The Snail signaling branch downstream of the TGF-ß/Smad3 pathway mediates Rho activation and subsequent stress fiber formation.

Cancer cells acquire malignant phenotypes through an epithelial-mesenchymal transition, which is induced by environmental factors or extracellular signaling molecules, including transforming growth factor-ß (TGF-ß). Among epithelial-mesenchymal transition-associated cell responses, cell morphological changes and cell motility are closely associated with remodeling of the actin stress fibers. Here, we examined the TGF-ß signaling pathways leading to these cell responses. Through knockdown experiments in A549 lung adenocarcinoma cells, we found that Smad3-mediated induction of Snail, but not that of Slug, is indispensable for morphological changes, stress fiber formation, and enhanced motility in cells stimulated with TGF-ß. Ectopic expression of Snail in SMAD3-knockout cells rescued the defect in morphological changes and stress fiber formation by TGF-ß, indicating that the role of Smad3 in these responses is to upregulate Snail expression. Mechanistically, Snail is required for TGF-ß-induced upregulation of Wnt5b, which in turn activates RhoA and subsequent stress fiber formation in cooperation with phosphoinositide 3-kinase. However, ectopic expression of Snail in SMAD3-knockout cells failed to rescue the defect in cell motility enhancement by TGF-ß, indicating that activation of the Smad3/Snail/Wnt5b axis is indispensable but not sufficient for enhancing cell motility; a Smad3-dependent but Snail-independent pathway to activate Rac1 is additionally required. Therefore, the Smad3-dependent pathway leading to enhanced cell motility has two branches: a Snail-dependent branch to activate RhoA and a Snail-independent branch to activate Rac1. Coordinated activation of these branches, together with activation of non-Smad signaling pathways, mediates enhanced cell motility induced by TGF-ß.

Incidence, Etiology, Risk Factors, and Outcomes of Bloodstream Infection after a Second Hematopoietic Stem Cell Transplantation.

Objective Infections after a second hematopoietic stem cell transplantation (HSCT) occur commonly and are associated with high mortality. However, studies on bloodstream infection (BSI) after a second HSCT are lacking. We therefore evaluated the details of BSI after a second HSCT. Methods We retrospectively evaluated the incidence, etiology, risk factors, and outcomes of BSI after a second HSCT. Patients Fifty-two adult patients with hematological malignancies who underwent allogeneic HSCT, including cord blood transplantation (CBT; n=33), as the second transplantation were enrolled. The second transplantation was limited to allogeneic HSCT. Patients who underwent HSCT for graft failure were excluded. Results The median HSCT interval was 438 (range: 39-3,893) days. Overall, 31 (59.6%) patients received autologous HSCT as the first HSCT. The cumulative incidence of BSI was 40.4% at 100 days after the second HSCT, with Gram-positive bacteria accounting for the majority (30.8%) of pathogens. Overall, 92.0% of BSIs occurred during the pre-engraftment period, and Enterococcus faecium accounted for 29.6% of pathogens. On a multivariate analysis, CBT was most closely associated with pre-engraftment BSI after the second HSCT (hazard ratio: 3.43, 95% confidence interval: 1.05-11.23, p=0.042). The 1-year survival rate after the second HSCT was lower in patients with BSI than in patients without BSI (p=0.10). Conclusion BSI is common after a second HSCT, especially with CBT. During the pre-engraftment period, BSI caused by pathogens such as E. faecium should be anticipated and appropriately treated to improve transplant outcomes.

Selective determination of formaldehyde by high-performance liquid chromatography with porous graphitic carbon column using N,N'-bis(9-anthrylmethyl)propane-1,3-diamine as derivatizing reagent.

