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Multiple studies on PIK3CA mutations in breast cancer (BC) had been performed, which showed the controversial results among different countries and races even those from the same country. The present study aimed to explore the PIK3CA gene mutation status in BC patients in Northwest China and reveal the relationship between PIK3CA mutations and clinicopathological features along with prognosis.1002 BC patients from Northwest China were recruited in this study, genomic DNA was extracted from formalin-fixed paraffin-embedded (FFPE) tumor tissues, and hotspot mutations in the exon 9 and 20 of PIK3CA gene were detected by ARMS-PCR.PIK3CA mutations were found in 31.2% (313/1002) of BC patients, among them 66.1% were mutations in exon 20% and 32.6% were mutations in exon 9. H1047R was the most common mutation type, accounting for 56.5% of the total mutated samples. Significant correlations were observed between PIK3CA mutation status and age (P = 0.035), histopathologic types (P = 0.004), pathological grade (P = 0.013), ER positivity (P 0.001), PR positivity (P 0.001), molecular subtypes (P = 0.004) and family history (P = 0.007). Cox multivariate analysis showed that patients with mutations in exon 9 or 20 had shorter DFS and OS than wild-type patients. Those with exon 9 mutations subgroup had the worst prognosis. Interestingly, patients with H1047L mutation had the best prognosis than others.PIK3CA mutations could be used as an indicator of clinical outcome or targeted therapy for multiple breast cancer subgroups in Northwest China.

Dopamine receptors are involved in several immunological diseases. We previously found that dopamine D3 receptor (D3R) on mast cells showed a high correlation with disease activity in patients with rheumatoid arthritis, but the mechanism remains largely elusive. In this study, a murine collagen-induced arthritis (CIA) model was employed in both DBA/1 mice and D3R knockout mice. Here, we revealed that D3R-deficient mice developed more severe arthritis than wild-type mice. D3R suppressed mast cell activation in vivo and in vitro via a Toll-like receptor 4 (TLR4)-dependent pathway. Importantly, D3R promoted LC3 conversion to accelerate ubiquitin-labeled TLR4 degradation. Mechanistically, D3R inhibited mTOR and AKT phosphorylation while enhancing AMPK phosphorylation in activated mast cells, which was followed by autophagy-dependent protein degradation of TLR4. In total, we found that D3R on mast cells alleviated inflammation in mouse rheumatoid arthritis through the mTOR/AKT/AMPK-LC3-ubiquitin-TLR4 signaling axis. These findings identify a protective function of D3R against excessive inflammation in mast cells, expanding significant insight into the pathogenesis of rheumatoid arthritis and providing a possible target for future treatment.

Ovarian cancer is one of the most common gynecological diseases with high mortality rates. Previous studies have shown that microRNA (miR)-638 is associated with tumorigenesis. The present study aimed to assess the role and underlying mechanisms of miR-638 in ovarian cancer. miR-638 expression was detected in ovarian cancer tissues and miR-638 was overexpressed or knocked down in ovarian cancer OVCAR-3 and Caov-3 cells. The clinical results revealed that miR-638 expression was downregulated in ovarian cancer tissues compared with in adjacent normal tissues. miR-638 expression was also found to be relatively low in OVCAR-3 cells whilst being relatively high in Caov-3 cells among the five ovarian cancer cell lines tested. miR-638 overexpression inhibited cell viability, arrested the cell cycle at the G1 phase and promoted apoptosis in OVCAR-3 cells. By contrast, miR-638 knockdown increased Caov-3 cell viability, facilitated cell cycle progression and inhibited apoptosis. miR-638 reduced the expression of high mobility group A1 (HMGA1) by directly targeting its 3' untranslated region. HMGA1 overexpression reversed the inhibition of proliferation induced by miR-638 overexpression in OVCAR-3 cells. These results suggest that miR-638 may serve to be a suppressor of ovarian cancer by regulating HMGA1, which may provide a potential therapeutic target for ovarian cancer.

