Development in biomarkers of breast cancer: a bibliometric analysis from 2011 to 2020.

OBJECTIVE: Breast cancer (BC) is a prevalent cancer all over the world. We conducted a bibliometric study to analyze global scientific results over the past 10 years, including the hotspots and frontiers of biomarker research in BC. MATERIALS AND METHODS: From 2011 to 2020, literature research from the Web of Science Core Collection (WoSCC) was performed. VOSviewer was applied to analyze and visualize the frontiers and hotspots related to biomarker research in BC. RESULTS: 13,680 papers were retrieved. There was an increasing number of annual publications (Np) related to biomarkers in BC during the past decade. The United States (US) published the greatest number of papers, which had the highest number of citations (Nc) and ranked first in terms of H-index. PLoS One and the University of Texas System were the most productive journals and affiliations, respectively. In 2014, Chetan Bettegowda published a paper with the world's highest global citation score (GCS). In recent years, keywords such as "expression", "microRNA", and "cell" have appeared most frequently. In addition, research related to COVID-19 in this field has become a hot topic in recent years. This bibliometric study found an increasing trend in publications related to biomarkers in British Columbia and the US was found to be an influential producer in this field. CONCLUSIONS: In the past decade, most research has focused on basic and clinical studies, of which microRNAs (miRNAs) and circulating tumor DNAs (ctDNAs) associated with the inhibition and attenuation of BC have become the focus of recent research.

[Analysis of factors related to systemic embolism in patients≥75 years old with non-valvular atrial fibrillation].

Objective: To explore the related risk factors for systemic embolism (SE) in patients aged≥75 years with non-valvular atrial fibrillation (NVAF). Methods: A case-control study. NVAF patients aged≥75 years who were hospitalized at the First Affiliated Hospital of Xinjiang Medical University from October 2018 to October 2020 were divided into no SE (n=1 127) and SE (n=433) groups according to the occurrence of SE after NVAF. Multivariate logistic regression was used to analyze SE-related factors in patients with NVAF without anticoagulation treatment. Results: In the multivariate model, the following factors were associated with an increased risk of SE in patients with NVAF: history of AF≥5 years [odds ratio (OR)=2.75, 95% confidence interval (CI) 1.98-3.82, P<0.01], lipoprotein(a)>300 g/L (OR=2.07, 95%CI 1.50-2.84, P<0.01), apolipoprotein (Apo)B>1.2 g/L (OR=1.91, 95%CI 1.25-2.93, P=0.003), left ventricular ejection fraction (LVEF) of 30%-49% (OR=2.45, 95%CI 1.63-3.69, P<0.01), left atrial diameter>40 mm (OR=1.54, 95%CI 1.16-2.07, P=0.003), and CHA2DS2-VASc score≥3 (OR=15.14, 95%CI 2.05-112.13, P=0.01). ApoAI>1.6 g/L was negatively correlated with the occurrence of SE (OR=0.28, 95%CI 0.15-0.51, P<0.01). Conclusions: History of AF≥5 years, lipoprotein(a)>300 g/L, elevated ApoB, left atrial diameter>40 mm, LVEF of 30%-49%, and CHA2DS2-VASC score≥3 are independent risk factors for SE whereas ApoAI>1.6 g/L is a protective factor against SE in patients with NVAF.

[Correlation between diameter and primary closure rate by internal limiting membrane peeling and air tamponade in large idiopathic macular holes].

