tailieunhanh - Helicobacter pylori and mucosa-associated lymphoid tissue: What’s new

With a relatively high incidence and unique clinicopathological features, gastric lymphoma has recently become an important area of cancer research. In 1983, Isaacson and Wright described a group acquisition of gastric MALT in H pylori infection facilitates the of extranodal low-grade B-cell lymphomas derived from Peyer development of gastric MALT patch–like structures of mucosa-associated lymphoid tissue(MALT)in the stomach, salivary glands, lungs and thyroid gland. | I Bad BUGS Infections Causing Lymphoma I Helicobacter pylori and mucosa-associated lymphoid tissue what s new Sung-Hsin Kuo1-4 andAnn-Lii Cheng1-4 Departments of10ncology and 2Internal Medicine National Taiwan University Hospital and National Taiwan UniversityCollege of Medicine Taipei Taiwan and 3CancerResearch Centerand4Graduate Institute of Oncology NationalTaiwanUniversityCollegeofMedicine Taipei Taiwan Low-grade mucosa-associated lymphoid tissue MALT lymphoma of the stomach gastric MALT lymphoma is associated with Helicobacter pylori infection. The eradication of Hpylori using antibiotics is successful in 60 to 80 of affected patients. In contrast to the previous paradigm we and other investigators have shown that a certain proportion of patients with Hpylori-positive early-stage diffuse large B-cell lymphoma DLBCL of the stomach with histological evidence of MALT lymphoma including high-grade transformed gastric MALT lymphoma and gastric DLBCL MALT achieved long-term complete pathological remission pCR after first-line Hpylori eradication therapy indicating that the loss of Hpylori dependence and high-grade transformation are separate events in the progression of gastric lymphoma. In addition patients with Hpylori-positive gastric DLBCL without histological evidence of MALT gastric pure DLBCL may also respond to Hpylori eradication therapy. A long-term follow-up study showed that patients who achieved pCR remained lymphoma free. Gastric MALT lymphoma is indirectly influenced by Hpylori infection through T-cell stimulation and recent studies have shown that Hpylori-triggering chemokines and their receptors Hpylori-associated epigenetic changes Hpylori-regulated miRNA expression and tumor infiltration by CD4 CD25 regulatory T cells contribute to lymphomagenesis of gastric MALT lymphoma. Recent studies have also demonstrated that the translocation of CagA into B lymphocytes inhibits apoptosis through p53 accumulation BAD phosphorylation and the up-regulation of

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