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Background: Mucormycosis is a rare and life-threatening invasive fungal infection. Pulmonary mucormycosis commonly occurs in patients with severe neutropenia. Typically, pulmonary mucormycosis causes tissue necrosis resulting from angioinvasion and subsequent thrombosis, so most cases can occur with necrotizing pneumonia and/or hemoptysis. Some complex cases may invade adjacent organs, such as the mediastinum, pericardium, and chest wall. However, to the best our knowledge there is little known regarding bronchoesophageal fistula due to pulmonary mucormycosis after induction chemotherapy for acute myeloid leukemia. We present a case report about this unusual presentation.Case Presentation: A 51-year-old Korean man was diagnosed as having acute myeloid leukemia and received induction chemotherapy. After prolonged severe neutropenia, he complained of coughing with aspiration. Imaging showed a bronchoesophageal fistula with extensive necrotizing pneumonia in the middle and lower lobes of his right lung. Bronchoscopy showed near total tissue necrosis in the middle lobe of his right lung, creating an orifice. A bronchial scope was passed through and was able to be connected with his esophagus; a bronchial wall biopsy was performed. Esophagoscopy revealed a large linear defect of his esophageal wall 30 cm from the incision that may have connected with the bronchus. A bronchial biopsy showed typical hyphae with necrotic tissue, indicating pulmonary mucormycosis. He was given amphotericin B, and a wide excision of lung and esophagus was planned. However, he suddenly died due to massive hemoptysis.Conclusion: Here we present an extremely rare case of bronchoesophageal fistula with severe necrotizing pneumonia due to pulmonary mucormycosis. [ABSTRACT FROM AUTHOR]

Introduction: Condyloma acuminatum are caused by human papillomavirus. Giant condyloma acuminatum is a locally invasive, destructive, and large sized mass. Risk factors for the development of giant condyloma acuminatum include an immunodeficient state, such as human immunodeficiency virus infection, post-organ transplantation, or post-allogeneic bone marrow transplantation. However, reports of giant condyloma after bone marrow transplantation are extremely rare (0.3 to 1.3%). The standard treatment for giant condyloma acuminatum is recommended as wide surgical resection due to its high rate of success and low rate of recurrence. Case presentation: A 31-year-old Korean man presented to our hospital with anal discomfort for more than one month due to a protruding mass. He had a history of BCR-ABL-positive acute lymphoblastic leukemia and had undergone an allogenic stem cell transplantation. Gross findings revealed a large perianal cauliflower-like mass over 7cm in size with invasion of the anal orifice. He was diagnosed with giant anal condyloma occurring after an allogeneic bone marrow transplantation. However, we achieved successful treatment using a combination of topical podophyllin and cryotherapy and transanal surgical excision, followed by bleomycin irrigation. Conclusions: We report an extremely rare case of giant condyloma acuminatum of anus due to human papillomavirus type six in a patient with acute lymphoblastic leukemia following an allogeneic bone marrow transplantation. The tumor was successfully treated with a combination of topical podophyllin and cryotherapy and transanal surgical excision, followed by bleomycin irrigation. [ABSTRACT FROM AUTHOR]

Desmoplastic small round cell tumor (DSRCT) is a rare and aggressive malignancy with a poor outcome that occurs in adolescents and young adults; <200 cases of DSRCT have been reported. Renin-producing tumors are also rare and cases of extrarenal renin-producing tumors are even rarer. The present study describes the case of a 20-year-old male that was diagnosed with DSRCT and presented with severe hypertension and hypokalemia, as well as metabolic alkalosis. The plasma renin activity (PRA) level was identified to be markedly elevated (normal range in standing and supine positions, 1.3-4.0 ng/ml/h and 0.15-2.33 ng/ml/h, respectively) and the plasma aldosterone level was also increased (normal range in standing and supine positions, 4.0-31.0 ng/dl and 1.0-1.6 ng/dl, respectively). The symptoms of the patient were consistent with the renin-secreting tumor triad, which comprises hypertension, hypokalemia and elevated PRA. Paraneoplastic syndromes must always be considered in cancer patients exhibiting unusual clinical findings, despite their rarity. The current patient was diagnosed with paraneoplastic secondary hypertension due to the presence of disseminated renin-secreting DSRCT. The patient was treated with the VAC/IE regimen (vincristine, adriamycin, cyclophosphamide, ifosfamide and etoposide) for six cycles. Following this treatment, the serum renin and aldosterone levels fell to within the normal range and the patient's blood pressure was normalized without antihypertensive medication. Although an immunohistochemical evaluation of renin was not conducted as the sample size was inadequate, the present study demonstrated that the tumor had produced renin. The biosynthesis of renin was identified by the presence of mRNA that coded for the renin precursor, which was observed in the ascites of the patient. The current study describes, to the best of our knowledge, the first reported case of paraneoplastic secondary hypertension in a patient presenting with a renin-producing DSRCT. [ABSTRACT FROM AUTHOR]

We have evaluated the role of mitogen-activated protein kinases (MAPKs) and their relationship with nuclear factor kappaB (NF-kappaB) and peroxisome proliferator-activated receptor gamma (PPARgamma) in indomethacin-induced apoptosis of colon cancer cells. We demonstrated that indomethacin can induce the prolonged activation of MAPKs in colon cancer cells; and that of these MAPKs, p38 MAPK may play a partial but significant role in indomethacin-induced apoptosis. Furthermore, indomethacin-induced p38 MAPK-mediated apoptosis of colon cancer cell lines is independent of caspase activation and not associated with indomethacin-induced NF-kappaB suppression and PPARgamma activation.