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Infantile hemangiomas as frequent infancy tumors have been a controversial issue of medical scientists worldwide. Their clinical aspects are various and their physiopathology is yet to be fully understood. Numerous publications outline the characteristics, causes, evolution possibilities and therapeutic approaches. Deciding whether to treat or not is the main question of this kind of pathology. Hemangiomas that have complications or can cause irreversible damage need therapy. This is a brief review of up-to-date information regarding the presentation of infantile hemangiomas and target-therapies.

Rhinocerebral mucormycosis in acute lymphoblastic leukemia is manageable with sequential therapy including, amphotericin B, surgery, and risk-adapted chemotherapy.

ObjectivesThe aim of the study was to describe the historical and clinical characteristics of hemangiomas in a series of cases of our clinic.MethodsThis is a retrospective study of 36 patients with infantile hemangiomas consulted in our clinic.ResultsWe had 14 multiple hemangiomas, and 1 kaposiform hemangioendothelioma. Almost two-thirds involved the cephalic extremity, and 76% of the cases were treated. Pregnancy risk factors included prematurity, low-birth weight and respiratory distress syndrome. Propranolol was used in 22 cases, followed by prednisone in 3 cases. Vincristine and interferon were used as associated therapies or as second line therapies. Two hemangiomas had complications, one ulceration and a Kasabach-Merritt syndrome. All the patients had a good evolution.ConclusionsOur study results regarding the involvement of pregnancy and birth risk factors in developing infantile hemangiomas is similar to literature data. The majority of patients had at least one risk factor suggesting that at least one trigger to develop an infantile hemangioma is necessary. Our study shows that the cephalic extremity is mostly involved, and because of its potential complications they are most likely to be treated. The study shows that propranolol is the leading treatment option with few and mild side effects.

Patient: Female, 6 Final Diagnosis: Acute lymphoblastic leukemia Symptoms: Abdominal pain • bloody diarrhea • malaise • vomiting Medication: — Clinical Procedure: Chemotherapy Specialty: Oncology Objective: Unusual clinical course Background: Malignant hypercalcemia is a rare finding in the pediatric population, even more rare in hematological malignancies, such as leukemia. Case Report: We present a case of a 6-year-old female patient who was diagnosed with acute lymphoblastic leukemia, with secondary hypercalcemia. She started chemotherapy following the IC-BFM ALL2002 protocol with simultaneous calcitonin, diuretics and aggressive hydration for hypercalcemia, and went into complete remission after the induction therapy. After 4 months of chemotherapy, she was diagnosed with relapse associated again with malignant hypercalcemia, and underwent chemotherapy with the relapse protocol. There was no response after the first 2 cycles, so we decided to start her on clofarabine. Due to the severe hypercalcemia and consecutive osteolysis, she developed several bone fractures and needed gypsum immobilization. We started her again on calcitonin, but she developed severe adverse reactions, so we found it necessary to start bisphosphonates, first zoledronic acid intravenously, and afterwards clodronate orally. Consolidation of bone fractures was achieved, but due to prolonged immobilization she developed bedsores, superinfected with Lichtheimia corymbifera . We started posaconazole orally, but she rapidly went into severe sepsis with multiple organ failure. The leukemia showed no response to chemotherapy, progressed rapidly, and the patient died. Conclusions: Malignant hypercalcemia is associated with a poor prognosis in leukemia, and might need a more aggressive therapy.

Here we show that surface-enhanced Raman scattering (SERS) analysis captures the relative hypomethylation of DNA from patients with acute leukemia associated with Down syndrome (AL-DS) compared with patients diagnosed with transient leukemia associated with Down syndrome (TL-DS), an information inferred from the area under the SERS band at 1005 cm–1 attributed to 5-methycytosine. The receiver operating characteristic (ROC) analysis of the area under the SERS band at 1005 cm–1 yielded an area under the curve (AUC) of 0.77 in differentiating between the AL-DS and TL-DS groups. In addition, we showed that DNA from patients with non-DS myeloproliferative neoplasm (non-DS-MPN) is hypomethylated compared to non-DS-AL, the area under the SERS band at 1005 cm–1 yielding an AUC of 0.78 in separating between non-DS-MPN and non-DS-AL. Overall, in this study, the area of the 1005 cm–1 DNA SERS marker band shows a stepwise decrease in DNA global methylation as cells progress from a pre-leukemia to a full-blown acute leukemia, highlighting thus the potential of SERS as an emerging method of analyzing the methylation landscape of DNA in the context of leukemia genesis and progression.

Infantile hemangioma is one of the most common benign tumors affecting children, with ~10–15% requiring medical treatment. These tumors consist of endothelial cells and stromal components, including fibroblasts, pericytes and mast cells. Effects of propranolol treatment in combination with bevacizumab or vincristine on cell growth were compared in the current study using human umbilical vein endothelial cells (HUVECs) and BJ human normal fibroblasts (BJs) to determine potential synergic effects in vitro. Inhibition of cell growth was investigated using MTT assays and cytotoxicity of the drugs in various combinations was expressed as half inhibitory concentration (IC50). Apoptosis was investigated using flow cytometry, with Alexa Fluor 488 and propidium iodide. Propranolol inhibited BJ and HUVEC growth in a dose-dependent manner, with increased response observed in BJs (IC50, 148,32 µg/ml; standard error logIC50, 0.07). Treatment with vincristine induced the strongest growth inhibition in HUVECs (IC50, 17,89 µg/ml; standard error log IC50, 0.07) and BJs (IC50, 24,81 µg/ml; standard error log IC50, 0.08) compared with propranolol (HUVEC IC50, 81,94 µg/ml; standard error log IC50, 0.06; BJ-IC50, 148,32 µg/ml; standard error logIC50, 0.07) or bevacizumab (HUVEC IC50 96,91 µg/ml; standard error log IC50, 0.06; BJ IC50, 182,70 µg/ml; standard error log IC50, 0.09) alone. Bevacizumab was the weakest cytotoxic agent. Combination treatment of vincristine with bevacizumab induced the highest levels of apoptosis in HUVECs compared with all other treatments and triple-drug therapy induced the levels of apoptosis in BJs. Single treatment with vincristine, propranolol or bevacizumab induced apoptosis in BJs and HUVECs. In BJs, triple treatment exhibited the greatest influence on apoptosis, compared with single and dual treatments and in HUVECs, vincristine and bevacizumab combination treatment induced apoptosis to the highest level. The present study offers novel perspectives in drug repurposing studies for the three drugs, particularly in diseases where the pathogenesis is based on healthy endothelial cell proliferation, including hemangiomas.