Objective: To analyze surgical outcomes by internal limiting membrane peeling and air tamponade in large idiopathic macular holes (IMHs) and the correlation between the minimal diameter and the primary closure rate. Methods: Retrospective study. A total of 282 patients (300 eyes) with IMHs larger than 400 µm who underwent vitrectomy and internal limiting membrane peeling in Beijing Tongren Hospital from July 2015 to January 2019 were enrolled, including 56 males (61 eyes) and 226 females (239 eyes) with an medium age of 65(62, 68) years. Before July 2016, gas tamponade was applied while after that, air tamponade was used. The minimal diameter of the IMH was measured. IMHs were divided into intervals every 50 µm by minimal diameter, and the primary closure rate of the two tamponades were compared between intervals by Chi-square test. The receiver operating characteristic (ROC) curve was drawn to show the correlation between the minimal diameter and the primary closure rate by air tamponde. Results: The mean minimal diameter of all the IMHs was (615.7±126.0)µm. In general, the primary closure rate was 91.7% (275/300), and the BCVA at last visit (0.5(0.3, 0.7)) improved significantly (P<0.001) comparing to the preoperative one (0.1(0.05, 0.2)). A total of 187 eyes with air tamponade exhibited a primary closure rate of 88.2%, which was significantly lower (P=0.005) than that with gas tamponade (97.3%). For IMHs with air tamponade, the optimal closure rate was 100% among all intervals; from the interval of (650, 700)µm on, the primary closure rates of every interval gradually decreased and were significantly lower than the optimal one (P<0.05) respectively; the ROC curve revealed that IMHs larger than 664.5 µm tended to exhibit a smaller chance of primary closure. For IMHs ≤650 µm, the two tamponades exhibited comparable primary closure rate (96.1% for air, 100.0% for gas, P=0.17), while for IMHs>650 µm, air tamponade (71.2%) presented significantly lower rate (93.5% for gas, P=0.002). IMHs ≤650 µm exhibited significantly better BCVA compared to those larger (P<0.01), no matter which tamponade was applied. In IMHs ≤650 µm, BCVA exhibited no significant difference between the two tamponades, so as in IMHs>650 µm. Conclusions: For IMHs with air tamponade, the minimal diameter is closely related to both the primary closure rate and the postoperative BCVA. IMHs>650 µm exhibited evidently poorer anatomical and functional outcomes compared with those ≤650 µm, which suggested that maybe other techniques for the internal limiting membrane could be applied to improve surgical outcomes for these large IMHs. (Chin J Ophthalmol, 2019, 55:739-746).

[Application of ultrasound in diagnosis of uterine prolapse by measuring area of levator hiatus].

Objective: To investigate the value of the area of levator hiatusin diagnosis of uterine prolapse. Methods: From September 2017 to December 2018, 80 patients diagnosed with uterine prolapse by Department of Gynecology, Xiangya Hospital of Central South University were selected as the case group, and 80 cases of normal women in the same period were selected as the control group. All subjects in both groups were examined by transperineal three-dimensional ultrasound. The anteroposterior and transverse diameters and the area of levator hiatus were measured at rest and during maximum Valsalva maneuver respectively. The ROC curve was drawn to determine the cut-off value of area of levator hiatus in diagnosis of uterine prolapse and to evaluate its diagnostic value. Results: At rest and during maximum Valsalva maneuver, the anteroposterior and transverse diameters and the area of levator hiatus in study group were larger than those in control group, the difference was statistically significant (P<0.05). During maximum Valsalva maneuver, the above values in both groups were greater than those of the same group at rest state, but there was no significant difference between the two groups (P>0.05). During maximum Valsalva maneuver, the best cut-off value of area of levator hiatus for the diagnosis of uterine prolapse was 22.09 cm(2), the area under curve was 0.893. The sensitivity, specificity and accuracy were 90.0%, 95.0% and 92.5%, respectively. Conclusion: Transperineal three-dimensional ultrasound can evaluate the morphological changes of levator hiatus in patients with uterine prolapse, and the area of levator hiatus has high diagnostic value for uterine prolapse.

LncRNA NEAT1 alleviates sepsis-induced myocardial injury by regulating the TLR2/NF-κB signaling pathway.

