metastasis

Breast cancer (BC), as a global challenge, is one of the most prevalent malignant diseases among women. Idiopathic granulomatous mastitis (IGM) is a rare, chronic inflammatory breast disease that primarily affects women of fertility age. IGM mimics symptoms and radiographic patterns of BC. IL-18 plays a dual role in cancer, as it can promote tumor growth or reduce tumor growth. Therefore, this study aimed to compare the serum levels of IL-18 in BC and IGM patients. This case-control study was conducted on 45 patients with BC, 25 with IGM (I), and 30 healthy individuals (C) with normal screening tests as the control group. The BC group consisted of 25 newly diagnosed BC patients (N), and 20 patients with metastatic BC (M). Specialized pathologists confirmed the histopathological pattern of BC and IGM. Enzyme-linked immunosorbent assay (ELISA) sandwich technique was used for the measurement of IL-18 serum levels. All statistical analyses were performed using SPSS-23, and GraphPad Prism. P <0.05 was considered statistically significant. The serum level of IL-18 showed statistically significant higher values in the three patient groups than the control group (P < 0.001). In addition, the IL-18 levels in the M group were significantly higher than in the N and I groups (P < 0.01). There was no statistical significance between N and I groups (P > 0.05). IL-18 levels were significantly elevated in BC compared with the IGM and control groups. IL-18 has a potential role as a prognostic indicator in BC, particularly for patients with metastasis.

Hyperthermia, which involves heating body tissues to enhance cancer treatment efficacy, has been explored as an adjunctive therapy to improve chemotherapy outcomes. Whole-body hyperthermia (WBH) offers a potential synergistic approach by sensitizing cancer cells to chemotherapeutic agents and enhancing drug delivery.

This study aimed to evaluate the efficacy and safety of combining systemic chemotherapy with WBH in patients with metastatic gastrointestinal cancers.

A pilot study was conducted at Shohada Tajrish Hospital. Patients with pathologically confirmed metastatic gastrointestinal cancers were treated with standard systemic chemotherapy combined with WBH. Hyperthermia was applied using infrared devices, maintaining body temperatures between 39°C and 40.5°C. Patients were kept at this plateau for 1.5 hours, receiving chemotherapy concurrently. Chemotherapy drugs were administered at 80% of the standard dose. After the completion of WBH, patients were observed in the hospital for 24 hours to ensure safety. Data on patient demographics, tumor characteristics, chemotherapy regimens, and adverse events were systematically collected and analyzed.

A total of 20 patients (mean age: 54.8 years) participated in the study, with an equal distribution of male and female participants. The mean number of hyperthermia and chemotherapy cycles was 4.6 and 4.9, respectively. Clinical response rates included 5% (1 patient) with a complete response (CR), 40% (8 patients) with a partial response (PR), and 35% (7 patients) with stable disease (SD). The overall disease control rate (DCR) — comprising CR, PR, and SD — was 80%, and all responses were observed in patients who had received at least six cycles of hyperthermia.Most patients experienced either no adverse events or only grade 1 toxicities. The most frequently observed grade 1 adverse effects were diarrhea (45%) and vomiting (43%), indicating that gastrointestinal symptoms were common. Severe toxicities (grade 4) were rare, occurring in approximately 2% of cases.

Whole-body hyperthermia combined with chemotherapy is a viable and well-tolerated therapeutic strategy for metastatic gastrointestinal cancers, demonstrating a favorable toxicity profile and promising response rates.Additional large-scale studies are suggested to confirm these findings and investigate the mechanisms underlying the improved treatment efficacy.

Endometrial cancer (EC) is a particularly frequent gynecological cancer, and metastasis is the leading cause of death in patients with EC. Using publicly accessible gene expression data, a bioinformatics study was carried out to increase our knowledge and reveal treatment targets for EC metastasis. This study aimed to identify new important molecular actors and clarify the molecular processes and pathways underlying EC metastasis.

