The efficacy of simple oral nutritional supplements versus usual care in postoperative patients with gastric cancer: study protocol for a multicenter, open-label, parallel, randomized controlled trial.

BACKGROUND: Body weight loss (BWL) after gastrectomy impact on the short- and long-term outcomes. Oral nutritional supplement (ONS) has potential to prevent BWL in patients after gastrectomy. However, there is no consistent evidence supporting the beneficial effects of ONS on BWL, muscle strength and health-related quality of life (HRQoL). This study aimed to evaluate the effects of ONS formulated primarily with carbohydrate and protein on BWL, muscle strength, and HRQoL. METHODS: This will be a multicenter, open-label, parallel, randomized controlled trial in patients with gastric cancer who will undergo gastrectomy. A total of 120 patients who will undergo gastrectomy will be randomly assigned to the ONS group or usual care (control) group in a 1:1 ratio. The stratification factors will be the clinical stage (I or ≥ II) and surgical procedures (total gastrectomy or other procedure). In the ONS group, the patients will receive 400 kcal (400 ml)/day of ONS from postoperative day 5 to 7, and the intervention will continue postoperatively for 8 weeks. The control group patients will be given a regular diet. The primary outcome will be the percentage of BWL (%BWL) from baseline to 8 weeks postoperatively. The secondary outcomes will be muscle strength (handgrip strength), HRQoL (EORTC QLQ-C30, QLQ-OG25, EQ-5D-5L), nutritional status (hemoglobin, lymphocyte count, albumin), and dietary intake. All analyses will be performed on an intention-to-treat basis. DISCUSSION: This study will provide evidence showing whether or not ONS with simple nutritional ingredients can improve patient adherence and HRQoL by reducing BWL after gastrectomy. If supported by the study results, nutritional support with simple nutrients will be recommended to patients after gastrectomy for gastric cancer. TRIAL REGISTRATION: jRCTs051230012; Japan Registry of Clinical Trails. Registered on Apr. 13, 2023.

Pituitary pars intermedia dysfunction with pituitary gland melanotroph adenoma in a Grevy's zebra (Equus grevyi).

A 22-year and 9-month-old female Grevy's zebra (Equus grevyi) showed signs of polyuria, polydipsia, glucosuria, and muscle atrophy. Blood tests revealed hyperglycemia, hypertriglyceridemia, electrolyte imbalance, high levels of adrenocorticotropic hormone (ACTH) and cortisol, and low levels of hormones secreted by the pituitary pars distalis. Pathological examinations revealed a pituitary gland tumor and bilateral adrenal cortical hyperplasia. Pituitary tumor cells showed immunoreactivity for α-melanocyte-stimulating hormone and ACTH. The deposition of amyloid ß was observed in the parenchyma and vascular walls of the cerebrum. The zebra showed clinical signs of pituitary pars intermedia dysfunction and was histopathologically diagnosed with pituitary gland melanotroph adenoma. This case report provides insight into neoplastic and endocrine diseases associated with the aging of a zebra.

A case of mesenteric venous thrombosis complicating appendiceal diverticulitis.

BACKGROUND: Mesenteric venous thrombosis (MVT) and appendiceal diverticulitis are rare diseases. There has been no previous report on MVT complicating appendiceal diverticulitis. Herein, we report the first case of MVT complicating appendiceal diverticulitis. CASE PRESENTATION: A 70-year-old male patient with right lower abdominal pain presented to our hospital. Abdominal contrast-enhanced computed tomography (CT) suggested MVT complicating appendiceal diverticulitis. Initially, we started conservative treatment with antibacterial drugs, but on the 2nd hospital day his general condition deteriorated due to sepsis that seemed to be caused by appendiceal diverticulitis. Therefore, we performed laparoscopic appendectomy. Histopathological findings of the specimen showed appendiceal diverticulitis. After the operation, he gradually improved. He was discharged on the 30th hospital day. CONCLUSIONS: We report a successfully treated case of MVT complicating appendiceal diverticulitis by surgical intervention. This is the first case of MVT complicating appendiceal diverticulitis.

Orally Bioavailable Quinoxaline Inhibitors of 15-Prostaglandin Dehydrogenase (15-PGDH) Promote Tissue Repair and Regeneration.