Herein, the adsorption/desorption behaviors of benzoic acid (BA) and phthalic acid (PA) on three functionalized carbon nanotubes (CNTs) at various pH were investigated, and the charge-assisted H-bond (CAHB) was verified by DFT and FTIR analyses to play a key role. The results indicated that the adsorption order of BA and PA on CNTs was different from Kow of that at pH 2.0, 4.0, and 7.0 caused by the CAHB interaction. The strength of homonuclear CAHB (≥78.96 kJ·mol−1) formed by BA/PA on oxidized CNTs is stronger than that of heteronuclear CAHB formed between BA/PA and amino-functionalized CNTs (≤51.66 kJ·mol−1). Compared with the heteronuclear CAHB (Hysteresis index, HI ≥ 1.47), the stronger homonuclear CAHB leads to clearly desorption hysteresis (HI ≥ 3.51). Additionally, the contribution of homonuclear CAHB (≥52.70%) was also greater than that of heteronuclear CAHB (≤45.79%) at pH 7.0. These conclusions were further confirmed by FTIR and DFT calculation, and the crucial evidence of CAHB formation in FTIR was found. The highlight of this work is the identification of the importance and difference of pH-dependent homonuclear/heteronuclear CAHB on the adsorption and desorption behaviors of ionizable organic compounds on carbonaceous materials, which can provide a deeper understanding for the removal of ionizable organic compounds by designed carbonaceous materials.

Exposure to bisphenol A (BPA) is considered to be associated with the increased incidence of breast cancer. As a widespread replacement of BPA, the effect of bisphenol S (BPS) on breast tumor programming has not been studied. We reported that BPS exposure significantly promoted proliferation and deterioration of breast tumor by nonmonotonic dose response. The mechanisms were investigated by molecular biology and mass spectrometry-based lipidomics, proteomics and imaging. BPS exposure induced the spatially intratumor heterogeneity of morphology-driven lipids and proteins. The more significant proliferation resulted from BPS-10 (10 μg/kg body weight /day) exposure was evidenced by the variations of spatial distribution of lipids related to ceramide-sphingomyelin signaling pathway, proteins related to chromosomal stability and cell proliferation in central necrotic regions of breast tumor. In contrast, the BPS-100 exposure obviously accelerated deterioration of breast tumor by the variations of spatial distribution of proteins that were associated with the stability of nucleic acid structure in peripheral neoplastic regions. Accordingly, dysregulation of metabolism and protein function as well as DNA methylation and hypoxic tumor microenvironment could be applied to predict the possibility of tumorigenesis, proliferation and metastasis that might be caused by other bisphenol analogs.

MicroRNAs (miRs) are endogenous non-coding RNAs that serve key functions in a wide range of biological processes, including cell growth, development, apoptosis and carcinogenesis. However, the association between miR-187 and B-cell lymphoma 6 (BCL6) has yet to be fully investigated in lymphoma cell apoptosis. The present study hypothesized that a post-translational mechanism may exist for BCL6 expression, which is regulated by miR-187 in lymphoma cells. The present study demonstrated that the expression of miR-187 in diffuse large B-cell lymphoma (DLBCL) cells was significantly decreased, and its expression was negatively correlated with BCL6 expression. It was also observed that miR-187 directly binds to the 3′-untranslated region of BCL6 mRNA and subsequently suppresses the expression of BCL6. Additionally, the induced expression of miR-187 significantly promoted DLBCL cell apoptosis in vitro. The drug sensitivity of human DLBCL SUDHL2 cells was increased following induction of miR-187 overexpression via an miR-187 mimic. In conclusion, the results of the present study suggest that the modulation of miR-187 expression in DLBCL cells may improve the sensitivity of chemotherapy through BCL6 targeting.

Background/Aims: The pathogenesis of hepatocellular carcinoma (HCC) is mainly characterized by persistent cycles of liver injury, inflammation, and compensatory hepatocyte proliferation. Angiotensin II (Ang II) behaves as an endogenous pro-inflammatory molecule playing a significant role in HCC, however, the molecular link between Ang II, proliferation and inflammation remains unclear. Methods: Human HCC cell lines (HepG-2, SMMC-7721, MHCC97-H) were incubated with Ang II at the indicated concentrations for 24, 48, 72 h. MTT, BrdU ELISA, plate colony formation assay, immunohistochemistry, ELISA, small-interfering RNA(siRNA) transfection, quantitative real-time PCR and western blot were applied to assess their functional, morphological and molecular mechanisms in HCC cell lines. Results: High expression of Ang II type 1 receptor (AT1) and low expression of AT2 in HCC cells and tissues were found. Next, Ang II could significantly enhance cell growth and proliferation. Albeit Ang II slightly increased the percentage of HCC cells in the G0/G1 phase using flow cytometry analysis, no statistically significant alterations were shown. Further studies suggested that Ang II could directly induce proliferation associated proteins C-myc and proliferating cell nuclear antigen (PCNA) expressions, and inflammatory cytokines tumor necrosis factor-alpha (TNF-α) and C-reactive protein (CRP) productions in HCC cells. Interestingly, blocking AT1 and AT1 siRNA evidently inhibited Ang II-induced cell proliferation and inflammatory responses in HCC cells. More importantly, these effects may be mediated by AT1/PKC/NF-κB signaling pathway in HCC cell lines. Conclusions: The results propose that Ang II/AT1/PKC/NF-κB signaling pathway is necessary for proliferation and inflammation of HCC cells, which increases our understanding of the pathogenesis and provides clues for developing new strategies against Ang II-related progress of HCC.

