CD4 + T cells promote renal cell carcinoma proliferation via modulating YBX1.

Renal cell carcinoma (RCC) is a common urologic tumor and the third leading cause of death among urological tumors. Recent studies demonstrate that RCC tumors are more heavily infiltrated by lymphocytes than other cancers. However, the exact roles played by CD4 + T cells in RCC proliferation remain unknown. In this study, we cocultured RCC cells with CD4 + T cells. Stable knockdown of YBX1 in RCC cells was constructed. The effects of CD4 + T cells, TGFß1 and YBX1 on RCC cells were investigated using cell viability assays. In situ RCC nude mouse model was used to observe the tumor growth. The potential mechanisms of CD4 + T cells and YBX1 in RCC cells proliferation were explored by qRT-PCR and western blot. Expression of CD4, Foxp3 and TGFß1 in RCC were quantified by immunohistochemical staining. The results indicated that CD4, Foxp3 and TGFß1 were significantly up-regulated in RCC tissues. Human clinical sample and in vitro cell lines studies showed that RCC cells had better capacity than its surrounding normal kidney epithelial cells to recruit the CD4 + T cells. In vivo mouse model studies were consistent with the results by in vitro cell lines studies showing infiltrating T cells enhanced RCC cell proliferation. qRT-PCR and western blot exhibited that CD4 + T cells could enhance RCC cell proliferation via activating YBX1/HIF2α signaling pathway. Furthermore, CD4 + T cells functioned through inducing TGFß1 expression. In a word, infiltrating CD4 + T cells promoted TGFß1 expression in both RCC and T cells and regulated RCC cells proliferation via modulating TGFß1/YBX1/ HIF2α signals.

[Correlation between the expression of Pim-1 and androgen-deprivation therapy for prostate cancer].

OBJECTIVE: To investigate the expression of the Pim-1 gene in the LNCaP cells of the animal model of orthotopically implanted prostate cancer by surgical castration simulating androgen-deprivation therapy. METHODS: We equally allocated 32 male BALBc-nu mice into 4 groups, androgen-dependent prostate cancer (ADPC), androgen-deprivation therapy (ADT) , castration-resistant prostate cancer (CRPC) and blank control, and established the models of orthotopically implanted tumor using human prostate cancer LNCaP cells. We detected and ,compared the expressions of Pim-1, PSA, and androgen receptor (AR) in the tumor tissues of different groups by RT-PCR. qRT-PCR, ELSIA and immunohistochemistry. RESULTS: The relative gray scales in the ADPC and CRPC groups were 0.59 ± 0.01 and 1.14 ± 0.02, with statistically significant differences from 0.62 ± 0.03 in the ADT group (P < 0.05), and the Δ Ct values of Pim-1 were 6.15 ± 0.34 and 4.56 ± 0.23 in the former two groups, also with significant differences from 5.11 ± 0.21 in the latter (P < 0.05). The results of 2-ΔΔ Ct relative quantification analysis showed that the amplification products of Pim-1 in the ADT and CRPC groups increased 2.05 and 3.01 times respectively that of the ADPC group. The concentration of PSA was significantly higher in the ADPC ([480 ± 25] pg/ml) and CRPC ([870 ± 23] pg/ml) than in the ADT ([170 ± 32] pg/ml) and blank control groups (0 µg/L) (P < 0.01). The mean optical densities of Pim-1 and AR proteins were 0.017 ± 0.002 and 0.032 ± 0.009 in the ADPC group and 0.024 ± 0.002 and 0.040 ± 0.011 in the CRPC group, both with significant differences from those in the ADT group (0.018 ± 0.001 and 0.019 ± 0.006) (P < 0.01). CONCLUSION: Pim-1 is highly expressed in nude mice with prostate cancer receiving androgen-deprivation therapy and plays an important role in the progression and metastasis of prostate cancer.

TGFß1 Leu10Pro polymorphism contributes to the development of prostate cancer: evidence from a meta-analysis.

