Intraluminal calcifications in the small bowel of newborn infants with total colonic aganglionosis

Intraluminal calcifications were found in the small bowel of 4 newborns with total colonic aganglionosis. Abdominal radiography demonstrated circular aggregations of small punctate calcific densities in the right lower quadrant and evidence of bowel obstruction. There was a microcolon in each case. The calcifications, which resemble those seen in small intestinal atresia and stenosis, are probably related to fetal intestinal stasis, and may be differentiated from those due to meconium peritonitis.     

Magnetic resonance imaging of the brainstem: normal structure and basic functional anatomy

Normal structure and basic functional anatomy of the brainstem were studied using anatomic sections obtained with a cryomicrotome whole-organ sectioning technique. Major tracts and nuclei were identified and their function summarized. Magnetic resonance imaging of the brainstem was performed on 10 normal volunteers. By comparing these images with the corresponding anatomic sections, normal structures, including major tracts and nuclei, were identified. Knowledge of location and function of clinically important brainstem nuclei and tracts is necessary for optimal magnetic resonance image interpretation.     

Iron chelation: a potential therapeutic strategy in oesophageal cancer

Raised intracellular iron has been identified as a potential aetiological factor in the development of several epithelial malignancies, including those of the gastrointestinal tract. The mechanism behind this increase is thought to include disorders of iron uptake and storage. Several iron chelators have been identified as potential anti-tumour agents, with much work undertaken to ascertain the exact mode of action. Despite this, there is little known about the role that these drugs play in the cellular iron metabolism of oesophageal cancer. Consequently, the present study looks to review the relationship of two clinically important iron-chelating agents, deferoxamine and deferasirox, on cellular iron uptake and storage in oesophageal squamous and adenocarcinoma. This provides important evidence for the debate about the role these agents have in the clinical management of such tumours.

Linked Article

This article is a commentary on Ford et al., pp. 1316–1328 of this issue. To view this paper visit http://dx.doi.org/10.1111/bph.12045     

Abnormal methylation of the calcitonin gene marks progression of chronic myelogenous leukemia

The clinical aspects of disease progression in chronic myelogenous leukemia (CML) are well established, but the nature of the molecular events responsible is not known. We have previously reported a consistent pattern of novel sites of methylation in the 5' region of the calcitonin (CT) gene and other chromosome 11p loci in acute myelogenous and and lymphoid leukemias. In the present study, CT gene methylation patterns were investigated in peripheral blood from 51 patients with CML. Abnormal patterns were found in only 2 of 31 patients in chronic phase, but in 5 of 8 patients in accelerated phase, and in 11 of 12 patients in blast crisis (P less than .005). For one patient studied in blast crisis, abnormal CT gene methylation was found in the peripheral blast cells but not in the granulocytes. In two of three patients studied with CML and having normal peripheral cell patterns, abnormal patterns were found in marrow blast cells. In one patient, only partial normalization of the CT gene methylation pattern was seen after chemotherapy induction of a second chronic phase and the patient relapsed 5 months later. Our findings indicate that abnormal methylation of the 5' region of the CT gene is regularly a marker of disease progression in CML which may prove clinically useful. This abnormal methylation site is part of an imbalance in DNA methylation that may play a role in the progressive genetic instability which characterizes the advancing stages of CML.     

Treatment of refractory adult lymphoblastic leukemia (ALL) with 4'(9- acridinylamino) methanesulfon-M-anisidide (AMSA)

Twenty-four adults with ALL were treated with AMSA alone or in combination. Twenty-two were treated at time of relapse and two patients after failing primary induction therapy. All had been treated with anthracyclines prior to receiving AMSA. Of the 22 patients with ALL in relapse, 4 achieved a complete remission. Two of these patients have relapsed while receiving maintenance chemotherapy; one died 1 mo after achieving remission due to the occurrence of cholycystitis in the setting of pancytopenia and one patient underwent bone marrow transplantation and is in remission at 8 mo after the second remission. Both patients who failed primary induction therapy remain in remission at 11 and 36 mo, respectively. The use of AMSA should be considered for patients with ALL who fail primary induction as well as those whose leukemia becomes resistant to conventional agents.