No abstract

(10%) patients were found to have serum ferritin >1000 ug/dl post-transplant. Of these, a total of 16 (70%) displayed clinically significant iron overload (IOL) that was defined as excess iron leading to organ dysfunction with serum ferritin (SF) of at least 1000 ug/dl. The median age of 18 males and 05 females was 58 years (24-72). Primary diagnosis for AHT included, AML/MDS (n¼16), ALL (n¼2), SAA (n¼2) and others (n¼3). Patients received median of 12 (7-60) lifetime cumulative PRBCs transfusions. The median pre-transplant SF and that at IOL was 1718 ug/dl (850-4658) and 3712 ug/l (1461-45598) respectively. IOL developed at median of 7 months (2-27) post AHT. All but 3 patients had cGvHD (limited skin¼11, extensive ¼9). Liver dysfunctions (median AST ¼ 149 u/l, ALT ¼ 230 u/l and alkaline phosphatase ¼ 249 u/l) was thought to be potentially IOL related. Therapeutic intervention for IOL comprised of phlebotomy in all 23 patients with 2 receiving concurrent oral chelation. With a median of 9 (1-115) phlebotomies, SF <1000 ensued in 15 (2-30) months. Liver functions normalized at median of 22 (4-110) weeks. HFE analyses of both donor and recipients available in 19 patients had no impact on IOL occurrence of its response to treatment. Figure 1 demonstrates relationship of SF decline and influence on hematopoiesis. At 12 months post phlebotomy, Improvement in hemoglobin and platelets was incremental but modest with rise of 4.6% and 13% respectively. Phlebotomy was well tolerated. At the median follow-up of 72 months, 16/23 (70%) patients are alive with median survival of 58 months (19-153). Cause of death included fungal infections in 4 patients. Phlebotomy produces predictable and safe iron reduction in patients with post AHT IOL. We found modest but encouraging improvement in hematopoiesis that requires further testing.

lized, immunoprecipitated, and sequentially immunoblotted using antibodies to mucin and transmembrane subunits. Results: MUC4 is identified by immunocytochemical staining throughout the normal UADT mucosa, in 24 of 29 primary UADT SCC, and in 6 of 6 metastatic cervical lymph nodes. A trend toward decreased staining of MUC4 in poorly differentiated tumors is suggested. Immunoblots show MUC4 in normal and tumor tissue in 3 of 4 SCCs analyzed, although electrophoretic migration patterns are similar between normal and tumor. Immunocytochemical staining of MUC4 in 11 major and minor salivary gland neoplasms reveals variable staining of normal and neoplastic tissue. MUC4 is consistently demonstrated in immunoblots of normal parotid tissue. Immunoblot with a carbohydrate-dependent antibody suggests carbohydrate differences in the MUC4 mucin subunit expressed in normal and neoplastic tissue from one parotid tumor. Conclusion: MUC4 is identified in SCCs of the UADT and neoplastic salivary tissue. Differential expression between normal and tumor MUC4 is demonstrated in some cases. Correlation of MUC4 expression with clinical outcomes may establish MUC4 as a potential molecular prognostic marker for these tumors.