer remains high globally. Protein arginine methyltransferases (PRMT) represent post-translational modifications that interact with multiple signalling pathways, playing a role in epithelial-mesenchymal transition. In complex with desmoglein-2 (DSG2), a cell adhesion protein, both participate in the progression of dysplastic changes with potential malignant development. The presented study was performed on archival paraffin-embedded blocks from adult women. The studied samples were categorised into low-grade and high-grade intraepithelial lesions. Immunohistochemical analysis was used to observe subcellular localisation, immunoreaction intensity, and percentage of PRMT5- and DSG2-expressing cells, followed by statistical analysis. Preliminary results identified statistically significant differences between the expression and subcellular localisation of proteins in question in low-grade and high-grade squamous intraepithelial lesions. The primary goal of the presented study is to perceive the involvement of PRMT5 and DSG2 in the initiation and progression of cervical lesions. Our observations indicate the potential of the assessed proteins as prognostic markers. However, further studies of PRMT5 and DSG2 are required to provide greater insight into cervical carcinogenesis.

Lobular carcinoma in situ (LCIS) with microinvasion is a rare entity which is rarely reported in the literature. We describe a case of microinvasive LCIS following excision of a fibroepithelial lesion. The lesion was graded as U3 and M3 on ultrasonography and mammography respectively, and on core needle biopsy was described as a fibroepithelial lesion with 'unusual features'. Microscopic examination revealed a fibroepithelial lesion focally colonised by florid E-cadherin negative LCIS with multiple foci of microinvasive classical lobular carcinoma, which lacked a myoepithelial layer on CK5 and S100 staining.

Primary sebaceous and lipid-rich carcinomas are extremely rare. Sebaceous carcinoma cells are large and oval with light, partially vacuolated cytoplasm. The second population consists of cells located mainly on the peripheral parts of tumour beaches. Those cells are of smaller calibre and are fusiform in appearance. Lipid- rich carcinoma is made up of multiple cell populations. The predominant cell type is with a distinctly light, vacuolated, and partially optically clear cytoplasm. Pathohistological analysis may be overlapping. On one side there is a tumour with a relatively excellent prognosis, and on the other, a highly aggressive carcinoma with a tendency for early metastases.

The normal subpopulation of CD34+CD38 - haematopoietic stem cells does not express CLL-1; therefore, the assessment of the expression of this protein can be used for the diagnosis of minimal residual disease. The aim of this study was to evaluate, using multi-colour flow cytometry, the level of CLL-1 protein expression on CD34+CD38- myeloid niche cells in acute myeloid leukaemia (AML) and myelodysplastic syndromepatients at the time of diagnosis and during disease monitoring on the example of 3 practical cases. The following conclusion was drawn: CD34+CD38-CLL-1+ cells in AML patients may serve as a biomarker to predict disease aggressiveness.

Breast carcinoma is one of the most common causes of cancer-related mortality among women worldwide. The primary objective of the present study was to eva-luate the expression of the epithelial-mesenchymal transition (EMT)-related markers Lin28, MUC1, and lipocalin-2 in invasive lobular carcinoma (ILC) and to investigate their correlation with clinicopathological characteristics and patient survival. This prospective cohort study included 120 classic ILC cases investigated for immunohistochemical expressions of Lin28, MUC1, and lipocalin-2 and followed them for five years or until death. The expression of markers in all tissue samples was assessed, analysed, and correlated with clinical-pathological parameters and outcomes. Lin28, MUC1, and lipocalin-2 were positively expressed in 55%, 75%, and 45%, respectively. The high expression of Lin28 and MUC1 and low lipocalin-2 were associated with poor clinicopathological characteristics and unfavourable overall survival. Lin28 and MUC1 were highly expressed in ILC and were associated with lower survival rates, poor outcomes, and a pessimistic prognosis in patients with ILC, while lipocalin-2 expression was associated with a positive outcome where its down-regulation was related to a poor prognosis in patients with ILC. Furthermore, we concluded that Lin28, MUC1, and lipocalin-2 could influence cancer behaviours, including proliferation, invasion, and migration, by regulating the EMT process and CSC criteria in ILC cells, making them potentially advantageous indicators and targeted treatments. Our research may have significant implications for understanding the pathophysiology and prognosis of ILC, which could help select treatment targets.

Long non-coding RNA LINC00908 is a functional biomarker in regulating tumour progression. Its dysregulation in gastric cancer implies its potential functional role. Few studies have noted the functional role of LINC00908 in gastric cancer. The potential of LINC00908 to serve as a biomarker in gastric cancer was evaluated. A total of 113 paired gastric cancer tissues and normal tissues were collected from patients with gastric cancer. LINC00908 levels were evaluated by polymerase chain reaction, and its significance in disease progression and patients' prognosis was assessed. In vitro, the function of LINC00908 in tumour-related cellular processes was evaluated with CCK8 and Transwell assay. Significant downregulation of LINC00908 was observed in gastric cancer and was negatively associated with disease development and overall survival of patients. LINC00908 showed significant inhibitory effects on the proliferation, migration, and invasion of gastric cancer cells. Additionally, miR-627-3p was sponged by LINC00908 and therefore mediated the function of LINC00908 in gastric cancer cells. LINC00908 functioned as a prognostic biomarker and tumour suppressor of gastric cancer, providing a therapeutic target for gastric cancer.

Breast cancer is the most common cancer and a leading cause of death in women in Saudi Arabia. P16 is a tumour suppressor gene that plays a crucial role in regulating cell cycle. Several studies have investigated the significance of p16 expression in various cancer types. However, the significance of p16 in breast cancer remains controversial and insufficiently studied. The present study aims to examine the association between p16 expression and clinicopathological factors in breast cancer using immunohistochemistry staining. The study utilised 475 prospectively collected tissue samples from 475 women with breast cancer in Saudi Arabia. Nuclear and cytoplasmic immunohistochemical staining of p16 was observed in 338 (71%) of the cases and showed significant direct associations with adverse tumour features, including high tumour grade (p < 0.0001), negative oestrogen receptor/progesterone receptor status (p < 0.001), and lymph node metastasis (p = 0.02). Our study revealed a significant association between p16 protein expression and the established negative prognostic parameters in breast carcinoma including tumour grade, lymph node metastasis, and oestrogen receptor and progesterone receptor status.