Thermochemical Mechanism of the Epoxy-Glutamic Acid Reaction with Sn-3.0 Ag-0.5 Cu Solder Powder for Electrical Joining.

An epoxy-based solder paste (ESP) is a promising alternative to conventional solder pastes to improve the reliability of fine-pitch electrical joining because the epoxy encapsulates the solder joint. However, development of an appropriate epoxy formulation and investigation of its reaction mechanism with solder powder is challenging. In this study, we demonstrate a newly designed ESP consisting of diglycidyl ether of bisphenol F (DGEBF) resin, Sn-3.0 Ag-0.5 Cu (SAC305) solder powder, and L-glutamic acid (Glu), which is a proteinogenic amino acid for biosynthesis of proteins in living systems. The mechanism of the thermochemical reaction was explored and tentatively proposed, which reveals that the products of the reaction between SAC305 and Glu function as catalysts for the etherification of epoxides and alcohols produced by chemical bonding between DGEBF and Glu, consequently leading to highly crosslinked polymeric networks and an enhancement of impact resistance. Our findings provide further insight into the mechanism of the reaction between various formulations comprising an epoxy, amino acid, and solder powder, and their potential use as ESPs for electrical joining.

Is There Pathological Uniformity between the Periphery and Center of a Gastrointestinal Stromal Tumor?

BACKGROUND: Gastrointestinal stromal tumors (GISTs) are mesenchymal tumors and have some malignant potential. Mitotic count is important for predicting the malignant potential of GISTs. Proper treatment of GISTs requires accurate pathological diagnosis. In general, endoscopic ultrasound-guided fine-needle aspiration and deep biopsy are used for pathological diagnosis of GIST before making decisions about surgery. This study sought to evaluate the pathological uniformity of gastric GISTs for mitotic index of the center and periphery of the GIST. METHODS: We retrospectively reviewed the data of 37 gastric GIST patients who underwent wedge resection at Hanyang University Hospital. We used Armed Forces Institute of Pathology criteria to classify gastric GISTs. To determine the pathological uniformity of gastric GISTs, we compared GIST risk stratification between the center and periphery of GISTs. RESULTS: The mean size of GISTs was 3.56 ± 2.10 cm. Three lesions were located in the antrum, 11 in the fundus, 9 in the cardia, and 14 in the body. The mean age of patients was 58.65 ± 9.44 years; 18 patients were male and 19 were female. Thirty-five patients (94.6%) showed the same level of risk stratification between the center and periphery of gastric GISTs, while two patients (5.4%) presented different levels of risk between the two sites. No significant difference in mitotic count was observed between the two sites (kappa value = 0.863; p = 0.001). CONCLUSIONS: Mitotic index category (either more than five mitoses per high-power field or five or fewer mitoses per high-power field) of GISTs showed good concurrence between the center and periphery.

Comparison of core-needle biopsy and repeat fine-needle aspiration for thyroid nodules with inconclusive initial cytology.

PURPOSE: We aimed to compare the efficacy of ultrasound-guided core-needle biopsy (CNB) with repeat fine-needle aspiration (rFNA) cytology in thyroid nodules with inconclusive results in initial fine-needle aspiration cytology. METHODS: We studied 402 patients who required a repeat biopsy of thyroid nodules using ultrasound-guided CNB (n = 192) or rFNA (n = 210) because of inconclusive results in initial FNA, corresponding to categories I, III, and IV of the Bethesda System for Reporting Thyroid Cytopathology. If repeat biopsy results were benign (category II), suspicious malignancy (category V), or malignancy (category VI), they were defined as "diagnostic results". The diagnostic yield and performances of repeat biopsy were analyzed and compared between the rFNA and CNB groups. RESULTS: The diagnostic results were obtained significantly higher in the CNB group than in the rFNA group (72.4% vs. 52.4%; P < 0.001). In the subgroup analysis, the diagnostic results were significantly higher in the CNB group than in the rFNA group for patients of categories I and III (P < 0.001 in both) in initial FNA. However, in patients with category IV nodules, there were no significant differences in diagnostic results between the two groups (P = 0.46). CONCLUSION: Compared to rFNA, ultrasound-guided CNB is useful and effective as a repeat biopsy option for thyroid nodules with non-diagnostic results (category I) and atypia of undetermined significance (AUS) or follicular lesion of undetermined significance (FLUS) (category III) in initial FNA.