Transforming growth factor-ß1 (TGFß1) plays a significant role in regulating cellular proliferation and apoptosis. A large number of studies related to the association between TGFß1 Leu10Pro polymorphism and prostate cancer (PC) risk, but get conflicting results. We performed a meta-analysis based on six studies, assessing the strength of the association using odds ratios (OR) with 95% confidence intervals (CI). Overall, our evidence has indicated that TGFß1 Leu10Pro polymorphism had significantly increased PC risk in the allele comparison model (OR = 1.081, 95% CI = 1.003-1.165, Pheterogeneity = 0.141, P = 0.041). In the stratified analysis by ethnicity, the same results were found among Caucasians (for heterozygote model, OR = 1.741, 95% CI = 1.004-3.020, Pheterogeneity = 0.000, P = 0.049; recessive model, OR = 1.339, 95% CI = 1.045-1.717, Pheterogeneity = 0.020, P = 0.021; allele comparison model, OR = 1.091, 95% CI = 1.005-1.184, Pheterogeneity = 0.048, P = 0.037). In conclusion, this meta-analysis suggested that TGFß1 Leu10Pro polymorphism contributed to the development of PC. A well-designed and larger study is still required to evaluate this polymorphism and PC risk.

MMPs-related risk model identification and SAA1 promotes clear cell renal cell carcinoma migration via ERK-AP1-MMPs axis.

Matrix Metalloproteinases (MMPs) have been demonstrated to be essential in facilitating the migration and metastasis of clear cell renal cell carcinoma (ccRCC). However, the ability of the MMP family to predict clinical outcomes and guide optimal therapeutic strategies for ccRCC patients remains incompletely understood. In this investigation, we initially conducted a thorough examination of the MMP family in pan-cancer. Notably, MMPs exhibited distinctive significance in ccRCC. Following this, we undertook an extensive analysis to evaluate the clinical value of MMPs and potential mechanisms by which MMPs contribute to the progression of ccRCC. A novel stratification method and prognostic model were developed based on MMPs in order to enhance the accuracy of prognosis prediction for ccRCC patients and facilitate personalized treatment. By conducting multi-omics analysis and transcriptional regulation analysis, it was hypothesized that SAA1 plays a crucial role in promoting ccRCC migration through MMPs. Subsequently, in vitro experiments confirmed that SAA1 regulates ccRCC cell migration via the ERK-AP1-MMPs axis. In conclusion, our study has explored the potential value of the MMP family as prognostic markers for ccRCC and as guides for medication regimens. Additionally, we have identified SAA1 as a crucial factor in the migration of ccRCC.

Evaluation of bi-directional causal association between periodontitis and benign prostatic hyperplasia: epidemiological studies and two-sample mendelian randomization analysis.

Background: Periodontitis and benign prostatic hyperplasia (BPH) are all common chronic diseases with higher incidence in middle-aged and old men. Several studies have indicated a potential association between periodontitis and BPH, although the findings remain inconclusive. However, there is no mendelian randomization (MR) studies to assess this association. Methods: The 40 men who had received health check-ups were included in an epidemiological study. Genetic data of BPH (13118 cases and 72799 controls) and periodontitis (3046 cases and 195395 controls) from FinnGen project was used to perform two-sample MR analysis. The inverse-variance weighted (IVW) model was identified as the primary analytical method, with MR Egger, weighted median, simple mode, and weighted mode serving as additional approaches. Results: The epidemiological analysis demonstrated a lack of statistically significant differences in the prevalence of clinical BPH between severe periodontitis group and non-severe periodontitis group. Similarly, no statistically significant differences were found in the prevalence of severe periodontitis among individuals with clinical BPH compared to those without. Additionally, Among the five models utilized in MR analysis, including the IVW model, no evidence of a causal link between periodontitis and BPH was observed. Conclusion: The findings from our epidemiological investigation and MR analysis do not provide support for a causal relationship between periodontitis and BPH.

[Giant prostatic calculus with neurogenic bladder disease and prostate diverticulum: a case report and review of the literature].

