54 research outputs found

    A Case of an Invasive Lobular Carcinoma with Extracellular Mucin: Radio-Pathological Correlation

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    A case of 77-year-old female with an invasive lobular carcinoma with extracellular mucin is presented. She felt palpable mass in her left breast. Then, she came to our hospital for further examination. Mammography of right in full view revealed architectural distortion in left upper portion. And ultrasonography demonstrated low-echoic mass about 2 cm in diameter and invasion of the fat tissue was observed. Hence, malignancy was suspected and magnetic resonance imaging (MRI) was performed. MRI findings showed irregular shaped and margined mass with small T2-high-signal intensity. These findings suggested invasive carcinoma with mucin. Because the cancer lesion was not large, partial mastectomy was performed. Interestingly, pathological diagnosis was invasive lobular carcinoma with extracellular mucin. Extracellular mucinous lesion was concordant with small T2-high-signal intensity. This type of carcinoma was previously reported only in three cases, and rare but important, because the treatment and prognosis might change by histological subtypes. We suggest one of the MRI special features of our case is not only irregular shaped and margined mass but also small T2-high-signal intensity. These MR findings might be one of the valuable findings for the diagnosis and differentiation between this type of carcinoma from other tumors

    Prospective cohort study of febrile neutropenia in breast cancer patients administered with neoadjuvant and adjuvant chemotherapies: CSPOR-BC FN study

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    Background As Asians are more vulnerable to febrile neutropenia (FN) than Caucasians, evaluations of FN incidence and risk factors in Asians are important for the appropriate use of primary pegfilgrastim (PEG-G). Patients and methods Japanese breast cancer patients receiving standard adjuvant chemotherapies were prospectively enrolled in multicenter institutions from August 2015 to July 2017. FN was evaluated from 2 treatment policies: true FN (T-FN): ≥37.5 °C, grade 4 neutropenia, mandatory hospital visit (visiting); surrogate FN (S-FN): ≥37.5 °C, oral antibiotic, no mandatory visit (non-visiting). PEG-G was used at the physicians’ discretion. The primary endpoint was FN incidence during all cycles. Multivariate logistic regression analysis was performed to identify T-FN risk factors. Results Of 1005 enrolled patients, 980 women treated with FEC, E(A)C, and TC were analyzed. The FN incidence proportions in all patients were 22.5%, 27.5%, and 33.9% for FEC, E(A)C, and TC, respectively. Those of T-FN were 27.7%, 22.4%, and 36.6%; those of S-FN were 17.3%, 32.4%, and 31.5% with more frequent primary PEG-G usage. The relative dose intensity (RDI) of the 3 regimens was ≥0.85 in both groups. In the analysis of risk factors, TC (odds ratio = 2.67), age ≥ 65 years (2.24), and pretreatment absolute neutrophil count (ANC)/1000 μl (0.8) remained significant. Conclusions FN incidences were above 20% in the 3 regimens, with TC showing the highest. RDI was maintained at a high level in both visiting and non-visiting groups. Patient-related risk factors were age and pretreatment ANC

    Lack of impact of the ALDH2 rs671 variant on breast cancer development in Japanese BRCA1/2‐mutation carriers

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    The aldehyde degrading function of the ALDH2 enzyme is impaired by Glu504Lys polymorphisms (rs671, termed A allele), which causes alcohol flushing in east Asians, and elevates the risk of esophageal cancer among habitual drinkers. Recent studies suggested that the ALDH2 variant may lead to higher levels of DNA damage caused by endogenously generated aldehydes. This can be a threat to genome stability and/or cell viability in a synthetic manner in DNA repair-defective settings such as Fanconi anemia (FA). FA is an inherited bone marrow failure syndrome caused by defects in any one of so far identified 22 FANC genes including hereditary breast and ovarian cancer (HBOC) genes BRCA1 and BRCA2. We have previously reported that the progression of FA phenotypes is accelerated with the ALDH2 rs671 genotype. Individuals with HBOC are heterozygously mutated in either BRCA1 or BRCA2, and the cancer-initiating cells in these patients usually undergo loss of the wild-type BRCA1/2 allele, leading to homologous recombination defects. Therefore, we hypothesized that the ALDH2 genotypes may impact breast cancer development in BRCA1/2 mutant carriers. We genotyped ALDH2 in 103 HBOC patients recruited from multiple cancer centers in Japan. However, we were not able to detect any significant differences in clinical stages, histopathological classification, or age at clinical diagnosis across the ALDH2 genotypes. Unlike the effects in hematopoietic cells of FA, our current data suggest that there is no impact of the loss of ALDH2 function in cancer initiation and development in breast epithelium of HBOC patients

    A Clinical Trial Evaluating the Usefulness of Tailored Antimicrobial Prophylaxis Using Rectal-culture Screening Media Prior to Transrectal Prostate Biopsy: A Multicenter, Randomized Controlled Trial

