Adult T-cell leukemia (ATL) is an aggressive type of leukemia, originating from T-cells infected with human T-cell leukemia virus type 1. Accumulating evidence suggests the aberrant activation of NF-κ κ κ κB to be a causative factor mediating the abnormal proliferation of leukemic cells, thus resulting in the development of ATL. A rearranged NF-κ κ κ κB2/p100 gene was isolated from an ATL-derived cell line, which was generated by a chromosomal translocation. The isolated NF-κ κ κ κB2 mutant is fused with the with no (lysine) deficient protein kinase 1 gene, coding for a 58 kDa protein that retains the DNA binding Rel homology domain, but it lacks the entire ankyrin repeat inhibitory domain, thus suggesting its constitutive activation. This rearranged NF-κ κ κ κB2 gene product (p58) was localized in the nucleus, and formed a complex with NF-κ κ κ κB p65 or RelB. Moreover, a T-cell line expressing p58 increased the amount of an NF-κ κ κ κB2-inducible gene, NF-κ κ κ κB2/p100 by itself. These results suggest that such NF-κ κ κ κB2 gene rearrangement may therefore be a factor in the constitutive activation of NF-κ κ κ κB in ATL, and thereby playing a role in the ATL pathogenesis. A dult T-cell leukemia (ATL) is a highly aggressive leukemia, characterized by the clonal proliferation of CD4 positive T-cells infected with human T-cell leukemia virus type 1 (HTLV-1).(1-5) HTLV-1 establishes a life-long persistent infection through the immortalization of infected T-cells. (6,7) This immortalization is, however, not sufficient for ATL development, since only a minority of HTLV-1 infected individuals (approximately 5%) develop ATL after a long latency period (approximately 60 years).(4,5) Accumulating evidence indicates that genetic and epigenetic changes of the host genome and HTLV-1-associated deterioration of host immunity may therefore be major factors in ATL development. (4,5) Primary leukemic cells in the patients, as well as ATL-derived cell lines demonstrate the constitutive activation of transcription factor NF-κB.(8-11) Moreover, agents which block the NF-κB activity induce apoptosis in these ATL cells.(12-14) Although HTLV-1 Tax protein potently activates NF-κB, primary leukemic cells as well as ATL derived cell lines express little, if any, tax mRNA. This indicates that the NF-κB activation in ATL cells is caused by genetic and/or epigenetic changes in the host genome. (4,10,15,16) However, precisely how NF-κB is deregulated in ATL cells still remains poorly elucidated.NF-κB plays a crucial role in cell proliferation, apoptosis, as well as inflammation, differentiation and development, by regulating the transcription of numerous genes.(17,18) NF-κB is a family of factors containing the DNA binding Rel homology domain including p50, p65, c-Rel, RelB, and p52. NF-κB is normally sequestered in the cytoplasm through physical interaction with ankyrin-repeat-containing inhibitor proteins, including IκBα, IκBβ, IκBε, and NF-κB2/p100. NF-κB is activated by either the canonical or non-canonical pathway. In the canonical ...
Diverticulitis and diverticular abscesses are rare and potentially serious complications of duodenal diverticulum. These conditions often lead to perforation of the diverticulum, necessitating surgical treatment. There have been few reported cases of duodenal diverticulitis with or without perforation treated by endoscopic drainage. Here, we present a case of duodenal diverticulitis accompanied by abscess formation that was treated successfully with an endoscopic nasobiliary drainage catheter. We suggest this treatment could be an acceptable option for selected patients with a localized abscess that is resistant to conservative treatment.
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