OBJECTIVE: To study the etiology, clinical manifestation, diagnosis and treatment of giant prostatic calculus with neurogenic bladder disease and prostate diverticulum. METHODS: We retrospectively analyzed the clinical data of a case of giant prostatic calculus with neurogenic bladder disease and prostate diverticulum and reviewed the relevant literature. The patient was a 37-year-old man, with urinary incontinence for 22 years and intermittent dysuria with frequent micturition for 9 years, aggravated in the past 3 months. He had received surgery for spina bifida and giant vesico-prostatic calculus. The results of preoperative routine urinary examination were as follows: WBC 17 -20/HPF, RBC 12 - 15/HPF. KUB, IVU and pelvic CT revealed spina bifida occulta, neurogenic bladder and giant prostatic calculus. RESULTS: The patient underwent TURP and transurethral lithotripsy with holmium-YAG laser. The prostatic calculus was carbonate apatite in composition. Urinary dynamic images at 2 weeks after surgery exhibited significant improvement in the highest urine flow rate and residual urine volume. Seventeen months of postoperative follow-up showed dramatically improved urinary incontinence and thicker urine stream. CONCLUSION: Prostate diverticulum with prostatic giant calculus is very rare, and neurogenic bladder may play a role in its etiology. Cystoscopy is an accurate screening method for its diagnosis. For the young patients and those who wish to retain sexual function, TURP combined with holmium laser lithotripsy can be employed, and intraoperative rectal examination should be taken to ensure complete removal of calculi.

Benefits of lymphadenectomy for upper tract urothelial carcinoma only located in the lower ureter: a bicentre retrospective cohort study.

Background: Upper tract urothelial carcinoma (UTUC) is a rare and highly malignant urothelial tumor originating from the renal pelvis and ureter associated with poor prognosis. It has been established that 70% of ureteral tumors occur in the lower ureter. Radical nephroureterectomy (RNU) with ipsilateral bladder cuff excision is regarded as the standard treatment for UTUC. Current evidence supports the role of lymph node dissection (LND) in determining tumor staging, but no consensus has been reached on the potential survival benefits. The present study retrospectively analyzed cases of UTUC limited to the lower ureter to evaluate the survival benefits of LND during RNU. Methods: The present study retrospectively analyzed data from patients with UTUC limited to the lower ureter from two medical centers from 2000 to 2016 and assessed the survival outcomes, including recurrence-free survival (RFS) and cancer specific survival (CSS). During subgroup analysis, we stratified by pathological tumor (pT) stages and postoperative adjuvant chemotherapy (AC). Results: The study cohort included 297 patients separated into LND (n=111) and non-LND (n=186) groups. The two groups were comparable except for the pathological N stage. The LND group was associated with superior survival in terms of RFS (27.0% vs. 18.3%, p=0.044) and CSS (53.2 vs. 39.8%, p=0.031) compared to the non-LND group (n=186). In pT2-4 patients, the LND group was associated with better 3-year RFS (50.5% vs. 32.3%, p<0.05), 5-year RFS (29.7% vs. 12.0%, p<0.05), and overall RFS (18.7% vs. 6.0%, p<0.05) than the non-LND group. Besides, the LND group was associated with a significantly better 3-year CSS (68.1% vs. 49.6%, p=0.003), 5-year CSS (51.6% vs. 30.8%, p<0.05) and overall CSS (45.1% vs. 24.1%, p<0.05). In patients that underwent AC, the LND group had better survival benefits in terms of RFS (29.4 vs. 16.7%, p=0.023) and CSS (52.9% vs. 40.5%, p=0.038) compared to the non-LND group. Conclusion: LND has survival benefits in patients with UTUC localized to the lower ureter, especially for≥pT2 stage UTUC and AC cohorts. Overall, the therapeutic effect of LND in UTUC cannot be replaced by AC.

Six-transmembrane epithelial antigen of prostate 3 (STEAP3) is a potential prognostic biomarker in clear cell renal cell carcinoma that correlates with M2 macrophage infiltration and epithelial-mesenchymal.