Aromatic compounds containing two secondary amino groups were designed and prepared as new derivatizing reagents for aldehydes. One of them, N,N'-bis(9-anthrylmethyl)propane-1,3-diamine (APD), could achieve selective determination of formaldehyde (FA) on a porous graphitic carbon (PGC) column using xylenes, chlorobenzene, and 1-chloronaphthalene as mobile phases by high-performance liquid chromatography (HPLC). The APD-FA derivative was eluted from the PGC column, while the other APD-aldehyde derivatives remained on the column during the HPLC measurements. This specific elution was not observed using mobile phases such as acetonitrile, 1,4-dioxane, tetrahydrofuran, N,N-dimethylformamide, N,N-dimethylacetamide, N-methyl-2-pyrrolidone, chloroform, benzene, toluene, benzyl alcohol, 2-ethyl-1-hexanol, and pyridine. The APD-FA derivative had a six-membered ring of two tertiary amines identified using 1H NMR spectroscopy. When the π-π interaction of the solvent molecule of the mobile phase with PGC overcame that between the APD-FA derivative and PGC, the APD-FA derivative could be eluted from the column. The best resolution between the peak of the APD-FA derivative and that of free APD was observed when using o-xylene. The optimum derivatization and the HPLC conditions for selective HPLC determination of FA were to conduct the derivatization of FA by heating in an aqueous phase with APD in o-xylene at 100 °C. In this method, FA could be derivatized with APD at a mildly neutral pH of 6.7, unlike the low pH required for the derivatization of aldehydes with 2,4-dinitrophenylhydrazine (DNPH), which is commonly used for the derivatization of aldehydes. The detection and quantification limits of FA were 0.8 and 3.5 ng mL-1 in this HPLC method with fluorescent detection, respectively. This selective HPLC method could be applied to the determination of FA in various water samples. It was found that only APD among the derivatizing reagents containing two secondary diamines was useful for the selective determination of FA.

5-Aminolevulinic acid-based photodynamic diagnosis for detection of urothelial carcinoma cells in bladder washing sediment suspension: A pilot study.

BACKGROUND: Bladder cancer is a common malignant disease in developed countries. Early detection of malignancy is important using urine cytology. The 5-aminolevulinic acid (ALA)-based photodynamic diagnosis (ALA-PDD) has not been routinely applied in urine cytology analysis yet, although it has been well accepted for tumor lesion marking in cystoscopy. METHODS: A total of eight volunteers were enrolled in this study. The cells of sediment suspension from bladder washing fluid and random urine were stained by ALA-induced protoporphyrin IX (ALA-PpIX) and the fluorescent intensity of ALA-PpIX was analyzed by ImageJ. RESULTS: The cutoff value of fluorescent intensity was 90.260 per pixel. The proposed protocol provided an objective fluorescent intensity for evaluation. Sensitivity was 0.931 and specificity was 1.000. CONCLUSIONS: The staining procedure applied was ALA-PpIX for suspicious cells in the cellular suspension from bladder wash fluid and random urine. ImageJ was applied to the objective measurement for the fluorescent intensity of the stained cells. The cutoff value for the positive result was 90.260 per pixel. Therefore, the protocol proposed in this study provides a potential means to enhance accuracy for urine cytology analysis.

BCL11A promotes myeloid leukemogenesis by repressing PU.1 target genes.

The transcriptional repressor BCL11A is involved in hematological malignancies, B-cell development, and fetal-to-adult hemoglobin switching. However, the molecular mechanism by which it promotes the development of myeloid leukemia remains largely unknown. We find that Bcl11a cooperates with the pseudokinase Trib1 in the development of acute myeloid leukemia (AML). Bcl11a promotes the proliferation and engraftment of Trib1-expressing AML cells in vitro and in vivo. Chromatin immunoprecipitation sequencing analysis showed that, upon DNA binding, Bcl11a is significantly associated with PU.1, an inducer of myeloid differentiation, and that Bcl11a represses several PU.1 target genes, such as Asb2, Clec5a, and Fcgr3. Asb2, as a Bcl11a target gene that modulates cytoskeleton and cell-cell interaction, plays a key role in Bcl11a-induced malignant progression. The repression of PU.1 target genes by Bcl11a is achieved by sequence-specific DNA-binding activity and recruitment of corepressors by Bcl11a. Suppression of the corepressor components HDAC and LSD1 reverses the repressive activity. Moreover, treatment of AML cells with the HDAC inhibitor pracinostat and the LSD1 inhibitor GSK2879552 resulted in growth inhibition in vitro and in vivo. High BCL11A expression is associated with worse prognosis in humans with AML. Blocking of BCL11A expression upregulates the expression of PU.1 target genes and inhibits the growth of HL-60 cells and their engraftment to the bone marrow, suggesting that BCL11A is involved in human myeloid malignancies via the suppression of PU.1 transcriptional activity.

Group V Secretory Phospholipase A2 Regulates Endocytosis of Acetylated LDL by Transcriptional Activation of PGK1 in RAW264.7 Macrophage Cell Line.