OBJECTIVE: To investigate the effect of long non-coding ribonucleic acid nuclear paraspeckle assembly transcript 1 (lncRNA NEAT1) on lipopolysaccharide (LPS)-induced myocardial injury in mice and the underlying mechanism. This study aims to provide some references for the prevention and treatment of sepsis-induced myocardial injury. MATERIALS AND METHODS: According to the random number table, 60 male C57 mice were divided into the Sham group (n=20), LPS group (n=20) and LPS + NEAT1 small interfering ribonucleic acid (siRNA) group (n=20). Sepsis-induced myocardial injury model in mice was established by intraperitoneal injection of LPS (10 mg/kg), and the NEAT1 knockout model was established by tail vein injection of NEAT1 siRNAs. After 12 h, the cardiac function of mice in each group was detected via the two-dimensional ultrasound; ejection fraction [EF (%)] and fraction shortening [FS (%)] were recorded. Hematoxylin and eosin (H&E) staining was conducted to evaluate the pathological changes in the heart tissues in each group. Terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) staining was used to detect the apoptotic levels of myocardial cells and fibroblasts in each group. In addition, the expression level of the oxidative stress marker 4-hydroxynonena (4-HNE) and the positive proportions of cluster of differentiation 45 (CD45) and CD68 in the mouse heart of three groups were detected via immunohistochemical staining. Moreover, the messenger RNA (mRNA) expression levels of inflammatory indicators [interleukin-1 (IL-1), IL-6, monocyte chemotactic protein 1 (MCP-1) and tumor necrosis factor-alpha (TNF-α)] in mouse serum of the three groups were examined by enzyme-linked immunosorbent assay (ELISA). Finally, the effects of NEAT1 siRNAs on the Toll-like receptor 2 (TLR2)/nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) signaling pathway were detected by Western blotting. RESULTS: ENEAT1 knockdown could significantly improve ischemia/reperfusion (I/R)-induced cardiac insufficiency in rats, and increase EF (%) and FS (%) (p<0.05). Besides, NEAT1 knockdown remarkably inhibited the LPS-induced myocardial injury. Compared with the LPS group, LPS + NEAT 1 siRNA group has more orderly arranged cardiac myofilament, a lower degree of degradation and necrosis, and significantly reduced cell edema. TUNEL staining showed that NEAT1 knockdown markedly reduced LPS-induced apoptosis of cardiac cells (p<0.05). Immunohistochemical results revealed that NEAT1 knockdown could remarkably reverse LPS-induced elevation of the myocardial 4-HNE expression and decrease the oxidative stress in the heart (p<0.05). At the same time, CD45+ and CD68+ cells were reduced after NEAT1 knockdown in myocardial tissues (p<0.05). Reverse Transcription-Polymerase Chain Reaction (RT-PCR) showed that the mRNA levels of inflammatory indicators in LPS + NEAT1 siRNA group were lower than that in the LPS group (p<0.05). According to Western blotting results, NEAT1 siRNAs could significantly downregulate the protein expressions of TLR2 and p-p65. CONCLUSIONS: NEAT1 knockdown can improve LPS-induced myocardial injury in mice by inhibiting the TLR2/NF-κB signaling pathway. LncRNA NEAT1 is expected to be a potential target for clinical treatment of the sepsis-induced myocardial injury.

[Application of transperineal pelvic floor ultrasonography in the diagnosis of female stress urinary incontinence].

Objective: To explore the application of transperineal pelvic floor ultrasonography in the diagnosis of female stress urinary incontinence(SUI). Methods: From March 2017 to December 2017, 60 patients diagnosed with SUI by department of gynecology, Xiangya Hospital of Central South University were selected as the case group, and 30 cases of normal women in the same period were selected as the control group. All subjects in both groups were examined by transperineal pelvic floor ultrasonography, that is, to be measured the bladder neck descent(BND), the urethral inclination angle(UIA), the posterior urethrovesical angle(PUVA) and the levator hiatus area(LHA) in resting state and during Valsalva maneuver. Results: (1)The differences in the measured values of the two groups were statistically significant(P<0.05). (2)The receiver operating characteristic curve(ROC) was used to find the cut-off values of SUI: when BND>31.5 mm; in Valsalva state, UIA>33.5°, PUVA>150.5° and LHA>20.6 cm2, with their sensitivity of 77.6%, 71.4%, 68.3% and 61.4%, respectively; the specificity of 68.9%, 74.6%, 73.9% and 78.0%, respectively. The area under the curve(AUC) were 0.753, 0.812, 0.721 and 0.712, respectively, when combined analysis of these indexes, reaching to 0.912. Conclusions: (1) Transperineal pelvic floor ultrasonography has a certain diagnostic value for SUI. (2)Combined analysis of various ultrasonic parameters can significantly improve the diagnostic efficiency of SUI.

Oncogenic activity of amplified miniature chromosome maintenance 8 in human malignancies.

Miniature chromosome maintenance (MCM) proteins play critical roles in DNA replication licensing, initiation and elongation. MCM8, one of the MCM proteins playing a critical role in DNA repairing and recombination, was found to have overexpression and increased DNA copy number in a variety of human malignancies. The gain of MCM8 is associated with aggressive clinical features of several human cancers. Increased expression of MCM8 in prostate cancer is associated with cancer recurrence. Forced expression of MCM8 in RWPE1 cells, the immortalized but non-transformed prostate epithelial cell line, exhibited fast cell growth and transformation, while knock down of MCM8 in PC3, DU145 and LNCaP cells induced cell growth arrest, and decreased tumour volumes and mortality of severe combined immunodeficiency mice xenografted with PC3 and DU145 cells. MCM8 bound cyclin D1 and activated Rb protein phosphorylation by cyclin-dependent kinase 4 in vitro and in vivo. The cyclin D1/MCM8 interaction is required for Rb phosphorylation and S-phase entry in cancer cells. As a result, our study showed that copy number increase and overexpression of MCM8 may play critical roles in human cancer development.