BACKGROUND: The six-transmembrane epithelial antigen of the prostate 3 (STEAP3) is a metalloreductase, which is essential for iron uptake. Existing literature has shown that STEAP3 may perform an important role in the onset and progression of tumors. Nonetheless, a complete pan-cancer investigation of the prognostic significance and immune properties of STEAP3 is currently unavailable. AIMS: As part of our investigation into the possible functions of STEAP3 in malignancies, we conducted a comprehensive analysis to examine the prognostic value and immune features of STEAP3 in human pan-cancer. METHODS AND RESULTS: R and Cytoscape programs were applied to analyze and visualize the data. The expression of STEAP3 in both cell lines and tissues was measured utilizing a variety of approaches. Using the shRNA knockdown technique, we tested the viability of the A498 and 786-O cell lines and validated their functions. Both CCK-8 and transwell assays were conducted to estimate cell proliferation and invasion. The expression of STEAP3 was substantially elevated and was shown to be linked to prognosis in the majority of malignancies, notably in clear cell renal cell carcinoma (ccRCC). In addition, the expression of STEAP3 was shown to have a strong correlation with immune infiltrates, which in turn triggered the recruitment and polarization of M2 macrophages in ccRCC. The protein STEAP3 shows promise as a predictor of responses to immune-checkpoint blockade (ICB) therapy. Positive links between STEAP3 and the epithelial-mesenchymal transition (EMT), the p53 pathway, and the immune-associated pathways were also found in the enrichment analysis. Our results illustrated that the STEAP3 expression level was substantially elevated in ccRCC tissues and suggested that it could stimulate EMT in ccRCC by downregulating CDH1. CONCLUSION: In a diverse range of cancers, STEAP3 might serve as a biomarker for determining the prognosis as well as a predictor of immunotherapy responsiveness. STEAP3 is a novel biological marker for determining prognosis, and it also performs a remarkable function in the promotion of tumor growth in ccRCC by enhancing invasion and EMT, as well as by triggering the recruitment and polarization of M2 macrophages.

HOXB3 drives WNT-activation associated progression in castration-resistant prostate cancer.

Enabled resistance or innate insensitiveness to antiandrogen are lethal for castration-resistant prostate cancer (CRPC). Unfortunately, there seems to be little can be done to overcome the antiandrogen resistance because of the largely unknown mechanisms. In prospective cohort study, we found that HOXB3 protein level was an independent risk factor of PSA progression and death in patients with metastatic CRPC. In vivo, upregulated HOXB3 contributed to CRPC xenografts progression and abiraterone resistance. To uncover the mechanism of HOXB3 driving tumor progression, we performed RNA-sequencing in HOXB3 negative (HOXB3-) and HOXB3 high (HOXB3 + ) staining CRPC tumors and determined that HOXB3 activation was associated with the expression of WNT3A and enriched WNT pathway genes. Furthermore, extra WNT3A and APC deficiency led HOXB3 to be isolated from destruction-complex, translocated to nuclei, and then transcriptionally regulated multiple WNT pathway genes. What's more, we also observed that the suppression of HOXB3 could reduce cell proliferation in APC-downregulated CRPC cells and sensitize APC-deficient CRPC xenografts to abiraterone again. Together, our data indicated that HOXB3 served as a downstream transcription factor of WNT pathway and defined a subgroup of CRPC resistant to antiandrogen which would benefit from HOXB3-targeted therapy.

[Paraganglioma of the prostate: a case report and review of the literature].

OBJECTIVE: To investigate the clinical presentation, pathologic features, treatment and prognosis of prostatic paraganglioma. METHODS: We retrospectively studied a case of prostatic paraganglioma and reviewed relevant literature. The patient was a 39-year-old man, admitted for repeated hematospermia for over 12 months. After misdiagnosed as having prostate cancer, he underwent suprapubic prostatectomy, with the tumor completely removed. RESULTS: Postoperative pathological examination confirmed the tumor to be prostatic paraganglioma, which was non-functional, with the immunohistochemical results of NSE (+), CGA (+), S100 (+), CK (-) and Desmin (-). Postoperative blood pressure was stable. Two weeks after surgery, the urethral catheter was removed and the patient discharged. No recurrence was found during 48 months of follow-up. CONCLUSION: Lacking specific clinical characteristics, paraganglioma of the prostate is easily misdiagnosed, and can be confirmed only by postoperative pathology and immunohistochemistry. For the treatment of this rare tumor, little experience has been accumulated, and further studies are needed.

Primary teratoma of the adrenal gland: a case report.

Background: Teratomas are unusual tumors derived from multiple germ layers but they usually arise from all three germ layers. Knowledge of this disease is still very limited because of its low incidence. Retroperitoneal teratomas are extremely rare neoplasms, especially adrenal teratomas, which frequently found to be large, cystic or cyst-solid lesions. Adrenal teratomas are easily confused with various benign or malignant tumors, such as myelolipomas, adenomas, and hamartomas. Case Description: In this case presentation, we report a rare case in which an adrenal gland mass without apparent discomfort was detected by abdominal computed tomography (CT) for 6 months in a 59-year-old female. Results from the patient's adrenal hormonal evaluation were normal. An abdominal enhanced CT scan revealed a heterogeneous mass in the right adrenal gland. The patient then underwent a laparoscopic right adrenalectomy and the lesion was diagnosed as mature teratoma through histopathological examination. The patient recovered well without any complications. Conclusions: Based on our knowledge, surgical resection is the first-choice intervention for the diagnosis and treatment of mature teratoma. Open surgery is the preferred method for the large tumors, while the laparoscopic adrenalectomy can be a better option in the small one. The patient's prognosis is usually good after complete resection, but close follow-up is also recommended.