Hepatocellular carcinoma (HCC) is one of the major causes of cancer-associated morbidity and mortality worldwide. Sphingosine-1-phosphate (S1P) and S1P receptor 1 (S1PR1) have been associated with the development and progression of HCC. Angiotensin II (Ang II) and Ang II receptor type 1 (AT1R) serve key roles in the progression and metastasis of HCC. However, the association and roles of Ang II/AT1R and S1P/S1PR1 in HCC have remained elusive. Therefore, the aim of the present study was to investigate the potential association between Ang II/AT1R and S1P/S1PR1 in HCC, as well as the association of AT1R and S1PR1 protein expression levels with the progression and prognosis of HCC. The results found that the serum levels of Ang II and S1P were significantly higher in patients with HCC compared with those in healthy donors. Furthermore, mRNA and protein levels of AT1R and S1PR1 were highly expressed in human HCC tissues. In addition, a positive correlation between Ang II/S1P and AT1R/S1PR1 in HCC was noted. Upregulation of AT1R and S1PR1 was associated with the progression of HCC. Patients with high AT1R and S1PR1 protein expression levels had unfavorable outcomes with respect to overall survival and recurrence-free survival compared with patients with low AT1R and S1PR1 expression levels. The present results demonstrated an association between AT1R and S1PR1 overexpression and the progression of HCC, indicating that Ang II/AT1R and S1P/S1PR may serve as valuable prognostic biomarkers for HCC.

Background: The widespread use of bisphenol A (BPA) substitutes has aroused great attention towards their toxicological evaluation in vivo and in vitro. Considering the intimate correlation between BPA and metabolic diseases, we explored whether bisphenol S (BPS), a major substitute to BPA, could cause the splenic toxicity by disturbing the lipid metabolism in mouse model. Methods: We investigated the splenic injury by combing the mass spectrometry (MS)-based lipidomics and imaging analysis, as well as molecular biological methods. Mice were divided into three groups (control-olive oil, 10 and 100 μg-BPS/kg body weight/day group) and treated by BPS in 56 days. Results: Two of BPS-treated concentrations induced the splenic morphological alterations and inflammation, including the decreased numbers and cellularity in the periarteriolar lymphoid sheath (T cell zone) and paucicellular primary lymphoid follicles (B cell zone) in splenic white pulp. Lipidome profiling of spleen after BPS treatment was also changed with up-regulated sphingosine [So], neutral glycosphingolipids [CerG], cholesteryl ester [ChE], diacylglycerols [DAG], lysophosphatidylcholine [LPC], lysophosphatidylethanolamine [LPE], phosphatidylglycerols [PG], phosphatidylinositols [PI] and phosphatidylserine [PS] as well as down-regulated ceramide [Cer], phosphatidylethanolamines [PE] and sphingomyelin [SM] compared to the control group. More importantly, significant different lipids in abundance and spatial distribution also implicated that white pulp were more sensitive to BPS treatment than other splenic sub-structures. Signaling lipids such as So (d18:0), Cer (d18:1/24:0), Cer (d18:1/22:0), SM (d18:1/22:1) and SM (d18:1/24:2) associated with inflammation were remarkable changed and co-localized in the splenic white pulp. Conclusions: Our finding indicated that BPS exposure promoted the splenomegaly, pro-inflammatory activation and morphological alterations, as well as induced the lipidome perturbation in the immune cells of white pulp, which might be expected to contribute a new perspective of bisphenol-induced organ injury. Keywords: Bisphenol S, Splenic injury, Mass spectrometry imaging, Lipidomics, Splenic white pulp