[An analysis of various diseases and hearing screening in NICU infants].

Objective:It is the first time to study the hearing screening results in NICU infants in Heilongjiang province,to analyze the various diseases and hearing loss distribution in NICU infants.Method:Three hundred and thirty four newborns(668 ears) in NICU received hearing screening with TEOAE and AABR test.We compared the results of different risk factors.Result:The failed ratio of different diseases in NICU are as follow: premature infants 61%,hypoxic-ischemic encephalopathy(HIE) 35%,neonatal infectious pneumonia 30%,neonatal sepsis 30%,neonatal aspiration pneumonitis 36%,neonatal jaundice 29%.Conclusion:The positive ratio of preterm infants was 61%,which is higher than the other diseases in NICU infants of Heilongjiang province.Both TEOAE and AABR failure have a high incidence of abnormal hearing status.Neonatal jaundice,neonatal infectious pneumonia and premature infants diseases are the high risk factors of auditory neuropathy spectrum disorder(ANSD) in NICU infants of Heilongjiang.

Effectiveness and security of CT-guided percutaneous implantation of (125)I seeds in pancreatic carcinoma.

OBJECTIVE: To assess the effectiveness and security of CT-guided percutaneous implantation of iodine-125 ((125)I)-labelled seeds in pancreatic carcinoma. METHODS: A total of 36 patients (25 males and 11 females) with an average age of 57 years (range, 39-84 years) were enrolled and categorized into Stage III (27 cases) and Stage IV (9 cases) of pancreatic cancer. There were 3 tumours in the pancreatic head and 33 tumours in the pancreatic body or tail. The average diameter of the tumours was 37.1 mm (range, 15-65 mm). The implantation of (125)I seeds was performed by using 18-G needles (length, 150-200 mm) through the anterior, lateral and posterior approaches. Then, (125)I seeds were loaded and released into the lesions. RESULTS: Implantations were performed via the anterior (23 patients), lateral (9 patients) and posterior (4 patients) approaches. During implantation, 3-14 punctures were performed for each patient, and a total of 164 punctures were recorded. Meanwhile, a total of 657 seeds were implanted with an average of 25.27 (range, 12-50) seeds per patient, and the success rate was 100%. The activity of each seed ranged from 0.55 to 0.65 mCi. A main adverse event occurred in one puncture and minor events in seven punctures. No significant relationship between the punctures or adverse events was identified. No serious complication was detected after the implantations during follow-up visits. CONCLUSION: This study suggested that CT-guided percutaneous implantation of (125)I seeds in a pancreatic carcinoma was relatively safe and effective for treating unresectable pancreatic cancer. ADVANCES IN KNOWLEDGE: The CT-guided percutaneous implantation of (125)I seeds in unresectable pancreatic cancer showed highly successful rates without serious complications.

(125)I particle implantation combined with chemoradiotherapy to treat advanced pancreatic cancer.

OBJECTIVE: To evaluate the therapy effects of (125)I implantation combined with chemoradiotherapy on pancreatic cancer patients. METHODS: 30 patients with Stage III or IV pancreatic cancer were equally divided into two groups (control and treatment group). The patients in the treatment group (nine males, six females) received chemotherapy in the first week and (125)I implantation in the third week, followed by combined chemoradiotherapy in the fifth week. The patients in the control group (10 males, 5 females) received the same treatment except (125)I implantation. The therapy in the control group and treatment group was repeated every 4 weeks. RESULTS: The median conformal radiotherapy dose in the treatment group (30.62 Gy) was significantly lower than that in the control group (47.86 Gy). The total radiation dose was 88.71 ± 27.39 Gy, and the surface activity was 0.6 mCi in the treatment group. After treatment, the average tumour size decreased both in the treatment group [9.17 cm(2), 95% confidence interval (CI): 5.60-12.74, p < 0.001] and in the control group (4.54 cm(2), 95% CI: 2.74-6.35, p < 0.001). The median survival time in the treatment group was 14 months (95% CI: 12.215-14.785) and in the control group was 12 months (95% CI: 10.884-13.116). There was no statistical significance in survival rates between the two groups (χ(2) = 0.908, p = 0.341). CONCLUSION: (125)I implanted into tumour combined with chemoradiotherapy has higher local control rate of advanced pancreatic cancer than chemoradiotherapy. ADVANCES IN KNOWLEDGE: We combined chemoradiotherapy with (125)I implantation to treat advanced pancreatic cancer and obtained a higher local control rate and better quality of life than when using chemoradiatherapy alone.