Nicotinamide inhibits growth of carcinogen induced mouse bladder tumor and human bladder tumor xenograft through up-regulation of RUNX3 and p300.

PURPOSE: Acetylation of chromatin interacting proteins is central to the epigenetic regulation of gene expression. Various tumor suppressors are inactivated by abnormal epigenetic modification. A great deal of effort has been devoted to developing anticancer agents that reactivate silenced tumor suppressors by modulating chromatin structure. Studies show that histone deacetylase inhibitors can act as anticancer agents and several histone deacetylase inhibitors are currently in clinical trials. We noted that the tumor suppressor RUNX3 is inactivated by promoter hypermethylation in human bladder cancer. We investigated whether reactivation of RUNX3 could suppress bladder cancer development in an animal model. MATERIALS AND METHODS: We analyzed RUNX3 reactivation and protein stabilization by a mild inhibitor of class III histone deacetylases, nicotinamide, by immunoprecipitation and immunoblot. Mouse bladder tumor was induced by N-butyl-N-(4-hydroxybutyl) nitrosamine. The effect of nicotinamide on Runx3 methylation status and tumor growth was measured. RESULTS: Nicotinamide induced RUNX3 expression at the transcriptional and posttranslational levels in a carcinogen induced mouse bladder tumor model and in human bladder tumor xenografts. Nicotinamide effectively inhibited the growth and progression of bladder tumors without decreasing body weight. CONCLUSIONS: Results suggest that nicotinamide has preventive and therapeutic effects on tumorigenesis through multiple mechanisms of RUNX3 expression up-regulation.

[Prostate cancer with five different histological features: a case report and review of the literature].

OBJECTIVE: To study the clinical manifestations, pathological characteristics and treatment methods of prostate cancer with five different histological features. METHODS: We reported 1 case of prostate cancer with five different histological features and further analyzed the diagnosis, pathology and treatment of the disease by reviewing the relevant literature. RESULTS: The patient was an 84-year-old male, admitted due to difficult urination and dribbling urine for 1 year, hematuria for 8 months and deterioration for 2 weeks. Prostate cancer was indicated by rectal examination, ultrasonography, CT, MRI and PSA, and confirmed by biopsy. Considering the general condition of the patient, we performed electrotransurethral resection under epidural anesthesia to alleviate his urinary symptoms and remove suspected tumor tissues. Postoperative pathology showed the case to be prostate adenocarcinoma, histologically characterized by cribriform carcinoma, acinar carcinoma, diffuse invasive carcinoma, ductal carcinoma, and mucinous adenocarcinoma, with a Gleason score of 9. Bicalutamide and goserelin were administered postoperatively. Systemic metastasis occurred 10 months later, and the patient died 1 year after the operation. CONCLUSION: Prostate cancer with five different histological features is extremely rare. Its early diagnosis is difficult and mainly depends on pathological and immunohistochemical examinations, and radical prostatectomy can be considered for its treatment.

[Undifferentiated prostate sarcoma with cartilage metaplasia: a case report and review of the literature].

OBJECTIVE: To investigate the clinical presentations and pathologic features of undifferentiated sarcoma of the prostate with cartilage metaplasia, and to clarify its category. METHODS: We analyzed the clinical data of a case of undifferentiated sarcoma of the prostate with cartilage metaplasia treated by surgical resection. The tumor tissue was subjected to routine HE and immunohistochemical staining, its histological structure and immunohistochemical expression were observed under the light microscope, and relevant literature on its manifestations was reviewed. RESULTS: The case was pathologically diagnosed as gray prostate tumor, with chondrosarcomatous and undifferentiated malignant mesenchymal components under the light microscope. Immunohistochemical staining revealed vimentin (+), local CD117 (+/-), SMA (-), Des (-), myoglobin (-), CD34 (-), CK7 (-), and CK8 (-). Tumor metastasis was found 2 months after the operation, and the patient died 4 months later. CONCLUSION: Undifferentiated sarcoma of the prostate with cartilage metaplasia is a very rare and highly malignant aggressive tumor, which can be diagnosed by biopsy and immunohistochemistry.