The GEOexplorer and R programming languages were used to analyze and visualize gene expression data from EC metastatic gene expression datasets, and differentially expressed genes (DEGs) and differentially expressed lncRNAs (DElncRNAs) were identified using bioinformatics with P-value thresholds of < 0.05, and |log2FC| > 1.5. KEGG pathway enrichment analysis and gene ontology enrichment was used to enrich the observed DEGs, protein-protein interactions were established, and hub genes were identified.

The findings revealed that DEGs were considerably enriched in a number of pathways, including the "Pathways in cancer", "Breast cancer", and "Rap1 signaling pathway." DEGs were also found to be involved in a number of biological processes, cellular components, and molecular activities. The PPI network included the hub genes CTNNB1, FGFR3, ESR1, and SRSF3 as well as a number of DElncRNAs, such as LINC01541, SNHG17, LINC00520, BHLHE22-AS1, LOC100509445, H19, and HOTAIRM1.

This study contributes to our understanding of the molecular processes driving EC metastasis, which may result in the development of new treatment targets and indicators for the early identification of EC metastasis. More studies are needed to validate these findings and to understand the functional roles of these key factors in EC metastasis.

The tumor microenvironment (TME) plays a pivotal role in cancer progression, influencing tumor initiation, growth, invasion, metastasis, and response to therapies. This study explores the dynamic interactions within the TME, particularly focusing on self-organization—a process by which tumor cells and their microenvironment reciprocally shape one another, leading to cancer progression and resistance. Understanding these interactions can reveal new prognostic markers and therapeutic targets within the TME, such as extracellular matrix (ECM) components, immune cells, and cytokine signaling pathways.

A comprehensive search method was employed to investigate the current academic literature on TME, particularly focusing on self-organization in the context of cancer progression and resistance across the PubMed, Google Scholar, and Science Direct databases.

Recent studies suggest that therapies that disrupt TME self-organization could improve patient outcomes by defeating drug resistance and increasing the effectiveness of conventional therapy. Additionally, this research highlights the essential of understanding the biophysical properties of the TME, like cytoskeletal alterations, in the development of more effective malignancy therapy.

This review indicated that targeting the ECM and immune cells within the TME can improve therapy effectiveness. Also, by focusing on TME self-organization, we can recognize new therapeutic plans to defeat drug resistance.

Increasing evidence has reported gene expression alterations in breast cancer (BC) tissues, necessitating their investigating to highlight the molecular basis of the disease development or progression. This study investigated the expression of miR-141, E2F3, CDK3, TP53, and KAT2B, and their association with histologic grade and metastasis in BC tissues.

The RNA expression level of miR-141, E2F3, CDK3, TP53, and KAT2B genes was analyzed in 23 BC and 23 normal tissue samples by RT-qPCR. The associations of the expression level of these genes with clinicopathological features of the BC tissue samples were evaluated. The study also explored the correlation between RNA levels of genes and miR-141.

Expression of miR-141, E2F3, CDK3, and KAT2B demonstrated significantly higher levels in BC tumor than normal tissues. TP53 expression showed an increase in tumor compared to normal tissues, although it was insignificant. Moreover, increased RNA expression of miR-141, E2F3, CDK3, and KAT2B corresponded to the advanced stage and regional metastasis of BC. Additionally, the results demonstrated a significant correlation between RNA expression levels of miR-141 with CDK3 and E2F3 with KAT2B.

Our findings highlighted clinicopathologic indicators that were relevant to aggressive BC. Besides, Correlations between overexpression of miR-141, E2F3, CDK3, and KAT2B in BC tissues suggest regulatory effects. Taken together, it seems results of this study could provide evidence that dysregulation of gene expression contributes significantly to unveiling the underlying molecular basis of BC.

