A case of giant nipple adenoma.

BACKGROUND: Nipple adenoma is a relatively rare benign disease. Clinically, it often presents with nipple erosions, and it should be differentiated from Paget's disease. CASE PRESENTATION: The patient was a 63-year-old woman who complained of a lump in her left nipple for more than 30 years. Computed tomography performed for screening congestive heart failure suggested a left nipple mass of 40 mm in size. Needle biopsy revealed nipple adenoma, and skin biopsy was also performed to confirm the diagnosis. Nipple tumor resection was performed under local anesthesia, and we confirmed that the final diagnosis was nipple adenoma with negative margins. The patient has been free from recurrence for 2 years since the surgery. CONCLUSIONS: We have reported our experience of a case of giant nipple adenoma.

Combination of DYRK2 and TERT Expression Is a Powerful Predictive Marker for Early-stage Breast Cancer Recurrence.

BACKGROUND/AIM: DYRK2 is a dual-specificity tyrosine-(Y)-phosphorylation-regulated kinase induces degradation of telomerase reverse transcriptase (TERT). The expression of both proteins in breast cancer were investigated as predictors of recurrence. PATIENTS AND METHODS: Two hundred and twenty-one patients with early breast cancer treated at our institute between 2000 and 2009, were included. We used immunohistochemical analyses to measure the expression of DYRK2 and TERT and correlated it with clinicopathological factors and survival. RESULTS: DYRK2 and TERT were positive in 58 (26%) and 86 (39%) of 221 patients, respectively. There was no correlation between DYRK2 and TERT expression and clinicopathological factors. Better disease-free survival was observed in the DYRK2-positive group (p=0.032), and poorer disease-free survival was noted in the TERT-positive group (p=0.023). The DYRK2-positive TERT-negative group exhibited significantly better disease-free survival than the other groups (p=0.006). CONCLUSION: The combination of DYRK2 and TERT may be a powerful tool to stratify breast cancer patients.

[Paclitaxel plus Bevacizumab Therapy plus Surgical Resection Results in Local Control of Stage â ¢C Breast Cancer].

The case was a 40-year-old female who was aware of a right breast mass for 1 year before her first visit. She had visited her previous doctor because the mass was gradually increasing in size. After close examination, she was diagnosed with Stage ⅢC triple-negative breast cancer. She underwent 4 courses of EC therapy and 7 courses of paclitaxel(PTX)plus bevacizumab( Bev)therapy and was then, referred to our hospital for resection. We instituted a 2-month break from Bev to prevent postoperative complications. She underwent a right mastectomy, combined chest wall resection, lymph node dissection, and chest wall reconstruction. Because the postoperative course was good and quality of life improved, the multidisciplinary treatment with surgery and pharmacotherapy was considered effective in locally advanced breast cancer.

[Comparison of the Incidence of Febrile Neutropenia in Doxorubicin/Cyclophosphamide(AC)and Docetaxel/Cyclophosphamide(TC) Perioperative Chemotherapies for Primary Breast Cancer].

Febrile neutropenia(FN)is an adverse event associated with chemotherapy. Because well-maintained dose intensity improves survival rate, suppression of FN is important. While the incidence of FN has been recognized to be higher with docetaxel/cyclophosphamide(TC)therapy, it is generally considered lower with doxorubicin/cyclophosphamide(AC)therapy, and primary prophylaxis with granulocyte-colony stimulating factor(G-CSF)is not recommended. FN with AC therapy is commonly experienced in our daily practice. Thus, we retrospectively compared the incidence of FN with AC and TC therapies. We examined the data of 48 patients with primary breast cancer, consisting of 26 patients treated with AC and 22 patients with TC as perioperative chemotherapy-from January 2014 to September 2018-to determine the incidence of FN. FN was observed in 7/26 patients who received AC(26.9%)and 5/22 patients who received TC(22.7%). Excluding patients with primary prophylaxis with G-CSF, FN was observed in 7/23 patients(30.4%)who received AC and 5/18 (27.8%)who received TC. The incidence of FN with AC therapy was higher than that with TC therapy in this study. Therefore, positive use of G-CSF is necessary for safety and to adequately maintain dose intensity for AC therapy.