Primary Renal Leiomyosarcoma.

To optimise the diagnosis and treatment of primary renal leiomyosarcoma, we present our experience with a similar case and review the literature. A 49-year woman was incidentally found to have a palpable mass in the right kidney. CT scan revealed an enhancing, heterogeneous, 6×7×9 cm right renal mass. On suspicion of renal carcinoma, a right radical nephrectomy was performed.  The pathological diagnosis was primary renal leiomyosarcoma. After 40 months of regular follow-up, local recurrence was found, and she had liver metastases. She died of cachexia due to tumor metastasis, and the survival period was just 44 months. With unobvious clinical manifestations, preoperative imaging and postoperative pathological examination might be helpful for an accurate diagnosis. Radical nephrectomy to completely remove the tumor is recommended, and the combination of neoadjuvant or postoperative therapy should also be considered. Key Words: Renal neoplasms, Leiomyosarcoma, Diagnosis, Therapy.

Progress in studies on pathological changes and future treatment strategies of obesity-associated female stress urinary incontinence: a narrative review.

With the increasing prevalence of obesity worldwide, obesity-related female stress urinary incontinence (FSUI) has become a key health problem. Recent studies indicated that FSUI is primarily caused by obesity-related pathological changes, such as fat droplet deposition, and results in pelvic floor nerve, vascular, and urethral striated muscle injury. Meanwhile, treatments for obesity-associated FSUI (OA-FSUI) have garnered much attention. Although existing OA-FSUI management strategies, including weight loss, pelvic floor muscle exercise, and urethral sling operation, could play a role in symptomatic relief; they cannot reverse the pathological changes in OA-FSUI. The continued exploration of safe and reliable treatments has led to regenerative therapy becoming a particularly promising area of researches. Specifically, micro-energy, such as low-intensity pulsed ultrasound (LIPUS), low-intensity extracorporeal shock wave therapy (Li-ESWT), and pulsed electromagnetic field (PEMF), have been shown to restore the underlying pathological changes of OA-FSUI, which might be related by regulation endogenous stem cells (ESCs) to restore urine control function ultimately in animal experiments. Therefore, ESCs may be a target for repairing pathological changes of OA-FSUI. The aim of this review was to summarize the OA-FSUI-related pathogenesis, current treatments, and to discuss potential therapeutic options. In particular, this review is focused on the effects and related mechanisms of micro-energy therapy for OA-FSUI to provide a reference for future basically and clinical researches.

Aberrant activation of super enhancer and choline metabolism drive antiandrogen therapy resistance in prostate cancer.

Next generation antiandrogens such as enzalutamide (Enz) are effective initially for the treatment of castration-resistant prostate cancer (CRPC). However, the disease often relapses and the underlying mechanisms remain elusive. By performing H3-lysine-27 acetylation (H3K27ac) ChIP-seq in Enz-resistant CRPC cells, we identified a group of super enhancers (SEs) that are abnormally activated in Enz-resistant CRPC cells and associated with enhanced transcription of a subset of tumor promoting genes such as CHPT1, which catalyzes phosphatidylcholine (PtdCho) synthesis and regulates choline metabolism. Increased CHPT1 conferred CRPC resistance to Enz in vitro and in mice. While androgen receptor (AR) primarily binds to a putative CHPT1 enhancer and mediates androgen-dependent expression of CHPT1 gene in Enz-sensitive prostate cancer cells, AR binds to a different enhancer within the CHPT1 SE locus and facilities androgen-independent expression of CHPT1 in Enz-resistant cells. We further identified a long-non coding RNA transcribed at CHPT1 enhancer (also known as enhancer RNA) that binds to the H3K27ac reader BRD4 and participates in regulating CHPT1 SE activity and CHPT1 gene expression. Our findings demonstrate that aberrantly activated SE upregulates CHPT1 expression and confers Enz resistance in CRPC, suggesting that SE-mediated expression of downstream effectors such as CHPT1 can be viable targets to overcome Enz resistance in PCa.