Colorectal cancer (CRC) ranks among the most prevalent cancers worldwide and is the fourth leading cause of cancer-related deaths. Metastasis poses a significant obstacle in CRC treatment, as distant metastasis, particularly to the liver, remains the primary cause of mortality. Colorectal liver metastasis (CRLM) occurs frequently due to the liver’s direct vascular connection to the colorectal region via the portal vein. Standard treatment approaches for CRLM are limited; only a few patients qualify for surgical intervention, resulting in a persistently low survival rate. Additionally, resistance to chemotherapy is common, emphasizing the need for more effective targeted therapies. Emerging evidence highlights the pivotal role of microRNAs (miRNAs) in modulating critical pathways associated with CRLM, including tumor invasion, epithelial-mesenchymal transition, and angiogenesis. MiRNAs exhibit dual functions as tumor suppressors and oncogenes by targeting multiple genes, thus playing a complex role in both the initiation and progression of metastasis. The regulatory mechanisms of miRNAs could help to identify novel biomarkers for early diagnosis and prognosis of CRLM, as well as promising therapeutic targets to overcome chemoresistance. Despite numerous studies on miRNA involvement in CRC metastasis, dedicated reviews focusing on miRNAs and CRLM remain scarce. This review aims to approach targeted therapies by examining the current understanding of miRNA involvement in CRLM and exploring their potential as diagnostic, prognostic, and therapeutic agents. Through an integrative approach, we aim to provide insights that could transform CRLM management and improve patient outcomes.

Chemotherapy remains a primary approach to cancer treatment, widely applied in bladder cancer (BC). However, the various side effects and resistance associated with chemotherapeutic drugs pose significant challenges in BC therapy, prompting interest in natural compounds like luteolin. Studies focus on its effects on key biological processes involved in BC, including metastasis, apoptosis, and autophagy.

This study investigated the regulation of mRNA expression of genes associated with apoptosis (BCL2, P53), autophagy (ULK1, ATG12), and metastasis (MMP2, MMP9) in malignant BC cells treated with luteolin.

This was an in vitro experimental study. EJ138 BC cells were treated with various concentrations of luteolin, and its impact on cell viability, proliferation, and gene expression was assessed. The cytotoxic effect of luteolin on EJ138 BC cells was evaluated using the MTT assay after 24- and 48-hour treatments with different luteolin concentrations. Flow cytometry was performed to examine luteolin’s anti-proliferative effect, and RT-PCR was used to analyze mRNA expression of BCL2, P53, ULK1, ATG12, MMP2, and MMP9 genes.

MTT assay results confirmed that luteolin reduced the proliferation rate of BC cells. Flow cytometry indicated increased cell death in EJ138 BC cells following luteolin treatment. RT-PCR findings demonstrated that luteolin upregulated P53, ULK1, and ATG12 expression while downregulating BCL2 mRNA expression. However, luteolin treatment in EJ138 cells did not significantly alter MMP2 and MMP9 expression levels.

These findings indicate that luteolin exerts cytotoxic effects on EJ138 BC cells by dysregulating mRNA expression of genes involved in apoptosis and autophagy. Therefore, luteolin shows potential as an effective anti-cancer agent for BC therapy.

In the 21st century, the main cause of death in both sexes worldwide are cardiovascular diseases, in second place are neoplasms. In the case of women, the fourth cause of mortality is breast cancer despite the screening.

Understanding the epigenetic mechanisms associated with cervical cancer progression and metastasis, considering its correlation with poor prognosis.

To prepare the present article, the search was done on platforms PubMed and Google Scholar, the search was carried out using the following medical subject headings (MeSH) in the search engine: “metastatic cervical cancer”, “cervical cancer epigenetics”, “cervical cancer genetics”, “cervical cancer mirnas”, “cervical cancer lncrnas”, “cervical cancer clinical trials” and “metastatic cervical cancer hpv”, in combination with boolean connectors ‘AND’ and ‘OR’. A total of 114 articles were reviewed, published between 1989 and 2022.