15-Prostaglandin dehydrogenase (15-PGDH) regulates the concentration of prostaglandin E2 in vivo. Inhibitors of 15-PGDH elevate PGE2 levels and promote tissue repair and regeneration. Here, we describe a novel class of quinoxaline amides that show potent inhibition of 15-PGDH, good oral bioavailability, and protective activity in mouse models of ulcerative colitis and recovery from bone marrow transplantation.

Evaluation of soccer team defense based on prediction models of ball recovery and being attacked: A pilot study.

With the development of measurement technology, data on the movements of actual games in various sports can be obtained and used for planning and evaluating the tactics and strategy. Defense in team sports is generally difficult to be evaluated because of the lack of statistical data. Conventional evaluation methods based on predictions of scores are considered unreliable because they predict rare events throughout the game. Besides, it is difficult to evaluate various plays leading up to a score. In this study, we propose a method to evaluate team defense from a comprehensive perspective related to team performance by predicting ball recovery and being attacked, which occur more frequently than goals, using player actions and positional data of all players and the ball. Using data from 45 soccer matches, we examined the relationship between the proposed index and team performance in actual matches and throughout a season. Results show that the proposed classifiers predicted the true events (mean F1 score > 0.483) better than the existing classifiers which were based on rare events or goals (mean F1 score < 0.201). Also, the proposed index had a moderate correlation with the long-term outcomes of the season (r = 0.397). These results suggest that the proposed index might be a more reliable indicator rather than winning or losing with the inclusion of accidental factors.

Robot-assisted laparoscopic low anterior resection for rectal cancer with persistent descending mesocolon: A case report.

INTRODUCTION: Persistent descending mesocolon (PDM) is a fixed abnormality in which the descending to sigmoid colon adheres to the small intestinal mesentery or right pelvic wall through right displacement. Surgery for colorectal cancer with PDM is difficult. Therefore, in addition to the anatomical characteristics of PDM, the extent of adhesion and characteristics of vascular courses need to be assessed in individual patients. The number of patients now undergoing laparoscopic or robot-assisted surgery for colorectal cancer has rapidly increased. We herein report a rectal cancer patient with PDM who safely underwent robot-assisted laparoscopic low anterior resection (RLAR). PRESENTATION OF CASE: A 71-year-old male was referred to our hospital for a detailed examination following a fecal occult blood-positive reaction. Lower gastrointestinal endoscopy revealed a type 2 lesion of the rectum. Moderately differentiated adenocarcinoma was diagnosed based on the results of a histopathological examination. Preoperative contrast-enhanced thoracoabdominal computed tomography showed abnormalities in the colonic course and characteristic vascular courses, suggesting rectal cancer with PDM. RLAR was performed. DISCUSSION: In surgery, it is important to initially perform adhesiolysis accurately in order to reconstruct the original shape of the colonic mesentery and confirm/dissect vascular bifurcations due to the risk of marginal arterial injury. CONCLUSION: In the present case, a detailed anatomical understanding of the site of intestinal adhesion and vascular courses, as well as surgical procedures, facilitated safe RLAR. We described this case and reviewed the anatomical characteristics of PDM and cautions for surgery.

Dual blockade of macropinocytosis and asparagine bioavailability shows synergistic anti-tumor effects on KRAS-mutant colorectal cancer.

Mutations of KRAS gene are found in various types of cancer, including colorectal cancer (CRC). Despite intense efforts, no pharmacological approaches are expected to be effective against KRAS-mutant cancers. Macropinocytosis is an evolutionarily conserved actin-dependent endocytic process that internalizes extracellular fluids into large vesicles called macropinosomes. Recent studies have revealed macropinocytosis's important role in metabolic adaptation to nutrient stress in cancer cells harboring KRAS mutations. Here we showed that KRAS-mutant CRC cells enhanced macropinocytosis for tumor growth under nutrient-depleted conditions. We also demonstrated that activation of Rac1 and phosphoinositide 3-kinase were involved in macropinocytosis of KRAS-mutant CRC cells. Furthermore, we found that macropinocytosis was closely correlated with asparagine metabolism. In KRAS-mutant CRC cells engineered with knockdown of asparagine synthetase, macropinocytosis was accelerated under glutamine-depleted condition, and albumin addition could restore the glutamine depletion-induced growth suppression by recovering the intracellular asparagine level. Finally, we discovered that the combination of macropinocytosis inhibition and asparagine depletion dramatically suppressed the tumor growth of KRAS-mutant CRC cells in vivo. These results indicate that dual blockade of macropinocytosis and asparagine bioavailability could be a novel therapeutic strategy for KRAS-mutant cancers.