AIMS: It was suggested that group V secretory phospholipase A2 (sPLA2-V) existed in the nucleus. This study examined whether nuclear sPLA2-V plays a role in endocytosis of acetylated low-density lipoprotein (AcLDL) in monocyte/macrophage-like cell line RAW264.7 cells. METHODS: RAW264.7 cells were transfected with shRNA vector targeting sPLA2-V (sPLA2-V-knockdown [KD] cells) or empty vector (sPLA2-V-wild-type [WT] cells). AcLDL endocytosis was assessed by incubation with 125I-AcLDL or AcLDL conjugated with pHrodo. Actin polymerization was assessed by flow cytometry using Alexa Fluor 546-phalloidin. RESULTS: In immunofluorescence microscopic studies, sPLA2-V was detected in the nucleus. ChIP-Seq and ChIP-qPCR analyses showed binding of sPLA2-V to the promoter region of the phosphoglycerate kinase 1 (Pgk1) gene. In the promoter assay, sPLA2-V-KD cells had lower promoter activity of the Pgk1 gene than sPLA2-V-WT cells, and this decrease could be reversed by transfection with a vector encoding sPLA2-V-H48Q that lacks enzymatic activity. Compared with sPLA2-V-WT cells, sPLA2-V-KD cells had decreased PGK1 protein expression, beclin 1 (Beclin1) phosphorylation at S30, and class III PI3-kinase activity that could also be restored by transfection with sPLA2-V-H48Q. sPLA2-V-KD cells had impaired actin polymerization and endocytosis, which was reversed by introduction of sPLA2-V-H48Q or PGK1 overexpression. In sPLA2-V-WT cells, siRNA-mediated depletion of PGK1 suppressed Beclin1 phosphorylation and impaired actin polymerization and intracellular trafficking of pHrodo-conjugated AcLDL. CONCLUSIONS: Nuclear sPLA2-V binds to the Pgk1 gene promoter region and increases its transcriptional activity. sPLA2-V regulates AcLDL endocytosis through PGK1-Beclin1 in a manner that is independent of its enzymatic activity in RAW264.7 cells.

[Rapid Recurrence of Dedifferentiated Liposarcoma of Occult Primary in the Abdomen-A Case Report].

A man in his 70s was referred to our hospital for the examination of an abdominal tumor detected incidentally. The tumor was resected with a preoperative diagnosis of gastric submucosal tumor. As a result of the histopathological examination, dedifferentiated liposarcoma was diagnosed. The tumor recurred 2 months after the operation, and resection was attempted again. However, the intraoperative findings showed multiple metastatic lesions, and radical resection was considered impossible. Chemotherapy was therefore administered with doxorubicin monotherapy and eribulin, but the tumor rapidly increased, and the patient ultimately died 8 months after the initial operation. Dedifferentiated liposarcoma is a histologic type with a poor prognosis among liposarcoma. Resection is the standard treatment, but it frequently develops in the retroperitoneum, and it is often found in an advanced state due to the lack of subjective symptoms compared to lesions of the extremities. In addition, its tendency to infiltrate into the surrounding area and to metastasize are also factors that make radical resection difficult. We herein report a case of dedifferentiated liposarcoma that was detected asymptomatically but had a rapid outcome.

The Target Differences of Anti-Tumorigenesis Potential of Curcumin and its Analogues Against HER-2 Positive and Triple-Negative Breast Cancer Cells.

Purpose: The current study aims to evaluate the in vitro cytotoxic and cell migration effects of synthetic curcumin and its analogues on HER2 and nuclear factor kappa B (NFκB) pathways, as well as the in vivo inhibitory effect on cancer growth of metastatic breast cancer. Methods: Cell viability, protein expression, and protein localization were determined in vitro using MTT assay, western blotting, and immunofluorescence, respectively. Meanwhile, scratch wound healing assay and gelatin zymography were conducted to investigate the metastasis inhibitory effect. The in vivo anti-tumor ability was evaluated in xenograft mouse model using triple-negative breast cancer (TNBC) cells. Results: Curcumin, PGV-0, and PGV-1 exhibited cytotoxic effect against HER2-overexpressing breast cancer cells. Although PGV-1 showed the best activity in the single cytotoxic assay, curcumin showed the strongest synergism with doxorubicin. Curcumin and PGV-0 inhibited membrane localization of HER2. In contrast, PGV-1 neither inhibited localization nor decreased the expression of HER2, nonetheless showed the most potent inhibition against nuclear localization of p65 indicating the different mechanisms of curcumin, PGV-0, and PGV-1. Regarding cancer metastasis, curcumin and PGV-1 showed inhibitory activities against cell migration and inhibited MMP-2 and MMP-9 protein expression. Lastly, PGV-1 was more potent compared to curcumin to suppress the tumor formation of metastatic breast cancer xenograft model in nude mice. Conclusion: Overall, our study strengthens the potency of curcumin analogue, PGV-1, for treating several types of cancer, including metastatic breast cancer.

