Atopic dermatitis (AD) is the most common chronic and relapsing inflammatory skin disease. Both abnormal barrier function and abnormal immune function are closely involved in the etiology of AD. Patients with AD have been subdivided into abnormal filaggrin, normal filaggrin, high immunoglobulin E, normal IgE groups, and so on. Regarding local cytokine profiles in the skin of patients with AD, the involvement of Th2, Th22, and Th17 cells at the acute stage, and the involvement of Th2, Th22, and Th1 cells at the chronic stage have been suggested. The IL-9 level has been reported to be higher in patients with AD than in healthy individuals, but it has also been reported that there are no differences in IL-9 levels between patients with AD and normal individuals. Thus, the role of IL-9 is unclear. The serum IL-18 level is high and induces Th2 reactions in patients with AD. IL-21 is thought to suppress IgE formation, but its activity in relation to AD remains unknown. IL-22 is involved in hyperplasia, increased antimicrobial peptide formation, and reduced filaggrin in patients with AD. IL-25, IL-33, and thymic stromal lymphopoietin are produced in epidermal cells and activate type 2 innate lymphoid cells or premature dendritic cells, resulting in the induction of Th2 reactions. IL-31 is produced by Th2 cells, causing an itching sensation and scratching behavior. A correlation has been reported between serum IL-32 levels and the severity of dermatitis. IL-34 is an element of the control system that suppresses inflammation, but its activity in cases of AD is unknown. One published report describes a correlation between serum IL-37 levels and the severity of dermatitis, but this relationship has not been sufficiently clarified to date, and requires further analysis. In this review, the author has attempted to summarize reports on cytokine expression in patients with AD. The author expects that important cytokines and cells involved in the pathophysiology of AD will be revealed, contributing to strategies for treating AD.

Endometrial carcinoma arises from the endometrium lining of the uterus and is a common malignancy of the female genital tract. It is generally categorized into two subtypes, types I and II. Type I endometrioid tumors account for 70~80% of cases, and they occur predominantly in premenopausal and perimenopausal women. Type I tumors are low-grade, early-stage, hormonally sensitive carcinomas; invasion of the uterine wall is minimal, so the prognosis is usually good. By contrast, type II endometrial carcinomas, which are primarily serous, are less common, accounting for only 10~20% of endometrial carcinomas. Type II tumors occur mostly in older postmenopausal women, are independent of estrogen exposure, and patients with them have a poor prognosis. The Cancer Genome Atlas Research Network performed an integrated genomic, transcriptomic, and proteomic characterization of 373 endometrial carcinomas. The genetic analyses were based on a combination of somatic nucleotide substitutions, microsatellite instability (MSI), and somatic copy number alterations. On the basis of the results, endometrial cancers were classified into four groups: (1) those with unusually high mutation rates and a unique nucleotide change spectrum (POLE [ultramuted] group); (2) those with MSI tumors, most with MLH1 promoter methylation (MSI [hypermuted] group); (3) those with lower mutation frequency comprising most of the microsatellite stable endometrioid cancers (copy number-low [endometrioid] group); and (4) those consisting primarily of serous-like cancers with extensive somatic copy number alterations and a low mutation rate (copy number-high [serous-like] group). In addition, in respect to pathway alterations, endometrial cancer has frequent mutations in the PI3K/AKT pathway. Regarding the epigenetic regulation of endometrial carcinoma, microRNAs (miRNAs) have received a lot of attention in recent years. miRNAs are a large family of small (approximately 22 molecules) non-coding RNAs that negatively regulate protein-coding gene expression post-transcriptionally. Recent studies have revealed dysregulated expressions of several miRNAs, also termed "onco-miRs," in various cancer tissues. Therefore, these onco-miRs could be promising prognostic biomarkers of cancer progression and/or metastasis. For example, in a recent study based on array-based comprehensive analyses, we identified miRNAs and mRNAs significantly dysregulated in endometrioid endometrial carcinomas and demonstrated that miR-200a, miR-200b, and miR-429 are onco-miRs that possibly target PTEN in endometrioid endometrial carcinomas.

Understanding of the genetic and epigenetic alterations of endometrial carcinomas may influence adequate treatments for patients.

Although the number of patients with cancer is increasing, 5-year survival rates are also increasing as a result of combined treatment modalities. In particular, rapid progress has been made in cancer pharmacotherapy. Pharmacists have an important and highly specialized role in the field of cancer to ensure treatment efficacy and safety. To be part of the multidisciplinary team providing medical care to cancer patients, pharmacists need specific knowledge, techniques, and experience. In this article, we consider the role of the pharmacist in cancer therapy, including present conditions and future prospects.

The Helicobacter pylori (H. pylori) eradication rate has decreased slightly because of the increasing number of clarithromycin-resistant bacteria. However, vonoprazan-based triple therapy (vonoprazan 40 mg/day+amoxicillin 1,500 mg/day+clarithromycin 800 mg/day) retains the potential to eradicate H. pylori better than other proton pump inhibitor (PPI) -based triple therapies. Vonoprazan is a potassium-competitive acid blocker that differs from PPIs in its mechanism of action. We compared vonoprazan-based triple therapy and esomeprazole-based triple therapy (esomeprazole 40 mg/day+amoxicillin 1,500 mg/day+clarithromycin 800 mg/day) in terms of the H. pylori eradication rate. Vonoprazan-based triple therapy was used to treat patients with a history of H. pylori-infected gastritis and gastric or duodenal ulcers caused by H. pylori during the period April 2015 to April 2016, and the eradication rates were compared with those obtained in similar patients treated with esomeprazole-based triple therapy between August 2014 and March 2015. The first-line H. pylori eradication rate of vonoprazan-based triple therapy was 92%, and the second-line eradication rate was 100%. The corresponding figures for esomeprazole-based triple therapy were 84.8% and 60%. Subgroup analyses of the first-line H. pylori eradication rate showed almost the same trends. There was no statistically significant difference between the H. pylori eradication rate of vonoprazan-based triple therapy and the eradication rate of esomeprazole-based triple therapy.

There is no established surgical strategy to manage dissection of the infrapyloric lymph node in cases of gastric cancer occurring after a coronary artery bypass graft (CABG) with the right gastroepiploic artery (RGEA). We performed gastrectomy in three patients with gastric cancer who had undergone CABG using RGEA. In order to reduce the preoperative risk, we dissected the infrapyloric lymph node by skeletonizing the RGEA bypass graft without redoing the CABG. No recurrence of the disease has been observed in any of the three patients. It is important to implement a non-invasive surgical strategy for gastric cancer patients at high risk due to severe heart disease or advanced age. This gastrectomy procedure is an adequate noninvasive surgical strategy, because it enables a complete cure without coronary revascularization.