Laparoscopic approach to recurrence following multiple surgeries for external rectal prolapse: a case report.

INTRODUCTION: The optimal procedure for recurrent external rectal prolapse remains unclear, particularly in laparoscopic approach. In addition, pelvic organ prolapse (POP) is sometimes concomitant with rectal prolapse. We present a case who underwent laparoscopic procedure for the recurrence of full-thickness external rectal prolapse coexisting POP. CASE PRESENTATION: An 81-year-old parous female had a 10-cm full-thickness external rectal prolapse following the two operations: the first was perineal recto-sigmoidectomy and the second was laparoscopic posterior mesh rectopexy. Imaging study revealed that the recurrent rectal prolapse was concomitant with both cystocele and exposed vagina, what we call POP. We planned and successfully performed laparoscopic ventral mesh rectopexy (LVMR) with laparoscopic sacrocolpopexy (LSC) using self-cut meshes without any perioperative complication. CONCLUSION: This is the first report of LVMR and LSC for recurrent rectal prolapse with POP following the perineal recto-sigmoidectomy and laparoscopic posterior mesh rectopexy. Even for recurrent rectal prolapse with POP, our experience suggests that LVMR and LSC could be utilized.

Bone marrow-derived mesenchymal stem cells promote colorectal cancer progression via CCR5.

Mesenchymal stem cells (MSCs) are recruited from BM to the stroma of developing tumors, where they serve as critical components of the tumor microenvironment by secreting growth factors, cytokines, and chemokines. The role of MSCs in colorectal cancer (CRC) progression was controversial. In this study, we found that C-C chemokine receptor type 5 (CCR5) ligands (i.e., C-C motif chemokine ligand 3 (CCL3), CCL4, and CCL5) were highly produced from MSCs using a chemokine array screening with conditioned media from the cultured human MSCs. A relatively strong CCR5 expression could be detected within the cytoplasm of several CRC cell lines. Regarding the effect of MSC, we found that the xenografts in which CCR5-overexpressing HCT116 cells were inoculated into immunocompromised mice were highly promoted in vivo by a mixture with MSCs. Notably, the CCR5 inhibitor, maraviroc, significantly abolished the MSC-induced tumor growth in vivo. In human clinical specimens (n = 89), 20 cases (29%) were high for CCR5, whereas 69 cases (71%) were low. Statistical analyses indicated that CCR5 expression in primary CRC was associated with CRC patients' prognosis. Especially, stage III/IV patients with CCR5-high CRCs exhibited a significantly poorer prognosis than those with CCR5-low CRCs. Furthermore, we investigated the effects of preoperative serum CCR5 ligands on patients' prognosis (n = 114), and found that CRC patients with high serum levels of CCL3 and CCL4 exhibited a poorer prognosis compared to those with low levels of CCL3 and CCL4, while there was no association between CCL5 and prognosis. These results suggest that the inhibition of MSC-CRC interaction by a CCR5 inhibitor could provide the possibility of a novel therapeutic strategy for CRC, and that serum levels of CCL3 and CCL4 could be predictive biomarkers for the prognosis of CRC patients.

Enhanced anastomotic healing by Daikenchuto (TJ-100) in rats.

Daikenchuto (DKT), a traditional Japanese medicine, is widely used to treat various gastrointestinal disorders. This study aimed to investigate whether DKT could promote the anastomotic healing in a rat model. Pedicled colonic segments were made in left colon by ligation of the feeding arteries, and then intestinal continuity was restored. Colonic blood flow was analyzed by using ICG fluorescence imaging: Fmax, Tmax, T1/2, and Slope were calculated. Anastomotic leakage (AL) was found in 6 of 19 rats (31.6%) in the control group, whereas in 1 of 16 rats (6.2%) in the DKT group. The Fmax and Slope of DKT group were significantly higher than those of control group. DKT could promote the anastomotic healing, with the higher bursting pressure on postoperative day (POD) 2 and 5, the larger granulation thickness on POD 5, and neoangiogenesis on POD 5. Histological examination showed DKT exhibited a decreased inflammatory cell infiltration, enhanced fibroblast infiltration, and enhanced collagen density on POD 5. In the DKT group, the levels of TGFß1 on POD 2 and VEGFα on POD5 were significantly higher, whereas the level of TNFα on POD 2 was significantly lower. Therefore, DKT could be effective for the prevention of AL following colorectal surgery.