TGF-ß-induced cell motility requires downregulation of ARHGAPs to sustain Rac1 activity.

Transforming growth factor-ß (TGF-ß) signaling promotes cancer progression. In particular, the epithelial-mesenchymal transition (EMT) induced by TGF-ß is considered crucial to the malignant phenotype of cancer cells. Here, we report that the EMT-associated cellular responses induced by TGF-ß are mediated by distinct signaling pathways that diverge at Smad3. By expressing chimeric Smad1/Smad3 proteins in SMAD3 knockout A549 cells, we found that the ß4 region in the Smad3 MH1 domain is essential for TGF-ß-induced cell motility, but is not essential for other EMT-associated responses including epithelial marker downregulation. TGF-ß was previously reported to enhance cell motility by activating Rac1 via phosphoinositide 3-kinase. Intriguingly, TGF-ß-dependent signaling mediated by Smad3's ß4 region causes the downregulation of multiple mRNAs that encode GTPase activating proteins that target Rac1 (ARHGAPs), thereby attenuating Rac1 inactivation. Therefore, two independent pathways downstream of TGF-ß type I receptor contribute cooperatively to sustained Rac1 activation, thereby leading to enhanced cell motility.

A case of gastric and duodenal mucosa-associated lymphoid tissue lymphoma with multiple gastric cancers: a case report.

BACKGROUND: Gastric mucosa-associated lymphoid tissue (MALT) lymphoma is often caused by Helicobacter pylori and has a good prognosis. Rarely, patients with MALT lymphoma may have gastric cancer and have a poor prognosis. CASE PRESENTATION: We herein report a case in which surgical treatment was achieved for a 72-year-old male patient with gastric and duodenal MALT lymphoma coexisting multiple gastric cancers. He underwent upper endoscopy for epigastric discomfort, which revealed mucosal erosion on the posterior wall of the middle body of the stomach, an elevated lesion on the duodenal bulb, and a raised tumor on the antrum of the stomach. He was diagnosed with gastric and duodenal MALT lymphoma with early gastric cancer. One month after H. pylori eradication, a second upper endoscopy revealed no improvement in the gastric or duodenal mucosa, and areas of strong redness with a shallow recess just below the cardia of the stomach. As a result, a diagnosis of gastric and duodenal MALT lymphoma with two gastric cancers was made. Total gastrectomy with proximal duodenum resection using intraoperative upper endoscopy and regional lymph node dissection was performed. Pathologically, gastric and duodenal MALT lymphoma and three gastric cancers were detected. Since one of them was an advanced cancer, he started taking S-1 after his general condition improved. CONCLUSION: For early detection of gastric and duodenal MALT lymphoma or gastric cancer, appropriate upper endoscopy and a biopsy are important. It is necessary to select a suitable treatment, such as H. pylori eradication, endoscopic treatment, surgery, chemotherapy, and irradiation, according to the disease state.

Trib1 promotes acute myeloid leukemia progression by modulating the transcriptional programs of Hoxa9.

The pseudokinase Trib1 functions as a myeloid oncogene that recruits the E3 ubiquitin ligase COP1 to C/EBPα and interacts with MEK1 to enhance extracellular signal-regulated kinase (ERK) phosphorylation. A close genetic effect of Trib1 on Hoxa9 has been observed in myeloid leukemogenesis, where Trib1 overexpression significantly accelerates Hoxa9-induced leukemia onset. However, the mechanism underlying how Trib1 functionally modulates Hoxa9 transcription activity is unclear. Herein, we provide evidence that Trib1 modulates Hoxa9-associated super-enhancers. Chromatin immunoprecipitation sequencing analysis identified increased histone H3K27Ac signals at super-enhancers of the Erg, Spns2, Rgl1, and Pik3cd loci, as well as increased messenger RNA expression of these genes. Modification of super-enhancer activity was mostly achieved via the degradation of C/EBPα p42 by Trib1, with a slight contribution from the MEK/ERK pathway. Silencing of Erg abrogated the growth advantage acquired by Trib1 overexpression, indicating that Erg is a critical downstream target of the Trib1/Hoxa9 axis. Moreover, treatment of acute myeloid leukemia (AML) cells with the BRD4 inhibitor JQ1 showed growth inhibition in a Trib1/Erg-dependent manner both in vitro and in vivo. Upregulation of ERG by TRIB1 was also observed in human AML cell lines, suggesting that Trib1 is a potential therapeutic target of Hoxa9-associated AML. Taken together, our study demonstrates a novel mechanism by which Trib1 modulates chromatin and Hoxa9-driven transcription in myeloid leukemogenesis.