It is essential to understand and know the epigenetic mechanisms associated with the cervical cancer pathogenesis and progression, to create new targeted treatment schemes for metastatic cervical cancer to reduce the mortality rate and increase disease-free survival.

 Colorectal cancer (CRC) is one of the most common types of cancer in the world and is considered a leading cause of cancer-related death. The present study aimed to investigate the inhibitory effect of lactobacillus acidophilus (PTCC 1643) supernatant (LAS) and lactobacillus rhamnosus (PTCC 1657) supernatant (LRS) on the growth and invasiveness of the human colon carcinoma cell line (Caco2) in-vitro.  

Materials & Methods

 In this study, the antiproliferative activity and anti-invasion potential of LAS and LRS were determined by MTT and transwell chamber assays, respectively. Furthermore, the expression of mitochondrial membrane potential-9 (MMP-9) and matrix metalloproteinase-12 (MMP12) genes were analyzed by real-time PCR.

 The results of the MTT assay indicated that LAS and LRS had cytotoxic effects on Caco-2 cell proliferation at a concentration of 25% and higher after 72 hours (p<0.0001). Thus, the minimum concentrations (25%) of supernatants were chosen for further experiments. LRS and LAS could significantly suppress the invasiveness of cells, p= 0.028 and p=0.002, respectively. Also, the expression of MMP12 was significantly increased in cells when treated with LAS (p<0.001), whereas LRS had no significant effect on MMP-12 expression. Furthermore, the expression of MMP-9 was statistically decreased in cells treated with both supernatants (p<0.00001).

 In general, it was shown that LAS and LRS exert anti-cancer activity against the growth, invasion, and metastasis of Caco2 cells.

Breast cancer (BC) is the most prevalent and lethal cancer in women. Prognostic factors are used to guide treatment and predict the prognosis. This study aimedto assess the influence of prognostic factors on the survival of patients with non-metastatic invasive BC.

Data from invasive BC patients admitted to Medical Oncology Department of Süleyman Demirel University between October 2002 and October 2013 were retrospectively reviewed. Clinicopathologic features, treatment information, and follow-up data were noted. The Kaplan-Meier method was used to estimate survival functions. Multivariate Cox regression analysis was performed to identify prognostic factors for disease-free survival (DFS) and overall survival (OS), with P-values <0.05 for univariate results

A total of 717 patients entered the study.The median follow-up time was 41 months. Recurrence was detected in 17.4% of the patients, and 111 (15.5%) patients died. The 5-and 10-year DFS rates were 78% and 61%; OS rates were 86% and 70%, respectively. In multivariate analyses, DFS and OS were associated with axillary lymph node involvement (P<0.001 and P<0.05, respectively), tumor size (P<0.05), and histologic grade (P<0.05),whereas human epidermal growth factor receptor 2 positivity had only a statistically significant effect on poor OS (P=0.004).

Consistent withprevious studies, traditional prognostic factors had an important impact on prognosis in invasive BC patients. In the current era, where more conservative surgical approaches and new, effective systemic neoadjuvant and adjuvant therapies are widely used, the importance of the traditional prognostic factors highlighted in our study needs to be established by further studies.