Metachronous mediastinal lymph node metastasis from ascending colon cancer: A case report and literature review.

INTRODUCTION: Metachronous mediastinal lymph node metastasis without pulmonary metastasis is extremely rare in colorectal cancer, which makes the clinical diagnosis difficult and treatment strategy unclear. PRSENTATION OF CASE: A case was a 59-year-old man, who had undergone right hemicolectomy for ascending colon cancer 2 years and 8 months previously, presented with enlarged mediastinal lymph nodes. 18F-fluorodeoxyglucose (FDG) positron emission tomography revealed FDG was accumulated only into the mediastinal lymph nodes. Serum carcinoembryonic antigen (CEA) level was within the normal range. Six months later, the size and FDG uptake of the mediastinal lymph nodes had increased. We assumed a possibility that the mediastinal lymph nodes were metastasized from ascending colon cancer and so performed thoracoscopic-assisted resection of the mediastinal lymph nodes. Histopathological analysis revealed the resected lymph nodes were filled with moderately differentiated adenocarcinoma and a diagnosis of mediastinal lymph nodes metastasis from previously-resected ascending colon cancer was made. The patient was postoperatively followed for more than 1year and 8 months without any sign of recurrence. DISCUSSION: Only 7 cases of metachronous mediastinal lymph node metastasis from colorectal cancer, including our case, have been reported in the English literature. It is difficult to clinically diagnose mediastinal lymph node metastasis. CONCLUSION: We report a rare case of metachronous mediastinal lymph node metastasis from ascending colon cancer with literature review. If the mediastinal lymph nodes are enlarged after colorectal cancer resection, we need to make a treatment strategy as well as a diagnostic approach considering the possibility of mediastinal lymph node metastasis.

Clinical Role of ASCT2 (SLC1A5) in KRAS-Mutated Colorectal Cancer.

Mutation in the KRAS gene induces prominent metabolic changes. We have recently reported that KRAS mutations in colorectal cancer (CRC) cause alterations in amino acid metabolism. However, it remains to be investigated which amino acid transporter can be regulated by mutated KRAS in CRC. Here, we performed a screening of amino acid transporters using quantitative reverse-transcription polymerase chain reaction (RT-PCR) and then identified that ASCT2 (SLC1A5) was up-regulated through KRAS signaling. Next, immunohistochemical analysis of 93 primary CRC specimens revealed that there was a significant correlation between KRAS mutational status and ASCT2 expression. In addition, the expression level of ASCT2 was significantly associated with tumor depth and vascular invasion in KRAS-mutant CRC. Notably, significant growth suppression and elevated apoptosis were observed in KRAS-mutant CRC cells upon SLC1A5-knockdown. ASCT2 is generally known to be a glutamine transporter. Interestingly, SLC1A5-knockdown exhibited a more suppressive effect on cell growth than glutamine depletion. Furthermore, SLC1A5-knockdown also resulted in the suppression of cell migration. These results indicated that ASCT2 (SLC1A5) could be a novel therapeutic target against KRAS-mutant CRC.

Targeting metabolic reprogramming in KRAS-driven cancers.

Mutations of KRAS are found in a variety of human malignancies, including in pancreatic cancer, colorectal cancer, and non-small cell lung cancer at high frequency. To date, no effective treatments that target mutant variants of KRAS have been introduced into clinical practice. In recent years, a number of studies have shown that the oncogene KRAS plays a critical role in controlling cancer metabolism by orchestrating multiple metabolic changes. One of the metabolic hallmarks of malignant tumor cells is their dependency on aerobic glycolysis, known as the Warburg effect. The role of KRAS signaling in the regulation of aerobic glycolysis has been reported in several types of cancer. KRAS-driven cancers are characterized by altered metabolic pathways involving enhanced nutrients uptake, enhanced glycolysis, enhanced glutaminolysis, and elevated synthesis of fatty acids and nucleotides. However, Just how mutated KRAS can coordinate the metabolic shift to promote tumor growth and whether specific metabolic pathways are essential for the tumorigenesis of KRAS-driven cancers are questions which remain to be answered. In this context, the aim of this review is to summarize current data on KRAS-related metabolic alterations in cancer cells. Given that cancer cells rely on changes in metabolism to support their growth and survival, the targeting of metabolic processes may be a potential strategy for treating KRAS-driven cancers.

