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Articles by F Wan
Total Records ( 2 ) for F Wan
  R Zhao , J Zhu , X Ji , J Cai , F Wan , Q Li , B Zhong , S Tucker and D. Wang
  Objective

To assess the resectability rate of patients with initially unresectable liver-only metastases from colorectal cancer (CRC) after treatment with irinotecan/capecitabine.

Methods

Patients received irinotecan (240 mg/m2) as a 30 min intravenous infusion on day 1 and capecitabine (1000 mg/m2) orally bid for 14 days beginning on day 2. Treatment was repeated every 3 weeks. The protocol encouraged two to four cycles of irinotecan/capecitabine after recovery from surgery.

Results

Between May 2004 and February 2007, 48 patients entered in the study. Forty-seven (97.9%) of the 48 patients were assessable for response. The overall response rate before surgery was 56.3% (95% CI, 42.3–70.3%) in the treated population, including 2 non-confirmed complete response (CR), 18 partial responses (PR) and 7 non-confirmed PR. Twenty-three (47.9%) of 29 patients with tumor shrinkage proceeded to surgical intervention. Twenty of the 23 patients had a complete resection (S-CR). With a median follow-up time of 32 months (range, 24–38 months), the overall median time to progression and overall survival for all patients were 16.7 months (95% CI, 10.0–23.4 months) and 27.5 months (95% CI, 23.6–31.4 months) for all patients. The 1- 2- and 3-year overall survival estimates were 79.2% (95% CI, 67.7–90.7%), 60.4% (95% CI, 46.6–74.3%) and 29.2% (95% CI, 16.3–42.0%), respectively. Grade 3 diarrhea occurred in eight (17.0%) patients. The most common Grade 3/4 hematological adverse event was neutropenia in 8.5% of the patients. There were no treatment-related deaths during this study.

Conclusions

Irinotecan/capecitabine appears to be a safe and very effective regimen in selected patients with unresectable liver metastases from CRC, but who are treated with a curative intent.

  E. J Cadera , F Wan , R. H Amin , H Nolla , M. J Lenardo and M. S. Schlissel
 

Because of the extreme diversity in immunoglobulin genes, tolerance mechanisms are necessary to ensure that B cells do not respond to self-antigens. One such tolerance mechanism is called receptor editing. If the B cell receptor (BCR) on an immature B cell recognizes self-antigen, it is down-regulated from the cell surface, and light chain gene rearrangement continues in an attempt to edit the autoreactive specificity. Analysis of a heterozygous mutant mouse in which the NF-B–dependent IB gene was replaced with a lacZ (β-gal) reporter complementary DNA (cDNA; IB+/lacZ) suggests a potential role for NF-B in receptor editing. Sorted β-gal+ pre–B cells showed increased levels of various markers of receptor editing. In IB+/lacZ reporter mice expressing either innocuous or self-specific knocked in BCRs, β-gal was preferentially expressed in pre–B cells from the mice with self-specific BCRs. Retroviral-mediated expression of a cDNA encoding an IB superrepressor in primary bone marrow cultures resulted in diminished germline and rearranged transcripts but similar levels of RAG expression as compared with controls. We found that IRF4 transcripts were up-regulated in β-gal+ pre–B cells. Because IRF4 is a target of NF-B and is required for receptor editing, we suggest that NF-B could be acting through IRF4 to regulate receptor editing.

 
 
 
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