Pseudocapsule of Small Renal Cell Tumors: CT Imaging Spectrum and Correlated Histopathological Features.

PURPOSE: To systematically analyze histopathologic features of pseudocapsule in small renal cell tumor (diameter≤4cm), assess the integrity of pseudocapsules by Computed Tomography (CT), and provide theoretical basis for the safety of nephron sparing surgery. MATERIALS AND METHODS: The pathological data of 116 patients who underwent surgery with clear cell renal cell carcinoma admitted from May 2010 to October 2017 were retrospectively analyzed. All patients underwent a CT scan of the abdomen including an unenhanced and triple-phase (arterial, nephrographic and excretory) post contrast series."All patients underwent a CT scan of the abdomen including an unenhanced and triple-phase (arterial, nephrographic and excretory) post contrast series."All patients underwent a CT scan of the abdomen including an unenhanced and triple-phase (arterial, nephrographic and excretory) post contrast seriesAll patients underwent a CT scan of the abdomen including an unenhanced and three-phase (arterial, nephrographic and excretory) post contrast series. Thorough gross examination and histological sections were used to determine the integrity of the pseudocapsule by two uropathologists. The consistency between pathological findings and CT imaging were evaluated by Kappa consistency test. RESULTS: The mean diameter of tumor was 3.0cm, range (2.6 ± 0.8) cm. On CT the pseudocapsule can present with one of the three following feathers:1) A regular and distinct halo; 2)lobulated clear margins;3) blurred margins. On histopathology, complete psuedocapsule was found in 85 tumors, incomplete psuedocapsule in 25 and no psuedocapsule was found in 6 tumors; CT scan findings demonstrated a regular halo in 82 tumors, lobulated clear margins in 26 and blurred margins in 8 tumors(Kappa=0.833,P=0.000). CONCLUSIONS: Most small renal cell tumors have an obvious psuedocapsule. Preoperative determination of the psuedocapsule's integrity is particularly important. CT scan can reliably evaluate the tumor margins and demonstrate the psuedocapsule when present. The imaging results are well correlated with the pathologic findings.

Loss of epithelial AR increase castration resistant stem-like prostate cancer cells and promotes cancer metastasis via TGF-ß1/EMT pathway.

BACKGROUND: Previous study has reported that loss of epithelial androgen receptor (AR) may promote tumor progression and cause TRAMP mouse model die earlier. The detail mechanisms, however, remain unclear. METHODS: Immunohistochemistry assay, Western blot and real-time PCR were used to detect the expression of epithelial and mesenchymal markers. RNA extraction, RT-PCR, quantitative RT-PCR, BrdU incorporation assays, flow cytometry and other experimental technics were also used in present work. RESULTS: Decreased expression of epithelial markers (Cytokeratin 8, NKX3.1 and E-cadherin) and increased expression of mesenchymal markers (α-SMA, Vimentin, and N-cadherin) in were found in AR knockout TRAMP tumors. Further investigation indicated that AR signal deprivation is associated with cell morphology transition, high cell mobility, high cell invasion rate and resistance to anoikis in TRAMP prostate tumor cells. Together, these findings implied knockout AR in TRAMP prostate tumor may lead to EMT, which may result in earlier metastasis, and then cause TRAMP mice die earlier. TGF-ß1 is responsible for EMT in AR knockout TRAMP tumor cells. CONCLUSIONS: In conclusion, ADT therapy induced hormone refractory prostate cancer may gain the ability of metastasis through cell's EMT which is a phase of poor differentiation. Anti-EMT drugs should be developed to battle the tumor metastasis induced by ADT therapy.

Role and mechanism of micro-energy treatment in regenerative medicine.

With the continuous integration and intersection of life sciences, engineering and physics, the application for micro-energy in the basic and clinical research of regenerative medicine (RM) has made great progress. As a key target in the field of RM, stem cells have been widely used in the studies of regeneration. Recent studies have shown that micro-energy can regulate the biological behavior of stem cells to repair and regenerate injured organs and tissues by mechanical stimulation with appropriate intensity. Integrins-mediated related signaling pathways may play important roles in transducing mechanical force about micro-energy. However, the complete mechanism of mechanical force transduction needs further research. The purpose of this article is to review the biological effect and mechanism of micro-energy treatment on stem cells, to provide reference for further research.