The goal of this study was to observe the bacterial colonization in the intestinal mucosa in the patients with diarrhea predominant irritable bowel syndrome (IBS-D) and ulcerative colitis (UC), and compare the mucosa-associated microbiota among the IBS-D patients, UC patients and the healthy control, and explore the correlation of the mucosa-associated microbiota with clinical manifestations.A total of 20 IBS-D patients, 28 patients with UC (16 active, 12 inactive) and 16 healthy subjects were enrolled in the study. They all underwent colonoscopies in the Gastrointestinal Endoscopy Center in the Second Affiliated Hospital of Xi'an Jiaotong University from June 2016 to October 2016. The mucosa specimens were taken at the junction of rectum and sigmoid colon for fluorescent in situ hybridization (FISH). Then the observed mucosa-associated microbiota was counted and compared.(1) In the IBS-D patients, the mucosa-associated bacteria were found to colonize in the surface of mucosa and the adjacent mucin layer. And in active UC, Escherichia coli, and Bacteroides were found in the lamina propria, in addition to bacterial colonization in the above-mentioned areas. (2) The total count of mucosa-associated bacteria and the individual counts of E. coli, Clostridium, and Bacteroides were significantly increased, and Bifidobacteria significantly decreased (P0.05) in the IBS-D patients and UC patients. Counts of Lactobacillus were decreased only in UC patients compared with the healthy control. And a significantly larger variation of the above-mentioned bacterial counts was found in the patients with UC, particularly in those with active UC, compared with those with IBS-D (P0.05); the counts in the UC group were 1.3 to 5.3 times more or less than those in the IBS-D group. (3) Compared with healthy controls and IBS-D, the total count of bacteria and the individual counts of E. coli and Bacteroides in the lamina propria in active UC were significantly increased (P0.05). (4) A significant negative correlation of the counts of Lactobacillus and Bifidobacteria with the defecation frequency and fecal characteristics (P0.05) was found in the IBS-D patients; in those with UC, both the total count of bacteria and the individual counts of E. coli, Clostridium, Bacteroides, Lactobacillus, and Bifidobacteria were significantly correlated, positively or negatively, with the related clinical manifestations and the activity of the disease (P0.05).Compared with the healthy control, intestinal microecology was changed most obviously in UC with much smaller differences though in the same direction in IBS-D. The translocation of some bacteria into the lamina propria was found in UC, particularly in active UC. The changes of mucosa-associated microbiota were related more or less to some clinical manifestations in IBS-D and UC.

Osteoporosis is a kind of metabolic bone disorder. MicroRNA-21 (miR-21) has been proven to play an important role in bone formation, whereas its role in osteoporosis is unclear. In the present study, miR-21 expression was inhibited by TNF-α in mesenchymal stem cells (MSCs). TNF-α induced cell apoptosis, and inhibited cell proliferation and differentiation of MSCs. Whereas the effect was reversed by miR-21 mimics. Expression of reversion-inducing cysteine-rich protein with Kazal motifs (RECK) which is a predicted target of miR-21 was inhibited by miR-21 mimics. A luciferase reporter gene assay showed that miR-21 directly bound to RECK 3'-UTR. The effect of TNF-α on MSCs was reversed by RECK siRNA which was consistent with miR-21 mimics. The expression of MT1-MMP was inhibited by TNF-α and enhanced by RECK siRNA and miR-21 mimics. For the in vivo study, an osteoporosis model (OVX) was established by bilateral oophorectomy in mice. The expression of miR-21 decreased and RECK increased in the OVX mice. When treated with lentiviral RECK shRNA, the osteocalcin concentration and alkaline phosphate activity of the OVX mice decreased. The bone mineral density of the right femur mid-diaphysis was improved by RECK shRNA. Collectively, miR-21 modulated the osteoporosis by targeting RECK. These results emphasize the role of miR-21 during osteoporosis and suggest RECK might be a new medical target for osteoporosis.

Background Insulin-like growth factor binding protein 3 (IGFBP3) plays an important role in cellular proliferation, differentiation, apoptosis, and mammary carcinogenesis. Genetic variations in IGFBP3 have been identified to influence the circulating IGFBP3 level. The present study determined the impact of an important promoter polymorphism (A-202C, rs2854744) on susceptibility and progression of breast cancer in a Chinese population. Methods We genotyped the IGFBP3 A-202C polymorphism in a case-control study involving 465 breast cancer patients and 799 age-matched, cancer-free controls using the TaqMan method. Logistic regression was used to assess the genetic association between the occurrence and progression of breast cancer. Results Compared with the wild genotype (-202AA), we found a statistically significant increased risk of breast cancer associated with the variant genotypes (CC vs. AA: OR = 2.00, 95% CI = 1.25–3.21; AC + CC vs. AA: OR = 1.34, 95% CI = 1.06–1.70). In the stratified analysis, the increased risk was more apparent among the subgroups of older subjects (OR = 1.70, 95% CI = 1.20–2.42). Furthermore, we found that patients carrying variant genotypes (AC + CC) had a significantly greater prevalence of large tumor size (OR = 1.72, 95% CI = 1.13–2.64; P = 0.021). Conclusion Our results suggest that the functional IGFBP3 A-202C polymorphism may influence the susceptibility and progression of breast cancer in the Chinese population.