Long-Term Survival After Pelvic Exenteration for Locally Recurrent Rectal Cancer Associated With Crohn's Disease With, Adjuvant Chemotherapy, and Immunosuppressive Therapy.

Crohn's disease (CD) is associated with an increased risk of developing colorectal cancer. In particular, cases in which long-term survival is achieved by patients with local recurrence of CD-associated rectal cancer are rare. We report a case in which curative resection was achieved for a 47-year-old man with long-standing CD and locally recurrent rectal cancer. In this case, the patient obtained a long-term survival without recurrence after surgical resection with adjuvant chemotherapy and immunosuppressive therapy. In the management of inflammatory bowel disease patients with cancer, the management of both cancer and inflammatory bowel disease treatment is important for the long-term prognosis.

Pseudosarcomatous myofibroblastic proliferation of the appendix with an abdominal abscess due to diverticulum perforation: a case report.

BACKGROUND: Pseudosarcomatous myofibroblastic proliferation is a rare proliferative lesion of the submucosal stroma characterized by myofibroblast proliferation and inflammatory cell infiltration, and is mainly reported in the urinary system. CASE PRESENTATION: We report a 65-year-old male who was referred to our emergency room with right-side iliac fossa pain. The pain gradually worsened for approximately 2 months, and rebound tenderness was positive. Blood examination showed severe inflammatory findings, and enhanced computed tomography revealed a heterogeneous contrast-enhancing mass lesion measured to be 55 × 50 mm in size at the lower right abdomen. Based on these results, the patient was diagnosed with appendicitis with an abdominal abscess. As the inflammation was severe, we drained the abscess before performing surgery. Approximately 1 month after the abscess diminished, interval appendectomy was performed. Macroscopic findings of the resected specimen showed a perforated diverticulum of the appendix and a small adjacent nodule measured to be 14 mm in size. Histopathological examination with hematoxylin and eosin staining revealed that the nodule consisted of fibroblast proliferation and inflammatory cell infiltration. Furthermore, immunohistochemical examination showed positive for smooth muscle actin and desmin and negative for S-100, c-kit, and anaplastic lymphoma kinase. Based on these histopathological results, we diagnosed the nodule as an unusual case of a pseudosarcomatous myofibroblastic proliferation associated with perforation of the diverticulum of the appendix. CONCLUSION: Herein, we report a rare case of a pseudosarcomatous myofibroblastic proliferation that occurred in the appendix with diverticulitis.

Urinary Mulberry Cells as a Biomarker of the Efficacy of Enzyme Replacement Therapy for Fabry Disease.

Mulberry cells are often present in the urinary sediments of patients with Fabry disease (FD). We herein report two patients with FD undergoing enzyme replacement therapy (ERT). A 41-year-old man was diagnosed based on lack of α-galactosidase A activity. ERT was subsequently administered. A 40-year-old woman was diagnosed based on urinary Mulberry cells and genetic testing, and ERT was initiated. While the renal function of the male patient deteriorated, the Mulberry cells disappeared in the female patient after ERT was administered. The detection of urinary Mulberry cells can contribute to the diagnosis as well as serve as a biomarker for the response to treatment.

[Mastectomy Followed by Skin-Transplantation Restored QOL and Enabled Chemotherapy in Two Cases of Locally Advanced Breast Cancer with Uncontrollable Bleeding].

Here, we report 2 cases of locally advanced breast cancer with uncontrollable bleeding treated with mastectomy followed by skin transplantation. The operation restored the QOL and enabled chemotherapy in postoperative periods. Case 1: A woman in her 70s was brought by an ambulance because of heart failure symptoms. She had a huge breast tumor on her left chest wall that bled repeatedly, necessitating frequent blood transfusions. An operation was performed, and chemotherapy was provided until she died of brain metastasis 1 year and 8 months after surgery. Case 2: A woman in her 70s was urgently hospitalized with a lumbar vertebrae bone fracture. She had a huge breast tumor on her right chest wall that bled repeatedly. Blood examination revealed severe anemia. An operation was performed, and chemotherapy was introduced sequentially. She is alive with a good status 2 years and 1 month after surgery.