Voriconazole-induced Severe Hyperkalemia Precipitated by Multiple Drug Interactions.

Voriconazole, a triazole antifungal agent used to treat serious fungal infections, has a pharmacokinetic characteristic of undergoing hepatic metabolism by the cytochrome P450 system. Few cases of hyperkalemia have been reported, which presented only when the serum voriconazole level was exceptionally elevated by drug-drug interactions. Additionally, azole antifungals may interfere with the biosynthesis of adrenal steroids and therefore can predispose patients to aldosterone deficiency. However, it is unclear whether voriconazole itself can induce hypoaldosteronism or hyperkalemia. Here, we report a case of voriconazole-induced hyperkalemia in a patient administered concurrent medications to treat comorbidities. Voriconazole was orally administered for pulmonary aspergillosis, and three episodes of severe hyperkalemia recurred, which improved with emergency treatment. In the first episode, renin-angiotensin-aldosterone system inhibitors were associated. We found that dronedarone might have increased the voriconazole level in the second episode. At that time, severe hypercalcemia was concurrent, which improved with acute hemodialysis and eliminating dronedarone. Finally, severe hyperkalemia recurred without concurrent medications known to interact with voriconazole. Upon switching from voriconazole to itraconazole, the hyperkalemia was resolved. Drug level monitoring is necessary when voriconazole is used. Genetic susceptibility, such as through CYP2C19 polymorphism, may be investigated for patients with adverse reactions to voriconazole.

CDK12 drives breast tumor initiation and trastuzumab resistance via WNT and IRS1-ErbB-PI3K signaling.

Cyclin-dependent kinase 12 (CDK12) has emerged as an effective therapeutic target due to its ability to regulate DNA damage repair in human cancers, but little is known about the role of CDK12 in driving tumorigenesis. Here, we demonstrate that CDK12 promotes tumor initiation as a novel regulator of cancer stem cells (CSCs) and induces anti-HER2 therapy resistance in human breast cancer. High CDK12 expression caused by concurrent amplification of CDK12 and HER2 in breast cancer patients is associated with disease recurrence and poor survival. CDK12 induces self-renewal of breast CSCs and in vivo tumor-initiating ability, and also reduces susceptibility to trastuzumab. Furthermore, CDK12 kinase activity inhibition facilitates anticancer efficacy of trastuzumab in HER2+ tumors, and mice bearing trastuzumab-resistant HER2+ tumor show sensitivity to an inhibitor of CDK12. Mechanistically, the catalytic activity of CDK12 is required for the expression of genes involved in the activation of ErbB-PI3K-AKT or WNT-signaling cascades. These results suggest that CDK12 is a major oncogenic driver and an actionable target for HER2+ breast cancer to replace or augment current anti-HER2 therapies.

Wound Healing Effect of Nonthermal Atmospheric Pressure Plasma Jet on a Rat Burn Wound Model: A Preliminary Study.