Metabolic Alterations Caused by KRAS Mutations in Colorectal Cancer Contribute to Cell Adaptation to Glutamine Depletion by Upregulation of Asparagine Synthetase.

A number of clinical trials have shown that KRAS mutations of colorectal cancer (CRC) can predict a lack of responses to anti-epidermal growth factor receptor-based therapy. Recently, there have been several studies to elucidate metabolism reprogramming in cancer. However, it remains to be investigated how mutated KRAS can coordinate the metabolic shift to sustain CRC tumor growth. In this study, we found that KRAS mutation in CRC caused alteration in amino acid metabolism. KRAS mutation causes a marked decrease in aspartate level and an increase in asparagine level in CRC. Using several human CRC cell lines and clinical specimens of primary CRC, we demonstrated that the expression of asparagine synthetase (ASNS), an enzyme that synthesizes asparagine from aspartate, was upregulated by mutated KRAS and that ASNS expression was induced by KRAS-activated signaling pathway, in particular PI3K-AKT-mTOR pathway. Importantly, we demonstrated that KRAS-mutant CRC cells could become adaptive to glutamine depletion through asparagine biosynthesis by ASNS and that asparagine addition could rescue the inhibited growth and viability of cells grown under the glutamine-free condition in vitro. Notably, a pronounced growth suppression of KRAS-mutant CRC was observed upon ASNS knockdown in vivo. Furthermore, combination of L-asparaginase plus rapamycin markedly suppressed the growth of KRAS-mutant CRC xenografts in vivo, whereas either L-asparaginase or rapamycin alone was not effective. These results indicate ASNS might be a novel therapeutic target against CRCs with mutated KRAS.

Intramural metastasis of T1 rectal cancer: report of a case report.

BACKGROUND: Intramural metastasis (IM) is extremely rare in colorectal cancer, although it often occurred in esophageal cancer. CASE PRESENTATION: We report a rare case of T1 rectal cancer with IM which was successfully resected by laparoscopic surgery. A 62-year-old man was admitted to our institution for the treatment of rectal cancer detected by medical examination. Colonoscopy revealed two tumors in the rectum: a type II rectal cancer of 2 cm in diameter located 5 cm proximal to the anal verge and a submucosal tumor of 1 cm in diameter located approximately 1.5 cm proximal to the rectal cancer. Abdominal computed tomography (CT), magnetic resonance imaging (MRI), and transrectal ultrasonography indicated the rectal cancer invaded into the submucosal layer with no metastasis to regional lymph nodes or distant organs. The patient underwent laparoscopic intersphincteric resection.Histopathological analysis revealed that the rectal cancer was moderately differentiated adenocarcinoma (stage I; pT1N0M0 according to the 7th edition of UICC) with severe lymphovascular invasion (ly1, v3) and that the submucosal tumor was composed of moderately differentiated adenocarcinoma proliferating within the muscularis propria. A number of features of the submucosal tumor indicated that this was an IM of the rectal cancer: clearly distinct location from the rectal cancer, growth predominantly within the muscularis propria, similar structural and cellular heterogeneity, and the presence of tumor emboli within vascular vessels. The patient was postoperatively followed for more than 4 years without any sign of recurrence. CONCLUSIONS: To the best of our knowledge, this is the first report of the T1 rectal cancer with IM.

Relationship Between 18F-FDG PET/CT Scans and KRAS Mutations in Metastatic Colorectal Cancer.