Curcumin Derivatives Verify the Essentiality of ROS Upregulation in Tumor Suppression.

BACKGROUND: Curcumin has been shown to exert pleiotropic biological effects, including anti-tumorigenic activity. We previously showed that curcumin controls reactive oxygen species (ROS) levels through the ROS metabolic enzymes, to prevent tumor cell growth. In this study, we synthesized 39 novel curcumin derivatives and examined their anti-proliferative and anti-tumorigenic properties. METHODS AND RESULTS: Thirty-nine derivatives exhibited anti-proliferative activity toward human cancer cell lines, including CML-derived K562 leukemic cells, in a manner sensitive to an antioxidant, N-acetyl-cysteine (NAC). Some compounds exhibited lower GI50 values than curcumin, some efficiently induced cell senescence, and others markedly increased ROS levels, efficiently induced cell death and suppressed tumor formation in a xenograft mouse model, without any detectable side effects. A clustering analysis of the selected compounds and their measurement variables revealed that anti-tumorigenic activity was most well-correlated with an increase in ROS levels. Pulldown assays and a molecular docking analysis showed that curcumin derivatives competed with co-enzymes to bind to the respective ROS metabolic enzymes and inhibited their enzymatic activities. CONCLUSIONS: The analysis of novel curcumin derivatives established the importance of ROS upregulation in suppression of tumorigenesis, and these compounds are potentially useful for the development of an anti-cancer drug with few side effects.

Pentagamavunon-1 (PGV-1) inhibits ROS metabolic enzymes and suppresses tumor cell growth by inducing M phase (prometaphase) arrest and cell senescence.

We previously showed that curcumin, a phytopolyphenol found in turmeric (Curcuma longa), targets a series of enzymes in the ROS metabolic pathway, induces irreversible growth arrest, and causes apoptosis. In this study, we tested Pentagamavunon-1 (PGV-1), a molecule related to curcumin, for its inhibitory activity on tumor cells in vitro and in vivo. PGV-1 exhibited 60 times lower GI50 compared to that of curcumin in K562 cells, and inhibited the proliferation of cell lines derived from leukemia, breast adenocarcinoma, cervical cancer, uterine cancer, and pancreatic cancer. The inhibition of growth by PGV-1 remained after its removal from the medium, which suggests that PGV-1 irreversibly prevents proliferation. PGV-1 specifically induced prometaphase arrest in the M phase of the cell cycle, and efficiently induced cell senescence and cell death by increasing intracellular ROS levels through inhibition of ROS-metabolic enzymes. In a xenograft mouse model, PGV-1 had marked anti-tumor activity with little side effects by oral administration, whereas curcumin rarely inhibited tumor formation by this administration. Therefore, PGV-1 is a potential therapeutic to induce tumor cell apoptosis with few side effects and low risk of relapse.

Laparoscopic Percutaneous Endoscopic Gastrostomy Is Useful for Elderly.

BACKGROUND: In recent years, enteral nutrition has become relatively easy to perform through the penetration of percutaneous endoscopic gastrostomy (PEG). However, there have been reports of complications, such as mispuncture of other organs at the time of performing PEG. Previously, we had constructed a gastrostomy under the laparotomy for difficult PEG cases, and 2 years ago, we introduced laparoscopically assisted PEG. This study aimed to clarify the feasibility and safety of LAPEG for elderly people over 65 years old. METHODS: We evaluated the perioperative outcomes in 7 elderly patients who underwent LAPEG during these 2 years. In these subjects, the safety of LAPEG was evaluated retrospectively based on the surgical outcomes, perioperative complications, and postoperative course using the clinical archives. RESULTS: The subjects' mean age was 81.1 ± 8.03 years. LAPEG was successful in all 7 patients. The median operation time was 38 minutes (range, 31-71 minutes). Intraoperative and postoperative early or late complications from LAPEG were not observed in our cases. Enteral nutrition was commenced 2 days after PEG placement in all cases without complications. CONCLUSION: We summarized the LAPEG cases performed at our institution for the elderly, and have reported its feasibility and safety. The strongest advantage of LAPEG was that it allowed placement of the PEG without any complication under direct observation of the intraperitoneal cavity to confirm the safety of each organ.