Worldwide, an estimated 6 million patients seek medical attention for burns annually. Various treatment methods and materials have been investigated and developed to enhance burn wound healing. Recently, a new technology, plasma medicine, has emerged to offer new solutions in wound care. As the development of plasma medicine has shown benefit in wound healing, we aimed to assess the effects of plasma medicine on burn wounds. To investigate the effectiveness of a nonthermal atmospheric pressure plasma jet (NAPPJ) for burn wound treatment on a brass comb burn wound rat model. Burn wounds were made by applying a preheated brass comb (100°C) for 2 minutes, which resulted in four full-thickness burn wounds separated by three interspaces. Interspaces were exposed to NAPPJ treatment for 2 minutes and morphological changes and neutrophil infiltration were monitored at 0, 4, and 7 days post-wounding. The percentage of necrotic interspace was higher in the control group than in the plasma-treated group (51.8 ± 20.5% vs 31.5 ± 19.0%, P < .001). Moreover, the exposure of interspace to NAPPJ greatly reduced the number of infiltrating neutrophils. In addition, the percentage of interspace that underwent full-thickness necrosis in the plasma-treated group was smaller than that in the control group (28% vs 67%). NAPPJ exposure on interspaces has a positive effect on burn wounds leading to wound healing by reducing burn injury progression.

Inflammatory mediators of prostate epithelial cells stimulated with Trichomonas vaginalis promote proliferative and invasive properties of prostate cancer cells.

BACKGROUND: Trichomonas vaginalis (Tv) is the most common sexually transmitted parasite. It is detected in prostatic tissue of benign prostatic hyperplasia, prostatitis, and prostate cancer (PCa) and has been suggested to cause chronic prostatitis. Moreover, up to 20% of all cancers worldwide are associated with chronic inflammation. Here, we investigated whether inflammatory mediators produced by normal human prostate epithelial cells (RWPE-1) stimulated with Tv could promote growth and invasiveness of PCa cells. METHODS: Conditioned medium of RWPE-1 cells was prepared by stimulating them with Tv (trichomonad-conditioned medium [TCM]) and without Tv (conditioned medium [CM]). Promotion of PCa cells (PC3, DU145, and LNCaP) was assessed by wound healing, proliferation, and invasion assays. RESULTS: We observed that the production of interleukin (IL)-1ß, IL-6, CCL2, CXCL8, prostaglandin-E2 (PGE2 ), and COX2 by RWPE-1 cells was increased by stimulating them with Tv. When PCa cells were incubated with TCM, their proliferation, invasion, and migration increased. Moreover, they showed increased epithelial-mesenchymal transition (EMT)-related markers by a reduction in epithelial markers and an increase in mesenchymal markers. In vivo, xenograft tumor tissues injected with TCM also showed increased expression of cyclin D1 and proliferating cell nuclear antigen, as well as induction of EMT. Receptors and signal molecules of PCa cells increased in response to exposure to TCM, and blocking receptors (CXCR1, CXCR2, C-C chemokine receptor 2, glycoprotein 130, EP2, and EP4) reduced the proliferation of PCa cells with decreased production of cytokines (CCL2, IL-6, and CXCL8) and PGE2 , and expression of NF-κB and Snail1. CONCLUSIONS: Our results suggest that Tv infection may be one of the factors creating the supportive microenvironment to promote proliferation and invasiveness of PCa cells.

Experimental rat prostatitis caused by Trichomonas vaginalis infection.

BACKGROUND: Trichomonas vaginalis (T. vaginalis) is the most common sexually transmitted parasite. It has been detected in prostatic tissue of patients with prostatitis and reported to be associated with chronic prostatitis and benign prostatic hyperplasia as well as prostate cancer. Recently, experimental rodent models of prostatitis induced by pathogen infection have been developed. However, there have so far been no reports of prostatitis caused by T. vaginalis infection in animals. Here, we investigated whether infection with T. vaginalis via the rat urethra could cause prostatitis. METHODS: T. vaginalis was injected into prostate through urethra of rat (Wistar rats), and the rats were killed 1, 2, or 4 weeks later. The presence of T. vaginalis trophozoites in the rat prostates was examined by immunohistochemistry, and pathological changes of the prostate were observed by hematoxylin-eosin staining and evaluated by grading from 0 to 5 for inflammatory cell infiltration, acinar changes, and interstitial fibrosis. Infiltrated mast cells were observed by toluidine blue staining of rat prostate tissue. Chemokine C-C motif ligand 2 (CCL2) levels of the rat prostates were measured by ELISA. RESULTS: T. vaginalis trophozoites were observed in acini in the prostates of the injected rats. The prostate tissues had higher pathological scores, and 83% (5/6) and 100% (6/6) of the ventral and dorsolateral lobes (n = 6), respectively, were inflamed. Infiltration and degranulation of mast cells were observed at higher rates in prostate sections of the T. vaginalis-infected rats. Also, prostate tissues of the injected rats had increased CCL2 levels. CONCLUSIONS: Injection of T. vaginalis in rats caused prostatitis as revealed by pathologic changes, mast cell infiltration and increased CCL2 production. Therefore, this study provides the first evidence that T. vaginalis infection in rats causes prostatitis.