The aim of this study was to understand the interactions between tumor-associated mesenchymal stemcells (TA-MSCs) and triple-negative breast cancer (TNBC) cells, which appear to be necessary for developing effectivetherapies. In this experimental study, MDA-MB-231 and 4T1 TNBC cells were co-cultured with bonemarrow-derived MSCs, and TA-MSCs conditioned media (CM) were collected. TA-MSC CM-treated TNBC cells weresubjected to migration and invasion assays. Epithelial-mesenchymal transition (EMT) marker expression was quantifiedby real-time polymerase chain reaction (RT-PCR). Cell proliferation was measured using trypan blue exclusiontechnique, while cell cycle distribution and apoptosis were assessed by flow cytometry. The effects of TA-MSCs ontumor volume, survival rate, and lung metastasis were evaluated by subcutaneous co-injection of MSCs with 4T1 cellsin the right flanks of BALB/c mice (n=5 per group). Intratumoral interleukin-12 (IL-12) immunotherapy was performedusing lentiviral particles as a rescue experiment. The TA-MSCs RNA-seq dataset (PRJEB27694) was analyzed todetect elevated metastasis-associated oncogenes, downloaded from the European Nucleotide Archive database. Forvalidation of the RNA-seq data analysis, the expression levels of candidate oncogenes were evaluated in TA-MSCs,TNBC cells, and tumor tissue using RT-PCR. TA-MSCs enhanced migration, invasion, and EMT of TNBC cells in vitro without affecting cell proliferation orapoptosis. In vivo, TA-MSCs increased tumor growth and lung metastasis, while decreasing survival rates. IL-12 therapyelevated serum IL-12 and interferon-gamma (IFN-γ) expression, suppressed tumor volume and lung metastasis, andimproved overall survival in the TA-MSC group. RNA-seq data analysis identified upregulated oncogenes in TA-MSCs,among which MMP3, CXCL2, CXCL5, and ICAM1 were selected as the most relevant to metastasis. These genesshowed increased expression in TA-MSCs, TNBC cells, and tumor tissues. The findings of the present study revealed a complex interplay between TA-MSCs and TNBC cells thataffects tumor growth and metastasis. Preclinical results indicate that intratumoral IL-12 immunotherapy shows promisein overcoming TA-MSC-promoted tumor growth and metastasis.

The overall survival rates are below 10% in patients with metastatic renal cell carcinoma (RCC) posing a significant health challenge. There is a pressing need for novel and simple predictors of metastasis in patients with RCC to aid in early detection, thereby having prognostic and therapeutic implications.

To assess the efficacy of various inflammatory markers such as neutrophil-lymphocyte ratio (NLR), platelet-lymphocyte ratio (PLR), Systemic Inflammatory Response Index (SIRI), and Systemic Immune-Inflammatory Index (SII), in predicting metastasis amongst individuals diagnosed with RCC.

A retrospective study was undertaken at a tertiary hospital, focusing on individuals diagnosed with RCC. Patients were divided into two groups: Those with and without metastases. Patient demographics and clinical, pathological, and laboratory data were collected. The researchers evaluated the predictive capabilities of NLR, PLR, SIRI, and SII using ROC curves, with cut-off points determined via the Youden Index.

Of the 91 patients, 25 (27.5%) had metastatic RCC. Significant differences in NLR (P = 0.047), PLR (P = 0.004), SIRI (P = 0.006), and SII (P = 0.005) were noted between metastatic and non-metastatic groups. The ROC analysis showed that SIRI and SII had the highest predictive capacity with areas under the curve (AUCs) of 0.687 and 0.693, respectively. Logistic regression demonstrated NLR, PLR, SII, and SIRI as independent predictors of metastasis in RCC, with a combined predictive accuracy of 83.5%.

Neutrophil-lymphocyte ratio, PLR, SIRI, and SII are reliable predictors of metastasis in RCC, with their combined use enhancing predictive accuracy. These hematological parameters can be easily derived from routine blood tests, could help in the early diagnosis of metastases, and tailor the management of RCC, improving patient outcomes. Further multicentric studies are recommended to validate these findings and help integrate them into clinical practice.

Shikonin, a compound extracted from Lithospermum erythrorhizon , has demonstrated therapeutic effects on cancer; however, its effects on oral cancer remain unclear.

This study aimed to explore the therapeutic value of shikonin for the treatment of oral cancer.

