Mucosa-associated lymphoid tissue (MALT) lymphomas comprise 7.6% of non-Hodgkin’s lymphomas (NHLs) and they are recently recognized B-cell subset of NHLs. They are originated from gastrointestinal tract most frequently but may also occur in other organs including head and neck, lung, skin, thyroid and breast. Primary thyroid lymphomas (PTLs) constitute up to 5% of all thyroid malignancies. Diffuse large B-cell lymphoma is most common type of PTLs and MALT lymphoma is relatively rare subtype of PTLs. Thyroid MALToma arises in chronic inflammatory conditions with autoimmune or infectious etiologies. The optimal treatment regimen still remains controversial. However, It is reported that localized thyroid MALT lymphoma has excellent survival rate after surgical resection alone. We report a case of 48-years-old woman with primary thyroid MALToma.

Germline mutations in the BRCA1 and BRCA2 genes are strong genetic factors for predispositions to breast, ovarian, and other related cancers. This report describes a family with a history of breast and ovarian cancers that harbored a novel BRCA1 germline mutation. A single nucleotide deletion in intron 20, namely c.5332+4delA, was detected in a 43-year-old patient with breast cancer. This mutation led to the skipping of exon 20, which in turn resulted in the production of a truncated BRCA1 protein that was 1773 amino acids in length. The mother of the proband had died due to ovarian cancer and had harbored the same germline mutation. Ectopically expressed mutant BRCA1 protein interacted with the BARD1 protein, but showed a reduced transcriptional function, as demonstrated by the expression of cyclin B1. This novel germline mutation in the BRCA1 gene caused familial breast and ovarian cancers.
Adult ; Amino Acids ; BRCA1 Protein ; Breast Neoplasms* ; Breast* ; Cyclin B1 ; Exons* ; Genes, BRCA1 ; Genes, BRCA2 ; Germ-Line Mutation* ; Humans ; Introns ; Mothers ; Ovarian Neoplasms

BACKGROUND: Tumor necrosis factor-alpha (TNF-α) inhibitors (TNFis), which are the main treatment for ankylosing spondylitis (AS), have been reported not only to reduce the incidence of anterior uveitis (AU) but also to induce it, and these effects differ among the various types of TNFis in clinical use. The present study investigated the effect of TNFis on uveitis by analyzing the long-term clinical course of AU in AS patients treated with TNFi therapy. METHODS: Patients treated with at least one TNFi between January 2007 and July 2017 were reviewed, and 54 patients with at least one episode of AU were included in this study. The TNFis included anti-TNF-α antibodies (adalimumab, infliximab, and golimumab), and a soluble TNF receptor molecule (etanercept). The effect of prevention of AU, the likelihood of new-onset uveitis after the initiation of TNFi therapy, and the effects of drug switching and dose escalation were assessed. RESULTS: The first uveitis flare was observed before TNFi therapy in 39 patients and after TNFi therapy in 15 patients. Anti-TNF-α antibodies were more efficacious in decreasing the recurrence of AU than etanercept. Among patients in which uveitis first occurred after beginning TNFi therapy, patients on etanercept tended to first develop AU less than 1 year after starting the drug, and their AS tended to be well-controlled at the time of uveitis flares. Patients with a uveitis flare before their medication was switched did not recur afterwards, and five of eight patients showed no relapse after dose escalation. CONCLUSION: TNFis have various effects on AU. TNFis, particularly anti-TNF-α antibodies, should be considered in patients with AS and frequent AU relapse. Additionally, clinicians should consider whether AU is due to an absence of a therapeutic response of AS to TNFi treatment or to TNFi treatment itself, and appropriate treatment changes should be made accordingly.
Adalimumab ; Antibodies ; Drug Substitution ; Etanercept ; Humans ; Incidence ; Infliximab ; Receptors, Tumor Necrosis Factor ; Recurrence ; Spondylitis, Ankylosing ; Tumor Necrosis Factor-alpha ; Uveitis ; Uveitis, Anterior