NDR-effect vertical-illumination-type Ge-on-Si avalanche photodetector.

We present the enhanced performances of a vertical-illumination-type Ge-on-Si avalanche photodetector based on internal RF-gain effects operating up to 50 Gb/s. A fabricated Ge-on-Si avalanche photodetector (APD) exhibits three operational voltage regions associated with different aspects of the current (DC) gain and bandwidth characteristics. The measured current-voltage (I-V) curve of a Ge-on-Si APD exhibits a negative photoconductance (negative differential resistance [NDR]) in a high bias region beyond the avalanche breakdown voltage (V br ), where a device shows good eye openings up to 50 Gb/s (non-return-to-zero [NRZ] signal) with further improved signal-to-noise ratios and signal amplitudes. A ROSA packaged module, wherein a fabricated Ge-on-Si APD is wire-bonded to a commercial TIA with a ∼75% optical alignment for λ∼1310 nm and biased at a lower voltage than the V br , exhibits the sensitivities of -18.9 and -15.3 dBm for 30 and 35 Gb/s, respectively, and -13.9 dBm for 40 Gb/s at a 10-12 bit error rate. The experimental results indicate that considerable improvement in a module performance can be expected by utilizing the Ge-on-Si APD operated in the NDR region with a properly customized TIA.

Space Occupying Lesion in the Liver Caused by Hepatic Visceral Larva Migrans: A Case Report.

Visceral larva migrans (VLM) is one of the clinical syndromes of human toxocariasis. We report a case of hepatic VLM presenting preprandial malaise and epigastric discomfort in a 58-year-old woman drinking raw roe deer blood. The imaging studies of the abdomen showed a 74-mm hepatic mass featuring hepatic VLM. Anti-Toxocara canis immunoglobulin G (IgG) was observed in enzyme-linked immunosorbent assay (ELISA) and western blot. Despite anthelmintic treatment, the patient complained of newly developed cough and skin rash with severe eosinophilia. Hepatic lesion increased in size. The patient underwent an open left lobectomy of the liver. After the surgery, the patient was free of symptoms such as preprandial malaise, epigastric discomfort, cough, and skin rash. Laboratory test showed a normal eosinophilic count at postoperative 1 month, 6 months, 1 year, and 4 years. The initial optical density value of 2.55 of anti-T. canis IgG in ELISA was found to be negative (0.684) at postoperative 21 months. Our case report highlights that a high degree of clinical suspicion for hepatic VLM should be considered in a patient with a history of ingestion of raw food in the past, presenting severe eosinophilia and a variety of symptoms which reflect high worm burdens. Symptom remission, eosinophilia remission, and complete radiological resolution of lesions can be complete with surgery.

Adult Idiopathic Renal Fanconi Syndrome: A Case Report.