In China, the majority of ovarian cancer patients (80%–90%) are women who are diagnosed with epithelial ovarian cancer. The SYNPO2 gene has recently been reported to be associated with epithelial ovarian cancer in Europeans. To investigate the association of common variants of SYNPO2 gene with epithelial ovarian cancer in Han Chinese individuals, we designed a case–control study with 719 epithelial ovarian cancer patients and 1568 unrelated healthy controls of Han Chinese descent. A total of 49 tagging single-nucleotide polymorphisms were genotyped; single-single-nucleotide polymorphism association, imputation, and haplotypic association analyses were performed. The single-nucleotide polymorphism rs17329882 was found to be strongly associated with serous epithelial ovarian cancer and with ages ≤49 years, consistent with the pre-menopausal status of analyzed epithelial ovarian cancer cases. Odds ratios and 95% confidence intervals provided evidence of the risk effects of the C allele of the single-nucleotide polymorphism on epithelial ovarian cancer. Imputation analyses also confirmed the results with a similar pattern. Additionally, haplotype analyses indicated that the haplotype block that contained rs17329882 was significantly associated with epithelial ovarian cancer risk, specifically with the serous epithelial ovarian cancer subtype. In conclusion, our results show that SYNPO2 gene plays an important role in the etiology of epithelial ovarian cancer, suggesting that this gene may be a potential genetic modifier for developing epithelial ovarian cancer.

The genes encoding the immunoglobulin κ light chain are assembled during B cell development by V(D)J recombination. For efficient rearrangement, the Igκ locus must undergo a series of epigenetic changes. One such epigenetic mark is DNA methylation. The mechanism that the Igκ locus is selectively demethylated at the pre-B cell stage has not previously been characterized. Here, we employed bisulfite DNA-modification assays to analyze the methylation status of the Igκ locus in primary pre-B cells from RAG-deficient mice with pre-rearranged Igh knock-in allele. We observed that the Igκ locus was hypermethylated in RAG2-deficient pre-B cells but hypomethylated in RAG1-deficient pre-B cells, indicating that wild-type (WT) RAG2 involves the Igκ locus demethylation in a RAG1-independent manner prior to rearrangement. We generated a series of RAG2 mutants between residue 350 and 383. We showed that these mutants mediated the Igκ rearrangement but failed to regulate the Igκ gene demethylation. We further analyzed that these mutants could increase RAG recombinase activity in vivo. We conclude that residues 350-383 region are responsible for endogenous Igκ locus demethylation at pre-B cells. We propose that WT RAG2 has an intrinsic function to regulate the Igκ locus demethylation.

APE1 is an important DNA repair protein in the base excision repair pathway. Genetic variations in APE1 have been suggested to influence individuals' susceptibility to human malignancies. The present study was aimed to investigate the associations between two functional polymorphisms in APE1 (-656TG and 1349TG) and breast cancer risk.We genotyped the two polymorphisms in a case-control study of 500 breast cancer patients and 799 age-matched cancer-free controls using the TaqMan method. Unconditional logistic regression adjusted for potential confounding factors was used to assess the associations.We found that the variant genotypes of the -656TG were significantly associated with decreased breast cancer risk, compared with the wild genotype [TG/GG vs. TT: adjusted odds ratio (OR)=0.71, 95% confidence interval (CI)=0.56-0.91], and the protective effect of this polymorphism was more predominant among the subgroups of younger subjects (52 years) (OR=0.65, 95% CI=0.46-0.92). Besides, we found that the variant genotypes were associated with less frequent lymph node metastasis (P=0.020, OR=0.64, 95% CI=0.44-0.94). We did not observe any significant association between the 1349TG polymorphism and breast cancer risk.Our results suggest that the APE1 -656TG but not the 1349TG polymorphism may influence the susceptibility and progression of breast cancer in the Chinese population. Large population-based prospective studies are required to validate these findings.