OA-4 inhibits osteoclast formation and bone resorption via suppressing RANKL induced P38 signaling pathway.

Osteoclasts are one of the key therapeutic targets for a variety of orthopedic diseases such as osteoporosis and osteoarthritis. In this study, we synthesized a novel compound N-(3-(cyclohexylcarbamoyl) phenyl)-1H-indole-2- carboxamide (termed as OA-4) and investigated the effects of OA-4 on the differentiation and function of osteoclasts. OA-4 markedly diminished osteoclast differentiation and osteoclast specific gene expression in a dose-dependent manner. In addition, OA-4 dose-dependently suppressed osteoclastic bone resorption. Furthermore, we found OA-4 attenuated RANKL-induced p38 phosphorylation without affecting JNK or NF-κB signaling pathways. Collectively, we synthesized a novel compound OA-4 which can inhibit osteoclast formation and functions via the suppression of p38 signaling pathway.

OA10 is a novel p38alpha mitogen-activated protein kinase inhibitor that suppresses osteoclast differentiation and bone resorption.

In search of anti-bone resorbing agents for the potential treatment of osteoporosis, we synthesized a novel compound Tert-butyl 4-(3-[1H-indole-2-carboxamido]benzoyl)piperazine-1-carboxylate (OA10) and found that OA10 is capable of inhibiting RANKL-mediated osteoclast formation and osteoclastic bone resorption in a dose-dependent manner. This biological effect is further supported by the fact that OA10 suppressed osteoclastic-specific gene expression, including tartrate-resistant acid phosphatase, cathepsin K receptor, and calcitonin receptor. Further molecular mechanism investigation revealed OA10 inhibited p38 phosphorylation, suppressed c-fos and NFATc1 expression without affecting NF-κB or JNK signaling pathways. Taken together, this study suggested that OA10 can inhibit osteoclastogenesis by suppressing p38-c-Fos-NFATc1 cascade. OA10 may be developed as a therapeutic drug for osteoclast-related osteolytic diseases.

Phosphorylation and interaction of myopodin by integrin-link kinase lead to suppression of cell growth and motility in prostate cancer cells.

Myopodin is a tumor-suppressor gene that suppresses growth of prostate and urothelial carcinomas. However, the mechanism of myopodin tumor-suppressor activity or signaling that leads to activation of myopodin remains unclear. In this report, we showed that the N-terminus of myopodin binds integrin-linked kinase (ILK) both in vivo and in vitro. An ILK interaction motif of 78 amino acids (amino acids 82-157) was identified in the N-terminus region of myopodin. Induction of ILK-dependent kinase activity by integrin α7 led to phosphorylation of myopodin both in vivo and in vitro. Knocking down ILK dramatically reduced the inhibition of cell growth and motility mediated by myopodin. A mutant of myopodin lacking the ILK interaction motif is inactive in suppressing the growth and motility of PC3 cells. As a result, this study showed a novel and critical signaling pathway that leads to activation of myopodin.

Inhibition of prostate cancer growth and metastasis using small interference RNA specific for minichromosome complex maintenance component 7.

Minichromosome complex maintenance component 7 (MCM7) is a critical component of DNA replication licensing. Amplification and overexpression of MCM7 leads to high rate of prostate cancer metastasis. Recent studies indicate that MCM7 genome encodes a putative 'super-oncogene' cluster including MCM7 oncogene and a miRNA cluster that knocks down the expression of several critical tumor-suppressor genes. In this study, we constructed a vector that constitutively expresses small interference RNA (siRNA) specific for MCM7. Introduction of this vector into prostate cancer cell lines PC3 or Du145 decreases the expression of MCM7 by 80%. The vector inhibits DNA synthesis and generates growth arrest of these cancer cells. Severe combined immunodeficient mice were xenografted PC3 or Du145 tumors, and subsequently treated with this vector through tail vein injection with polyethylenimine. The animals had dramatically smaller tumor volume, less metastasis and better survival rate in comparison with the controls. As a result, intervention of MCM7 expression using siRNA approach may hold the promise for treating androgen refractory prostate cancer.