Renal Fanconi syndrome (RFS) is caused by generalized proximal tubular dysfunction and can be divided into hereditary and acquired form. Adult-onset RFS is usually associated with drug toxicity or systemic disorders, and modern molecular genetics may explain the etiology of previous idiopathic cases of RFS. Here, we report the case of a 52-year-old woman with RFS whose etiology could not be identified. She presented with features of phosphaturia, renal glucosuria, aminoaciduria, tubular proteinuria, and proximal renal tubular acidosis. Her family history was unremarkable, and previous medications were nonspecific. Her bone mineral density was compatible with osteoporosis, serum intact parathyroid hormone level was mildly elevated, and 25(OH) vitamin D level was insufficient. Her blood urea nitrogen and serum creatinine levels were 8.4 and 1.19 mg/dL, respectively (estimated glomerular filtration rate, 53 mL/min/1.73 m2). Percutaneous renal biopsy was performed but revealed no specific renal pathology, including mitochondrial morphology. No mutation was detected in EHHADH gene. We propose the possibility of involvement of other genes or molecules in this case of adult RFS.

Clinicopathological analysis of CD44 and CD24 expression in invasive breast cancer.

A subpopulation of breast cancer cells with cluster of differentiation (CD)44-positive and CD24-negative expression has been reported to have stem cell properties and to have a higher tumorigenic capacity than other cells. However, the clinicopathological characteristics of this subpopulation are not fully understood. In this study, we aimed to identify the correlations between the expression of CD44 and CD24 and clinicopathological parameters and overall survival. We studied specimens from 262 patients with invasive breast cancer. Immunohistochemical staining for CD44 and CD24 was performed using tissue microarrays. The clinicopathological factors were evaluated from the patients' medical records. In correlation analysis, CD44 expression was significantly associated with human epidermal growth factor receptor 2 (HER2)-negative status (P<0.001). Conversely, CD24 expression was significantly associated with HER2-positive status (P<0.001). CD44 and CD24 expression did not demonstrate any correlation with the age, tumor size, axillary lymph node metastasis status, tumor stage, histological grade, estrogen receptor status and progesterone receptor status of patients. Upon survival analysis, there was no statistical difference in overall survival according to the expression of CD44 and CD24. The results from this study suggest that CD44 and CD24 are clinically significant markers associated with breast tumorigenesis, but not sufficient factors in determining the prognosis of invasive breast cancer.

Strain sonoelastography of inflammatory myopathies: comparison with clinical examination, magnetic resonance imaging and pathologic findings.

OBJECTIVE: To evaluate strain sonoelastography (SSE) in patients with inflammatory myopathies (IM) compared with clinical examination, MRI and pathologic findings. METHODS: 18 lesions from 17 consecutive patients with IM (5 males and 12 females; mean age, 41.2 years; range, 11-67 years) were assessed with SSE after MRI. The ratio of strain in the target muscle (A) and a nearby normal muscle (B), defined as the strain index value (SR) (B/A), was calculated automatically. Elastograms were assigned an elasticity score according to the degree and distribution of strain induced by manual compression. Ultrasonography and MRI were analyzed in conjunction with clinical information, biochemical data, final clinical diagnosis and grading of pathology. Correlations between SR and qualitative analyses of MRI and ultrasonography, elasticity score, biochemical data and final clinical diagnosis were analyzed using Pearson's correlation coefficient. RESULTS: The SR of the target muscles was high in patients with IM (mean 3.14; range, 0.95-5.93 ± 1.42). The correlations between SR and pathologic grading and elasticity score were statistically significant (p < 0.05). There was no significant agreement between SR and other clinical and radiologic parameters. CONCLUSION: Muscle hardness, as semi-quantitatively measured by SSE, was increased in cases of IM. The correlation between the SR and the pathologic grading suggests that SSE could be an important tool in not only the diagnosis of but also in measuring the degree of muscular inflammation. ADVANCES IN KNOWLEDGE: This work describes a correlation between tissue elasticity and pathology in IM.

The Role of Steroid Sulfatase as a Prognostic Factor in Patients with Endometrial Cancer.

