Hypermethylation of CpG islands in the promoter region of the p15INK4B gene in childhood acute leukaemia

It has been reported that the cyclin-dependent kinase inhibitor (CDKI) gene p15INK4B is frequently inactivated by genetic alterations and may be responsible for various malignant tumours. Another way of inactivation of this CDKI is by hypermethylation of 5'CpG islands in the promoter region of the p15INK4B gene and this inactivation seems to be a frequent event in various haematological malignancies. In the present study, we investigated the methylation status of the p151NK4B gene to clarify its role in the pathogenesis of childhood acute myeloid (AML) and acute lymphoblastic leukaemia (ALL). The study included 23 cases of B-cell origin ALL, 13 cases of T-cell origin ALL, 32 cases of AML, and 10 apparently healthy controls. Hypermethylation was studied by methylation-specific polymerase chain reaction. Hypermethylation of the p15INK4B gene was more frequent in cases with T-cell origin ALL (46.2%), but similar among children with B-cell origin ALL (13.0%) and AML (18.8%). Hypermethylation of p15INK4B may be involved in the pathogenesis of T-cell origin ALL, but not in that of AML or B-cell origin ALL.     

Infected femoral artery pseudoaneurysm in drug addicts: the beneficial use of the internal iliac artery for arterial reconstruction

BACKGROUND: Infected femoral artery pseudoaneurysm (IFAP) is a severe complication in parenteral drug abusers, with difficult and controversial management. Ligation alone without revascularization is frequently associated with later intermittent claudication and limb amputation. Furthermore, arterial reconstruction with a synthetic or venous conduit is limited because of a contaminated field and, often, unavailability of autologous venous grafts. In this study, we present our experience with the internal iliac artery (IIA) as a graft for arterial reconstruction after IFAP excision in these patients. METHODS: Data of 14 consecutive patients who presented with IFAP secondary to parenteral drug abuse from 2001 to 2005 were analyzed. Twelve patients (85.7%) were male. The median age was 27 years (range, 19-42 years). In 13 cases, the IFAP involved the common femoral artery, and in 1 case it involved the profunda femoris artery (PFA). In nine patients, we used the IIA for arterial reconstruction (five as a patch and four as an interposition graft), whereas in two patients the arterial deficit was repaired with a great saphenous vein patch. In two cases, an extra-anatomic bypass with a synthetic polytetrafluoroethylene graft was performed. In one patient, the pseudoaneurysm involved the PFA and was treated with excision and ligation of the PFA. RESULTS: All nine patients who underwent revascularization with the use of IIA were free of claudication symptoms. None of them experienced any perioperative complications, had signs of reinfection, or required limb amputation during the follow-up period (median, 19 months; range, 4-52 months). Regarding the remaining five patients, one died 25 days after surgery because of multiorgan failure, and one underwent reoperation because of proximal anastomotic rupture of a synthetic graft. The latter patient finally underwent a transmetatarsal amputation. CONCLUSIONS: The use of IIA for arterial reconstruction after IFAP excision in drug abusers is safe and effective. These preliminary results indicate that the implementation of this technique offers many advantages compared with traditional treatment options.     

Malignant mixed tumor of the nasal cavity

Parotid gland is the most common location of malignant mixed tumors. Three different subtypes of these tumors exist: carcinoma ex pleomorphic adenoma, carcinosarcoma, and metastasizing mixed tumor. Carcinoma ex-pleomorphic adenoma is by far the most common subtype. Although unusual sites of these tumors have been published, we report an extremely rare case of a malignant mixed tumor located in the nasal cavity.     

Anti-survivin antibody responses in lung cancer

Existing evidence regarding spontaneous anti-survivin humoral responses in lung cancer is inconclusive. Moreover, despite that cancer cell death elicited by radiotherapy and some chemotherapeutic agents seems to be immunogenic, information about the possible effect of treatment on these responses, is lacking. Serum samples from 33 small cell lung cancer (SCLC) and 117 non-small cell lung cancer (NSCLC) patients upon diagnosis, and from 100 controls, were tested by ELISA for anti-survivin antibodies. Cutoff was set to the mean + 2SD of controls. 7.7% of NSCLC, none of the SCLC patients and 2% of the controls appeared with elevated antibody levels (OR 3.6, 95% CI 0.7–17.3 for NSCLC, OR 0.6, 95% CI 0.03–12.6 for SCLC). Measurement of antibodies in 76 NSCLC patients post therapies and during their follow-up, revealed that in 12 NSCLC patients the antibody levels increased up to 2–38 times, and in seven others, they decreased by 2–8 times. No significant correlation was uncovered between either the antibody levels upon diagnosis or their changes post therapies and during follow-up, and any clinicopathological parameter, their response to therapy and survival. Survivin does not induce considerable humoral responses in lung cancer. Potentially, however, strong anti-survivin antibody responses can be elicited during the post therapy and follow-up of the patients, whose clinical significance remains to be elucidated. These findings, together with our previous data concerning survivin expression and the related cytolytic T cell responses in lung cancer, signify a high tolerogenic potential of this tumor-associated antigen.     

Wound dehiscence: is still a problem in the 21th century: a retrospective study

Background  

The aim of this study was to evaluate the risk factors of wound dehiscence and determine which of them can be reverted.     

Probing the evolution of appendage specialization by Hox gene misexpression in an emerging model crustacean

Changes in the expression of Hox genes have been widely linked to the evolution of animal body plans, but functional demonstrations of this relationship have been impeded by the lack of suitable model organisms. A classic case study involves the repeated evolution of specialized feeding appendages, called maxillipeds, from anterior thoracic legs, in many crustacean lineages. These leg-to-maxilliped transformations correlate with the loss of Ultrabithorax (Ubx) expression from corresponding segments, which is proposed to be the underlying genetic cause. To functionally test this hypothesis, we establish tools for conditional misexpression and use these to misexpress Ubx in the crustacean Parhyale hawaiensis. Ectopic Ubx leads to homeotic transformations of anterior appendages toward more posterior thoracic fates, including maxilliped-to-leg transformations, confirming the capacity of Ubx to control thoracic (leg) versus gnathal (feeding) segmental identities. We find that maxillipeds not only are specified in the absence of Ubx, but also can develop in the presence of low/transient Ubx expression. Our findings suggest a path for the gradual evolutionary transition from thoracic legs to maxillipeds, in which stepwise changes in Hox gene expression have brought about this striking morphological and functional transformation.