CSR1 induces cell death through inactivation of CPSF3.

CSR1 (cellular stress response 1), a newly characterized tumor-suppressor gene, undergoes hypermethylation in over 30% of prostate cancers. Re-expression of CSR1 inhibits cell growth and induces cell death, but the mechanism by which CSR1 suppresses tumor growth is not clear. In this study, we screened a prostate cDNA library using a yeast two-hybrid system and found that the cleavage and polyadenylation-specific factor 3 (CPSF3), an essential component for converting heteronuclear RNA to mRNA, binds with high affinity to the CSR1 C terminus. Further analyses determined that the binding motifs for CPSF3 are located between amino acids 440 and 543. The interaction between CSR1 and CPSF3 induced CPSF3 translocation from the nucleus to the cytoplasm, resulting in inhibition of polyadenylation both in vitro and in vivo. Downregulation of CPSF3 using small interfering RNA induced cell death in a manner similar to CSR1 expression. A CSR1 mutant unable to bind to CPSF3 did not alter CPSF3 subcellular distribution, did not inhibit its polyadenylation activity and did not induce cell death. In summary, CSR1 appears to induce cell death through a novel mechanism by hijacking a critical RNA processing enzyme.

Pathological factors evaluating prostate cancer.

Prostate cancer is one of the most prevalent malignancies for men world wide. However, only a small fraction of prostate cancer cases are metastasizing and life-threatening. Even though the detection rate of prostate cancer has been steadily increased in the last two decades due to implementation of PSA screening, it is still not clear what factors govern its clinical outcomes. In this review, we will discuss several recent pathological advances that might contribute to the progression of prostate cancer. In addition, this review will cover a brief overview on conventional morphological evaluation of prostate cancer differentiation.

MCM7 amplification and overexpression are associated with prostate cancer progression.

The genomic DNA profiles of prostate cancers with aggressive features were compared to the profiles of matched normal DNA to identify genes that are selectively amplified in the cancer cells. One of the identified genes, MCM7, which is a component of the DNA replication licensing complex, has been studied extensively both at the DNA and protein levels in human prostate tissues. Approximately half of the prostate cancer specimens studied showed MCM7 gene amplification, and 60% of the aggressive prostate cancer specimens had increased MCM7 protein expression. Amplification or overexpression of MCM7 was significantly associated with relapse, local invasion and a worse tumor grade. Constitutive expression of MCM7 in a human prostate cancer cell line, DU145, resulted in markedly increased DNA synthesis and cell proliferation compared to vector-only controls, and an increased cell invasion in vitro. Indeed, MCM7 overexpression produced primary tumors 12 times larger than vector-only controls and resulted in a rapid demise of mice bearing those tumors. These studies implicate MCM7, and the DNA replication licensing gene family, in prostate cancer progression, growth and invasion.

Myopodin, a synaptopodin homologue, is frequently deleted in invasive prostate cancers.

Prostate cancer is one of the leading causes of cancer-related deaths for men in the United States. Like other malignancies, prostate cancer is underscored by a variety of aberrant genetic alterations during its development. Although loss of heterozygosity or allelic loss is frequently identified among prostate cancers, few genes have been identified thus far as critical to the development of invasive prostate cancers. In this report, we used the recently developed technology, the "differential subtraction chain," to perform a genome-wide search for sequences that are deleted in an aggressive prostate cancer. Among the deleted sequences, we found that one sequence was deleted in >50% of prostate cancers we tested. We mapped this sequence to chromosome 4q25 by screening the Genebridge 4 hamster radiation panel with primers specific to this probe, and subsequently identify a 54-kb minimal common deletion region that contains the sequence encoding myopodin. Sequence analysis indicates that myopodin shares significant homology with synaptopodin, a protein closely associated with podocyte and neuron differentiation. Further study shows that frequent complete or partial deletions of the myopodin gene occurred among invasive prostate cancer cases (25 of 31 cases, or 80%). Statistical analysis indicates that deletion of myopodin is highly correlated with the invasiveness of prostate cancers, and thus may hold promise as an important prognostic marker for prostate cancers.