PURPOSE: The aim of the study was to determine steroid sulfatase (STS) expression in endometrial cancer patients and its correlation with disease prognosis. MATERIALS AND METHODS: We conducted a retrospective study in 59 patients who underwent surgery with histologically confirmed endometrial cancer from January 2000 to December 2011 at Hanyang University Hospital. Immuno-histochemical staining of STS was performed using rabbit polyclonal anti-STS antibody. RESULTS: Sixteen of the 59 patients (27.1%) were positive for STS expression. Disease free survival (DFS) was 129.83±8.67 [95% confidence interval (CI): 112.84-146.82] months in the STS positive group (group A) and 111.06±7.17 (95% CI: 97.01-125.10) months in the STS negative group (group B) (p=0.92). Overall survival (OS) was 129.01±9.38 (95% CI: 110.63-147.38) months and 111.16±7.10 (95% CI: 97.24-125.07) months for the groups A and B, respectively (p=0.45). Univariate analysis revealed that FIGO stage and adjuvant therapy are significantly associated with DFS and OS. However, in multivariate analysis, FIGO stage and adjuvant therapy did not show any statistical significance with DFS and OS. STS was also not significantly associated with DFS and OS in univariate and multivariate analysis. CONCLUSION: STS expression was not significantly associated with DFS and OS, despite positive STS expression in 27% of endometrial cancer patients. Therefore, the role of STS as a prognostic factor in patients with endometrial cancer remains unclear and requires further research.

Single-chip photonic transceiver based on bulk-silicon, as a chip-level photonic I/O platform for optical interconnects.

When silicon photonic integrated circuits (PICs), defined for transmitting and receiving optical data, are successfully monolithic-integrated into major silicon electronic chips as chip-level optical I/Os (inputs/outputs), it will bring innovative changes in data computing and communications. Here, we propose new photonic integration scheme, a single-chip optical transceiver based on a monolithic-integrated vertical photonic I/O device set including light source on bulk-silicon. This scheme can solve the major issues which impede practical implementation of silicon-based chip-level optical interconnects. We demonstrated a prototype of a single-chip photonic transceiver with monolithic-integrated vertical-illumination type Ge-on-Si photodetectors and VCSELs-on-Si on the same bulk-silicon substrate operating up to 50 Gb/s and 20 Gb/s, respectively. The prototype realized 20 Gb/s low-power chip-level optical interconnects for λ ~ 850 nm between fabricated chips. This approach can have a significant impact on practical electronic-photonic integration in high performance computers (HPC), cpu-memory interface, hybrid memory cube, and LAN, SAN, data center and network applications.

Overexpression of Id1 in transgenic mice promotes mammary basal stem cell activity and breast tumorigenesis.

Inhibitor of differentiation/DNA binding (Id)1 is a crucial regulator of mammary development and breast cancer progression. However, its effect on stemness and tumorigenesis in mammary epithelial cells remains undefined. Herein, we demonstrate that Id1 induces mammary tumorigenesis by increasing normal and malignant mammary stem cell (MaSC) activities in transgenic mice. MaSC-enriched basal cell expansion and increased self-renewal and in vivo regenerative capacity of MaSCs are observed in the mammary glands of MMTV-Id1 transgenic mice. Furthermore, MMTV-Id1 mice develop ductal hyperplasia and mammary tumors with highly expressed basal markers. Id1 also increases breast cancer stem cell (CSC) population and activity in human breast cancer lines. Moreover, the effects of Id1 on normal and malignant stem cell activities are mediated by the Wnt/c-Myc pathway. Collectively, these findings provide in vivo genetic evidence of Id1 functions as an oncogene in breast cancer and indicate that Id1 regulates mammary basal stem cells by activating the Wnt/c-Myc pathway, thereby contributing to breast tumor development.

Silicon photonic receiver and transmitter operating up to 36 Gb/s for λ~1550 nm.

