Synovial tissues of patients with rheumatoid arthritis (RA) include factors regulating bone resorption, such as receptor activator NF-kappaB ligand (RANKL), TNF-alpha, IL-6, IL-17, and IFN-gamma. However, in addition to these cytokines, other factors expressed in synovial tissues may play a role in regulating bone resorption. In 2009, we demonstrated that novel peptides from T-cell leukemia translocation-associated gene (TCTA) protein expressed in synovial tissues from patients with RA inhibit human osteoclastogenesis, preventing cellular fusion via the interaction between TCTA protein and a putative counterpart molecule. Only a few studies on the role of TCTA protein have been reported, including our report published in 2009. In the current review paper, we summarized papers on TCTA protein before 2009 and our recent findings.

Autoantibodies impair acetylcholine receptor (AChR) in myasthenia gravis (MG) and P/Q-type voltage-gated calcium channel (VGCC) in Lambert-Eaton myasthenic syndrome (LEMS). (1) Some of MG and LEMS patients are "seronegative" for respective antibodies or modified by antibodies that recognize other proteins than AChR and VGCC such as MuSK, AChR allosteric site, membrane Na+ channel and ryanodine receptor-1 (RyR1) in MG, and synaptotagmin-1 in LEMS. (2) Autoimmune responses affect the proteins participating in the mechanisms to compensate for synaptic disorders on the basis of presynaptic Ca2+ homeostasis provided by VGCC and non-VGCC (receptor-operated TRPCs): they act as enhancers of Ca(2+) -mediated ACh release via phospholipase C signaling pathways including M1-type presynaptic muscarinic AChR, neurotrophin receptor (TrkB), and fast-mode of synaptic vesicle recycling. (3) The pathophysiology contributive to contractile fatigue in MG includes RyR1 and also TRPC3. The TRPC3 also forms a complex with STIM1 and Orail to make up for Ca2+ after sarcoplasmic Ca2+ release. The prevalent detection of anti-TRPC3 antibodies in MG with thymoma could affect muscle contractile machineries in addition to anti-RyR1-induced affection. (4) When one faces "seronegative" MG, one should be cautious to conformation-specific antibodies and also congenital myasthenic syndromes.

A 74-year-old-woman who had never smoked was diagnosed in 2004 with cT3N2M1, stage IV primary pulmonary adenocarcinoma. After seven courses of chemotherapy with carboplatin and paclitaxel, she was given gefitinib as second-line therapy and made satisfactory progress. However, gefitinib was discontinued after 3 years of treatment due to re-growth of the tumors. She was then given chemotherapy with docetaxel as a third-line therapy. Over the course of time, meningeal carcinomatosis occurred in conjunction with her previous disease. Upon re-treatment with gefitinib, her meningeal carcinomatosis showed some improvement despite the growing primary tumor, so her QOL was improved. She is now visiting a hospital as an outpatient. When analysis of the EGFR gene mutant was conducted, deletion mutation of E746-A750 in exon 19 was revealed in the 2004 pulmonary tissue, as well as the cytological examination of cerebrospinal fluid and pulmonary tissue after recurrence. No change has been observed. Once gefitinib proved effective, re-treatment with gefitinib was considered useful after its discontinuation.

Epigenetics is a mechanism of reversible and heritable regulation of gene transcription in contrast to genetic or DNA-coding information. In higher vertebrae, epigenetics consist of methylation of cytosine and histone modification. Mainly as detection is easier, aberrant DNA methylation was studied since the middle of '80s and recently convenient kit makes easy for study of histone modification. DNA methylation and histone modification meet in the end of '90s and regulation of transcription has being revealed. In this review, a history of epigenetics is commented briefly and recent proceedings of epigenetic change in lung cancer including micro RNA inactivation by DNA methylation and multigenetic analyses in non-small cell lung cancer is discussed.

The recent topics in the treatment and genetic aberrations of gastric MALT lymphoma were reviewed. The chromosomal translocation t(11;18) (q21;q21)/API2-MALT1 has been frequently detected not only in gastric MALT lymphoma cases, but also in gastric diffuse large B-cell lymphoma (DLBCL) cases in two studies. Conversely, IGH-involved translocations, including t(3;14) (p14;q32)/FOXP1-IGH, are rarely seen in gastric MALT lymphoma. Several large-scaled clinical series have revealed that Helicobacter pylori eradication therapy is the optimal first-line treatment for patients with gastric MALT lymphoma, which leads to a favorable long-term outcome. A number of modalities and/or regimens, including chemotherapy, immunotherapy, and radioimmuotherapy, have been developed as the second-line treatments for patients not responding to eradication therapy.

Helicobacter pylori infection is the most common chronic bacterial infection worldwide and the most important acquired risk factor for gastric cancer. Bacterial, environmental and host genetic factors combine to define the degree of gastric damage. The most relevant and consistent genetic factors are in the interleukin-1B and tumor necrosis factor-A gene clusters. These cytokines play a key role in the gastric carcinogenesis and their roles have been confirmed in mouse models. More genetic factors have also been uncovered recently and certain cytokine and innate immune response gene polymorphisms appear to influence risk of gastric cancer and its precursor conditions. In the near future, we will be able to define a more comprehensive genetic profile that would identify high risk groups of developing gastric cancer.