UNLABELLED: Several studies have shown that KRAS mutations in colorectal cancer (CRC) result in the lack of response to anti-epidermal growth factor receptor-based therapy; thus, KRAS mutational testing has been incorporated into routine clinical practice. However, 1 limitation of this test is the heterogeneity of KRAS status, which can be either intratumoral heterogeneity within an individual primary CRC or discordant KRAS status between a primary CRC and its corresponding metastases. We previously reported that (18)F-FDG accumulation was significantly higher in primary CRCs with mutated KRAS than in those with wild-type KRAS. However, the clinical utility of the previous report has been limited because endoscopic biopsy for testing KRAS status is safe and feasible only in primary CRC. The purpose of this study was to investigate whether KRAS status is associated with (18)F-FDG accumulation in metastatic CRC and whether (18)F-FDG PET/CT scans can be used to predict the KRAS status of metastatic CRC. METHODS: A retrospective analysis was performed on 55 metastatic CRC tumors that were identified by (18)F-FDG PET/CT before surgical resection. Maximum standardized uptake value (SUVmax) of the respective metastatic tumor was calculated from (18)F-FDG accumulation. RESULTS: From the analysis with the 55 tumors, no significant correlation was found between SUVmax and KRAS status. We next analyzed only tumors larger than 10 mm to minimize the bias of partial-volume effect and found that SUVmax was significantly higher in the KRAS-mutated group than in the wild-type group (8.3 ± 4.1 vs. 5.7 ± 2.4, respectively; P = 0.03). Multivariate analysis indicated that SUVmax remained significantly associated with KRAS mutations (P = 0.04). KRAS status could be predicted with an accuracy of 71.4% when an SUVmax cutoff value of 6.0 was used. CONCLUSION: (18)F-FDG accumulation into metastatic CRC was associated with KRAS status. (18)F-FDG PET/CT scans may be useful for predicting the KRAS status of metastatic CRC and help in determining the therapeutic strategies against metastatic CRC.

Regulation of 18F-FDG accumulation in colorectal cancer cells with mutated KRAS.

UNLABELLED: KRAS gene mutations occur in approximately 40% of colorectal cancers (CRCs) and are associated with resistance to anti-epidermal growth factor receptor antibody therapy. We previously demonstrated that (18)F-FDG accumulation in PET was significantly higher in CRCs with mutated KRAS than in those with wild-type KRAS in a clinical setting. Here, we investigated the mechanisms by which mutated KRAS increased (18)F-FDG accumulation. METHODS: Using paired isogenic human CRC cell lines that differ only in the mutational status of the KRAS gene, we measured (18)F-FDG accumulation in these cells in vitro and in vivo. We also investigated the roles of proteins that have a function in (18)F-FDG accumulation. Finally, we examined the relationship among mutated KRAS, hypoxia-inducible factor 1α (HIF-1α), and maximum standardized uptake value with 51 clinical CRC samples. RESULTS: In the in vitro experiments, (18)F-FDG accumulation was significantly higher in KRAS-mutant cells than in wild-type controls under normoxic conditions. The expression levels of glucose transporter 1 (GLUT1) and hexokinase type 2 (HK2) were higher in KRAS-mutant cells, and (18)F-FDG accumulation was decreased by knockdown of GLUT1. Hypoxic induction of HIF-1α was higher in KRAS-mutant cells than in wild-type controls; in turn, elevated HIF-1α resulted in higher GLUT1 expression and (18)F-FDG accumulation. In addition, HIF-1α knockdown decreased (18)F-FDG accumulation under hypoxic conditions only in the KRAS-mutant cells. Small-animal PET scans showed in vivo (18)F-FDG accumulation to be significantly higher in xenografts with mutated KRAS than in those with wild-type KRAS. The immunohistochemistry of these xenograft tumors showed that staining of GLUT1 was consistent with that of HIF-1α and pimonidazole. In a retrospective analysis of clinical samples, KRAS mutation exhibited a significantly positive correlation with expressions of GLUT1 and HIF-1α and with maximum standardized uptake value. CONCLUSION: Mutated KRAS caused higher (18)F-FDG accumulation possibly by upregulation of GLUT1; moreover, HIF-1α additively increased (18)F-FDG accumulation in hypoxic lesions. (18)F-FDG PET might be useful for predicting the KRAS status noninvasively.

[Mucoepidermoid carcinoma of the parotid gland as a secondary malignancy developed ten years after chemotherapy for childhood acute lymphoblastic leukemia].

We report on a case of mucoepidermoid carcinoma of the parotid gland following treatment of acute lymphoblastic leukemia (ALL) in childhood. The female patient was diagnosed as having T-cell ALL at the age of 13 years. Treatment included multidrug chemotherapy and prophylactic 18 Gy cranial irradiation. She developed low-grade mucoepidermoid carcinoma of the right parotid gland at the age of 24 years, the most probable cause of the secondary malignancy being radiation. In a literature review of mucoepidermoid carcinoma following ALL, 11 out of 14 cases received radiation therapy for the initial treatment of ALL, but 3 cases had no radiation therapy. The parotid gland carcinoma as a secondary malignancy following ALL in childhood is rare, but it highlights the need for concern about the secondary malignancy in patients with painless parotid swelling after chemoradiotherapy.