Temporal change in IL-6 mRNA and protein expression produced by cyclic stretching of human pulmonary artery endothelial cells.

The time courses of interleukin (IL)-6 gene expression and protein production were examined in human pulmonary artery endothelial cells (HPAECs) subjected to cyclic stretching. IL-6 protein was increased even in cells without stretching. Fold changes determined by dividing the level of IL-6 protein in stretched cells by that in unstretched cells at the same sampling times indicated that IL-6 protein was increased by stretching. At least 1 h of stretching was necessary to elicit an increase of IL-6 protein, and the levels peaked at 3 h after the start of stretching. After withdrawal of stretching, there was no further increase of IL-6 protein. The expression levels of the IL-6 gene were significantly increased by stretching and peaked at 30 min after the start of stretching. The difference in the peak times of IL-6 gene and protein expression likely reflects the process of protein synthesis after the appearance of IL-6 mRNA.

Genetic dissection of vasculitis, myeloperoxidase-specific antineutrophil cytoplasmic autoantibody production, and related traits in spontaneous crescentic glomerulonephritis-forming/Kinjoh mice.

The spontaneous crescentic glomerulonephritis-forming/Kinjoh (SCG/Kj) mouse is a model of human crescentic glomerulonephritis and vasculitis associated with the production of the myeloperoxidase (MPO)-specific antineutrophil cytoplasmic autoantibody (MPO-ANCA). Although the disease is mediated initially by mutation of the Fas gene (lpr), SCG/Kj mice also have non-Fas predisposing genetic factors. To define these factors, genome-wide quantitative trait locus (QTL) mapping was performed on female (B(6)x SCG/Kj) F(2) intercross mice. Fourteen non-Fas QTLs were identified. QTLs of glomerulonephritis were located on chromosomes 1, 10, 13, 16, and 17, vasculitis on chromosomes 1 and 17, splenomegaly on chromosome 1, hypergammaglobulinemia on chromosomes 1, 2, 4, 6, 7, 11, 13, and 17, antinuclear Ab on chromosomes 1, 8, 10, and 12, and MPO-ANCA production on chromosomes 1 and 10. Significant QTLs derived from SCG/Kj on chromosomes 1, 2, 7, and 13 were designated Scg-1 to Scg-5, respectively, and those derived from B(6) on chromosomes 4, 6, 17, and 10 were designated Sxb-1 to Sxb-4, respectively. Two loci linked to MPO-ANCA production on chromosomes 1 and 10 were designated Man-1 and Man-2 (for MPO-ANCA), respectively. Although both Scg-1 and Scg-2 were on chromosome 1 and shared several functions, it was of interest that aberrant MPO-ANCA production was exclusively controlled by Man-1, the centromeric half region of the Scg-2 chromosomal segment. We also examined the epistatic effects between the lpr mutation and non-Fas susceptibility genes. QTLs are discussed in relation to previously described loci, with emphasis on their candidate genes.

Histone H3 is aberrantly phosphorylated in glutamine-repeat diseases.

Double-labeling immunohistochemical studies staining with anti-ubiquitin and anti-phosphoserine antibodies and application of an enzymatic dephosphorylation technique reveal neuronal inclusions and affected nuclei to be aberrantly phosphorylated in brain tissues with patients with glutamine-repeat diseases. Regional distribution of the phosphorylated nuclei in neurons correlates with the pathology. To identify the target nuclear protein, transient expression of Huntington's disease exon 1 gene containing an expanded glutamine repeat was generated in a cell culture and nuclear inclusions were isolated with a fluorescence-activated cell sorting system. Immunoblotting studies of the aggregated nuclear proteins using anti-phosphoserine antibody demonstrate the protein of the aberrant phosphorylation as histone H3. The immunoblots of control and diseased brain tissues demonstrate that the phosphorylation of histone H3 is commonly increased in the diseased brains. Aberrant phosphorylation of histone H3 is surmised to be a shared pathological process in glutamine-repeat diseases.