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    The aim of this report is to introduce an on-going, multicenter, randomized controlled trial to evaluate whether tailored antimicrobial prophylaxis guided by rectal culture screening prevents acute bacterial prostatitis following transrectal prostate biopsy (TRPB). Patients will be randomized into an intervention or non-intervention group; tazobactam-piperacillin or levofloxacin will be prophylactically administered according to the results of rectal culture prior to TRPB in the intervention group whereas levofloxacin will be routinely given in the non-intervention group. The primary endpoint is the occurrence rate of acute bacterial prostatitis after TRPB. Recruitment begins in April, 2021 and the target total sample size is 5,100 participants

    Changes in Health State Utility Values in Japanese Patients with End-Stage Breast Cancer

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    We aimed to determine the dynamic trends in health state utility values (HSUVs) in patients with end-stage breast cancer. We selected 181 patients comprising 137 with primary breast cancer (PBC) and 44 with metastatic breast cancer (MBC) (28 survivors and 16 patients with MBC death). HSUVs were 0.90 and 0.89 in patients with PBC and 0.83 and 0.80 in those with MBC (survivors) at 6 and 3 months, respectively, before the end of the observation period; these values were 0.73 and 0.66, respectively, in those with MBC (deceased) during the aforementioned period. The root-mean-squared error (RMSE) for the decrease in HSUVs over 3 months was 0.10, 0.096, and 0.175 for patients with PBC, MBC (survivors), and MBC (deceased), respectively. One-way analysis of variance for differences in absolute error among the groups was significant (p = 0.0102). Multiple comparisons indicated a difference of 0.068 in absolute error between patients with PBC and those with MBC (deceased) (p = 0.0082). Patients with end-stage breast cancer had well-controlled HSUVs 3 months before death, with a sharp decline in HSUVs in the 3 months leading up to death

    DEVELOPMENT OF AUTOIMMUNE THROMBOCYTOPENIA AFTER HIGH-DOSE CHEMOTHERAPY AND AUTOLOGOUS PERIPHERAL BLOOD STEM CELL SUPPORT FOR METASTATIC BREAST CANCER

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    Autoimmune thrombocytopenia (AT) occurs after not only allogeneic but also autologous SCT following high-dose myeloablative chemotherapy against malignant tumors. A 50-year-old woman was diagnosed with metastatic breast cancer (MBC) and received myeloablative chemotherapy followed by autologous peripheral blood stem cell transplantation. Purpura developed on day +40 after transplantation, and a diagnosis of AT was made based on her bone marrow picture and elevation of serum PA-IgG level. Her thrombocytopenia was refractory to treatment with high-dose intravenous immune globulin (IVIG) and steroids. Although her platelet count recovered to within the normal range after splenectomy, 14 months after receiving SCT she died of disseminated intravascular coagulation syndrome caused by progression of cancer metastasis. There have been 10 reported cases of AT developing after high-dose myeloablative chemotherapy against malignant tumors followed by autologous SCT. We suggest that the thrombocytopenia after engraftment was caused by activation of dormant auto-immunity, which our patient potentially had, in conjunction with an insufficient quantity and quality of suppressor T-cells before complete reconstruction of the immune system after myeloablative conditioning. The clinical course of our patient was specific and different from previously reported cases since a splenectomy was necessary due to her thrombocytopenia being refractory to both steroid and IVIG therapy

    Use of immunohistochemical analysis of CK5/6, CK14, and CK34betaE12 in the differential diagnosis of solid papillary carcinoma in situ from intraductal papilloma with usual ductal hyperplasia of the breast

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    Objectives: The aim of this study was to use immunohistochemistry to differentiate solid papillary carcinoma in situ from intraductal papilloma with usual ductal hyperplasia (IPUDH). Three types of high-molecular-weight cytokeratins (CKs) – CK5/6, CK14, and CK34betaE12 – were targeted. Methods: We studied 17 patients with solid papillary carcinoma in situ and 18 patients with IPUDH diagnosed by at least two pathologists. Immunohistochemical analyses used antibodies to CK5/6, CK14, and CK34betaE12 to make the differential diagnosis of solid papillary carcinoma in situ versus IPUDH. Immunohistochemical staining was scored as 0–5 using Allred score. Results: Immunohistochemistry with CK5/6 and CK14 antibodies produced scores of 0–3 in all patients with solid papillary carcinoma in situ and 2–5 in all patients with IPUDH. Immunohistochemical staining with CK34betaE12 antibody produced scores of 1–3 in all patients with solid papillary carcinoma and 3–5 in all patients with IPUDH. In tissues from patients with IPUDH, significantly more cells were stained with CK34betaE12 than CK5/6 ( p  < 0.05) or CK14 ( p  < 0.05). Conclusion: The immunoreactivity of CK5/6, CK14, and CK34betaE12 antibodies was useful to differentiate solid papillary carcinoma in situ from IPUDH. CK34betaE12 is especially useful for distinguishing solid papillary carcinoma from IPUDH
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