MTT, colony formation, and Transwell assays were employed to evaluate the inhibitory effects of shikonin on the proliferation and migration abilities of human oral cancer cell lines (SCC-4 and SAS). Apoptosis and cell viability were assessed using the TdT-mediated deoxyuridine triphosphate-biotin nick end-labeling (TUNEL) assay. To investigate the potential anticancer mechanisms of shikonin, RNA sequencing, quantitative PCR, and western blotting were performed to analyze changes in the expression levels of oral cancer cell-related genes and proteins (matrix metalloproteinases-2 (MMP-2), matrix metalloproteinases-9 (MMP-9), VEGF-A, VEGF-C, Beclin-1, autophagy-related genes (ATG5), and light chain-3 (LC-3)). Additionally, animal xenograft experiments were conducted to examine the in vivo antitumor effects of shikonin.

The findings revealed that the external application of shikonin specifically targeted oral cancer cells without affecting normal cells and led to a dose-dependent inhibition of their growth. Even at non-lethal doses, shikonin effectively suppressed the production of metalloproteinases, thereby inhibiting cancer cell migration and wound healing. Furthermore, shikonin treatment reduced levels of tumor progression factors, such as vascular endothelial growth factor (VEGF)-A and VEGF-C, which are released during the early stages of cancer cell angiogenesis and lymphangiogenesis. Meanwhile, higher doses of shikonin induced cell autophagy and activated proteins such as ATG-5, LC-3B, and Beclin-1. At lethal doses, shikonin further decreased mitochondrial membrane potential, released calcium ions, and triggered apoptotic pathways. However, the administration of a calcium ion chelator (BAPTA-AM) inhibited shikonin-induced apoptosis.

These results demonstrate that shikonin induces autophagy and activates apoptotic pathways in oral cancer cells. Shikonin treatment significantly inhibited oral cancer growth and induced apoptosis in a rat model. In conclusion, shikonin effectively inhibited oral cancer cell growth, metastasis, and the expression of tumor progression-related proteins. Given the ease of drug delivery to the affected area in oral cancer, shikonin holds substantial potential for future applications that may improve patient recovery and enhance cure rates.

Breast cancer remains a formidable public health challenge worldwide, characterized by its initiation within the breast’s diverse tissues, particularly the ducts and lobules. This malignancy is predominantly categorized into three subtypes based on receptor status and genetic markers: hormone receptor-positive, HER2-positive, and triple-negative. Each subtype exhibits distinct biological behaviors and responses to treatment, which significantly influence the prognosis and management strategies. The development and metastatic spread of breast cancer are complex processes mediated by interactions between tumor cells and the host microenvironment, involving various cellular and molecular mechanisms. This review highlights the potential therapeutic role of celecoxib, a selective cyclooxygenase-2 (COX-2) inhibitor, in addressing the multifaceted aspects of breast cancer progression. Specifically, celecoxib modulates angiogenesis by reducing the levels of vascular endothelial growth factor (VEGF) through decreased PGE2 production, enhances the immune response by alleviating PGE2-mediated immunosuppression, and inhibits metastasis by limiting the activity of matrix metalloproteinases (MMPs). These mechanisms collectively hinder tumor growth, immune evasion, and metastatic spread. By synthesizing recent findings and analyzing the impact of celecoxib on these pathways, this paper seeks to delineate the integrated approaches necessary for managing metastatic breast cancer effectively.

Interleukin-2 (IL-2) is a well-known cytokine that plays a crucial role in stimulating immune cells, including natural killer (NK) cells and cytotoxic T cells. It has been studied as an immunotherapy for a variety of diseases, including cancer. However, due to its short serum half-life, high doses of IL-2 are required which can result in systemic toxicities like capillary leak syndrome.

To demonstrate the enhanced antitumor efficacy of Albumin Binding Domain-conjugated IL-2 (ABD-IL-2) at a lower dose compared to IL-2.

IL-2 and ABD-IL-2 were purified using Ni-NTA resin with a histidine sequence added to their C-terminal region for purification purpose. Peripheral blood lymphocytes were stimulated with IL-2 and ABD-IL-2 to assess their function. 4T1 cells were injected into BALB/c mice to establish a breast cancer model with metastasis evaluated in the lungs.