We present the hybrid-integrated silicon photonic receiver and transmitter based on silicon photonic devices and 65 nm bulk CMOS interface circuits operating over 30 Gb/s with a 10(-12) bit error rate (BER) for λ ~1550nm. The silicon photonic receiver, operating up to 36 Gb/s, is based on a vertical-illumination type Ge-on-Si photodetector (Ge PD) hybrid-integrated with a CMOS receiver front-end circuit (CMOS Rx IC), and exhibits high sensitivities of -11 dBm, -8 dBm, and -2 dBm for data rates of 25 Gb/s, 30 Gb/s and 36 Gb/s, respectively, at a BER of 10(-12). The measured energy efficiency of the Si-photonic receiver is 2.6 pJ/bit at 25 Gb/s with an optical input power of -11 dBm, and 2.1 pJ/bit at 36 Gb/s with an optical power of -2 dBm. The hybrid-integrated silicon photonic transmitter, comprised of a depletion-type Mach-Zehnder modulator (MZM) and a CMOS driver circuit (CMOS Tx IC), shows better than 5.7 dB extinction ratio (ER) for 25 Gb/s, and 3 dB ER for 36 Gb/s. The silicon photonic transmitter achieves the data transmission with less than 10(-15) BER at 25 Gb/s, 10(-14) BER at 28 Gb/s, and 6 x 10(-13) BER with the energy efficiency of ~6 pJ/bit at 30 Gb/s.

MEL-18 loss mediates estrogen receptor-α downregulation and hormone independence.

The polycomb protein MEL-18 has been proposed as a tumor suppressor in breast cancer; however, its functional relevance to the hormonal regulation of breast cancer remains unknown. Here, we demonstrated that MEL-18 loss contributes to the hormone-independent phenotype of breast cancer by modulating hormone receptor expression. In multiple breast cancer cohorts, MEL-18 was markedly downregulated in triple-negative breast cancer (TNBC). MEL-18 expression positively correlated with the expression of luminal markers, including estrogen receptor-α (ER-α, encoded by ESR1). MEL-18 loss was also associated with poor response to antihormonal therapy in ER-α-positive breast cancer. Furthermore, whereas MEL-18 loss in luminal breast cancer cells resulted in the downregulation of expression and activity of ER-α and the progesterone receptor (PR), MEL-18 overexpression restored ER-α expression in TNBC. Consistently, in vivo xenograft experiments demonstrated that MEL-18 loss induces estrogen-independent growth and tamoxifen resistance in luminal breast cancer, and that MEL-18 overexpression confers tamoxifen sensitivity in TNBC. MEL-18 suppressed SUMOylation of the ESR1 transactivators p53 and SP1, thereby driving ESR1 transcription. MEL-18 facilitated the deSUMOylation process by inhibiting BMI-1/RING1B-mediated ubiquitin-proteasomal degradation of SUMO1/sentrin-specific protease 1 (SENP1). These findings demonstrate that MEL-18 is a SUMO-dependent regulator of hormone receptors and suggest MEL-18 expression as a marker for determining the antihormonal therapy response in patients with breast cancer.

Bilateral granulomatous mastitis with a different etiology.

Idiopathic granulomatous mastitis (IGM) and Tuberculosis mastitis (TM) are rare inflammatory diseases of the breast that can clinically mimic malignancy causing misdiagnosis as breast cancer. We present a rare case of bilateral granulomatous mastitis with a different etiology. An initial lesion developed in the right breast was diagnosed as IGM, which was treated with antibiotics and surgery. A subsequent lesion developed in the contralateral breast 5 months later and was diagnosed as TM, which also completely responded to antituberculosis medication without surgical excision. Differential diagnosis was made using the results of the polymerase chain reaction for tuberculosis (TBC-PCR) of both of the breast lesions in addition to typical pathologic findings of IGM in the right breast and an antituberculosis medication response in the left breast. To the best of our knowledge, this is the first case of bilateral granulomatous mastitis with a different etiology.