PURPOSE: The purpose of this study was to compare the success rate of re-excision and breast-conserving surgery (BCS) between patients who received neoadjuvant chemotherapy and those who did not. METHODS: In this retrospective cohort study, 256 women who had clinical T2 breast cancer and planned to receive, as initial treatment either BCS (n=197) or neoadjuvant chemotherapy (n=59) between January 2009 and December 2012 were included. The data, including age, initial tumor size, mammographic microcalcification, ultrasound multifocality and axillary nodal status, were collected. The pathologic tumor size, p-multifocality, histologic type, estrogen receptor, progesterone receptor, human epidermal growth factor receptor 2, Ki-67, ductal carcinoma in situ (DCIS) and extensive intraductal component (EIC) were also reviewed. The re-excision and BCS success rates were investigated. Univariate analysis and regression model were used. To reduce the effect of selection bias, propensity score matching-based analysis was also performed. RESULTS: Of the 256 patients, 178 patients (90.4%, 178/197) in the non-neoadjuvant group and 56 patients (94.9%, 56/59) in the neoadjuvant group received BCS (p=0.406). In propensity-matched cohorts (n=118), the re-excision rate was similar in the two groups (35.6% in neoadjuvant group vs. 35.6% in non-neoadjuvant group, p=1.000). BCS success rate was slightly higher in neoadjuvant group (94.9%, 56/59) than in non-neoadjuvant group (86.4% [51/59], p=0.205). In logistic regression model, clinicopathologic factors associated with re-excision were pathologic multifocality (odds ratio [OR], 4.56; p=0.0142), high Ki-67 (≥50%) (OR, 0.7; p=0.0243) and DCIS component (OR, 2.67; p=0.0261). CONCLUSION: This study showed that neoadjuvant chemotherapy could increase the success rate of BCS but could not decrease that of re-excision. The re-excision rate is more associated with pathologic finding rather than the effect of neoadjuvant chemotherapy.
Breast Neoplasms ; Breast* ; Carcinoma, Intraductal, Noninfiltrating ; Cohort Studies ; Drug Therapy* ; Estrogens ; Female ; Humans ; Logistic Models ; Mastectomy, Segmental ; Propensity Score ; Receptor, Epidermal Growth Factor ; Receptors, Progesterone ; Retrospective Studies ; Selection Bias ; Ultrasonography

CTHRC1 (collagen triple-helix repeat-containing 1), a protein secreted during the tissue-repair process, is highly expressed in several malignant tumors, including pancreatic cancer. We recently showed that CTHRC1 has an important role in the progression and metastasis of pancreatic cancer. Although CTHRC1 secretion affects tumor cells, how it promotes tumorigenesis in the context of the microenvironment is largely unknown. Here we identified a novel role of CTHRC1 as a potent endothelial activator that promotes angiogenesis by recruiting bone marrow-derived cells to the tumor microenvironment during tumorigenesis. Recombinant CTHRC1 (rCTHRC1) enhanced endothelial cell (EC) proliferation, migration and capillary-like tube formation, which was consistent with the observed increases in neovascularization in vivo. Moreover, rCTHRC1 upregulated angiopoietin-2 (Ang-2), a Tie2 receptor ligand, through ERK-dependent activation of AP-1 in ECs, resulting in recruitment of Tie2-expressing monocytes (TEMs) to CTHRC1-overexpressing tumor tissues. Treatment with a CTHRC1-neutralizing antibody-abrogated Ang-2 expression in the ECs in vitro. Moreover, administration of a CTHRC1-neutralizing antibody to a xenograft mouse model reduced the tumor burden and infiltration of TEMs in the tumor tissues, indicating that blocking the CTHRC1/Ang-2/TEM axis during angiogenesis inhibits tumorigenesis. Collectively, our findings support the hypothesis that CTHRC1 induction of the Ang-2/Tie2 axis mediates the recruitment of TEMs, which are important for tumorigenesis and can be targeted to achieve effective antitumor responses in pancreatic cancers.
Angiopoietin-2 ; Animals ; Carcinogenesis ; Endothelial Cells ; Heterografts ; In Vitro Techniques ; Mice ; Monocytes* ; Neoplasm Metastasis ; Pancreatic Neoplasms ; Receptor, TIE-2 ; Transcription Factor AP-1 ; Tumor Burden ; Tumor Microenvironment