Both recombinant proteins significantly stimulated T lymphocyte proliferation compared to the negative control (P=0.000, P=0.001). Administration of both proteins reduced the size of isolated tumors in the breast cancer mouse model. The control group had more nodules and larger lung metastatic centers (P=0.000). Metastasis to secondary lymphoid organs occurred only in the control group.

By using ABD-IL-2 at a one-third concentration compared to IL-2, we aimed to reduce administration toxicity associated with high doses of IL-2 in immunotherapy. This approach shows potential for improving IL-2-based treatments while minimizing adverse effects.

Small cell lung cancer usually presents as a progressive disease in over 70% of patients. Common organs of metastasis include the liver, adrenal glands, bones, and brain. However, metastasis to the parotid gland is uncommon, as it has been discussed only in case reports. Among all parotid tumors, small cell cancer is rare, seen in only 1.7%.A 60-year-old man presented with a slow-growing, painless tumor of the left parotid gland and peripheral facial paralysis. Neck ultrasound identified a solid mass in the left parotid gland with enlarged lymph nodes in the parotid gland and ipsilateral neck lymphadenopathies with pathologic features in levels 2 and 3. Chest computed tomography (CT) demonstrated subsegmental collapse in the lingula with peribronchial cuffing in this lobe and mild cylindrical bronchiectatic changes in the left lower lobe. CT also showed multiple
mediastinal lymphadenopa thies in prevascular, paraaortic, and paratracheal spaces. Core needle biopsy was done, and initial analysis revealed small cell carcinoma in the left parotid gland. Immunohistochemical analysis of the specimen demonstrated and confirmed the diagnosis. The patient was then referred to the radiation oncology unit for treatment. Chemotherapy was initiated with a combination of cisplatin and etoposide. No complications of the chemotherapy were observed after three cycles; treatment and follow-up are ongoing. No irradiation was performed after evaluation by the radiation oncology department. Due to the advanced stage of his disease, treatment is set for palliative purposes only. Small cell lung cancer diagnosed from solitary etastasis to the parotid gland is very rare. Physicians should keep pulmonary origin in mind when faced with a parotid tumor, as without careful examination, the primary focus may be overlooked, negatively impacting survival rates and the prognosis of the patient. Overall, this finding carries a poor prognosis, but the mainstay of treatment is palliation with systemic chemotherapy and possibly irradiation to control symptoms.

Osteosarcoma (OS) is the most common cause of limb loss due to cancers. This study determines the mean survival time in patients with OS and prognostic factors.

This retrospective study was conducted on patients with OS who were referred to Shah Vali Hospital, Yazd, Iran, from 2004 to 2018. The data on patient-related factors (age and sex), tumor-related factors (recurrence, recurrence site, and metastasis), and living status were obtained and analyzed.

Overall, 29 patients were included, of which 21(72.4%) were male. The mean age of patients was 21.3±8.4 (age range of 8-42) years. The tumor site was the lower limb in 23 patients (79.3%), the upper limbs in 4 patients (13.8%), and the axial in 2 patients (6.9%). Meanwhile, 13(44.8%) patients died due to OS, and one (6.9%) died for other reasons. The mean survival time in the subjects was 83.1±14.71 months. The 1-year survival of patients was nearly 90%, 3-year survival was about 64%, and 5-year survival was 40%. Also, 7(24.1%) patients had primary metastasis. The mean survival period was 22.25 months in patients with primary metastasis and 98.87 months in patients without primary metastasis (P=0.011). Among the patients, 15(51.7%) had a recurrence, of which 6(20.7%) were local, and 9(31%) were distant recurrences. The mean survival period after the recurrence of patients was 21.27±5.07 months.

The mean survival period, according to sex, age, recurrence, and recurrence site, was not significant; however, it was significant according to metastasis.