Rheumatoid arthritis (RA) is an immune-mediated disease with a pathogenesis that involves CD4 T cell activation. Multiple immune regulatory molecules expressed on CD4(+) T cells were involved in RA pathogenesis. In this study, we investigated the role of T cell immunoglobulin and ITIM (immunoreceptor tyrosine-based inhibition motif) domain (TIGIT) in RA. The frequency of TIGIT-positive CD4(+) T cells in the synovial fluid (SF) of active RA patients was lower than that of inactive RA patients. And a negative correlation between RA disease activity and TIGIT expression was found. In CD4(+) T cells isolated from SF of active RA patients, TIGIT upregulation significantly decreased cell proliferation, as shown by MTT assay. TIGIT overexpression also significantly decreased the production of IFN-γ and IL-17, and increased that of IL-10, as determined by ELISA and qRT-PCR. In CD4(+) T cells isolated from SF of inactive RA patients, TIGIT was silenced by siRNA transfection. As expected, TIGIT knockdown resulted in an opposite effect on cell proliferation and the production of cytokines, including IFN-γ, IL-17 and IL-10. A RA mouse model was established using type II collagen induction. TIGIT was upregulated in RA mouse by lentivector infection. As expected, TIGIT overexpression in vivo significantly alleviated the disease severity and deceased the levels of anti-collagen II antibodies. TIGIT upregulation in the early stage was more effective to alleviate disease severity. Our data suggested the potential therapeutic role of TIGIT in RA patients.

MicroRNAs (miRNAs) have been reported to have diverse biological roles in regulating many biological processes, including osteogenic differentiation. In the present study, we identified that miR-24 was a critical regulator during osteogenic differentiation. We found that overexpression of miR-24 significantly inhibited osteogenic differentiation, which decreased alkaline phosphatase activity, matrix mineralization and the expression of osteogenic differentiation markers. In contrast, inhibition of miR-24 exhibited an opposite effect. Furthermore, we delineated that miR-24 regulates post-transcriptionals of T-cell factor-1 (Tcf-1) via targeting the 3'-untranslated region (UTR) of Tcf-1 mRNA. MiR-24 was further found to regulate the protein expression of Tcf-1 in the murine osteoprogenitors cells and bone mesenchymal stem cells. Additionally, the positive effect of miR-24 suppression on osteoblast differentiation was apparently abrogated by Tcf-1 silencing. Taken together, our data suggest that miR-24 participates in osteogenic differentiation by targeting and regulating Tcf-1 expression in osteoblastic cells.

To investigate the expression of TMEM16A in gastric carcinoma and its clinical implications.A total of 72 surgical specimens of gastric carcinoma were collected for examination of TMEM16A expression with immunohistochemical staining.TMEM16A expression was detected in the cytoplasm and cell membrane of the tumor cells. Of the 72 specimens of the tumor tissues, the total positivity rate of TMEM16A expression was 80.56% (58/72), significantly higher than the rate in the adjacent tissues (4.17%, 3/72, P0.005).Aberrant expression of TMEM16A occurs in the majority of gastric carcinoma cases. TMEM16A can be used as a new candidate target for diagnosis and treatment of gastric carcinoma.

IntroductionLipomas are ubiquitous and can occur anywhere in the body. Intrathoracic lipomata are rare benign lesions. However, a complete removal giant intrathoracic osteolipoma is achieved with only 18 cases previous cases described in medical literature from 1960 to 2008.Presentation of caseA 66-year-old female presented to our hospital suffered from mild chest pain and mild shortness of breath for more than 10 days. A subsequent chest X-ray and CT scans revealed a large homogeneous, low-attenuation fat density mass containing an oval calcification area in the center of the mass. Following surgical resection was performed successfully to remove the entire mass, which weighed a total of 1568g and measured 26cm×19cm×12cm in size. The histological analysis confirmed a giant intrathoracic osteolipoma without evidence of malignancy.DiscussionIntrathoracic lipomas are rare, slow-growing benign tumors without any symptom, which originate from the adipose tissue in submesothelial layers of the pleura parietalis, diaphragm, mediastinal and extrapericardial. They may extend into the chest cavity and fully encapsulate in most cases. Chest X-ray and CT and MRI scans are the most helpful tests in the diagnosis of intrathoracic lipomas. Complete enbloc removal of lipoma whenever possible, is the only definitive treatment option and the only way to prevent future recurrences.ConclusionThis case is the largest intrathoracic osteolipoma documented in the modern literature. Complete enbloc removal of lipoma whenever possible, is the only definitive treatment option.