Donor-Derived Ovarian Cancer in a Male Recipient After Kidney Transplant: A Case Report.

BACKGROUND: Patients who receive kidney transplants and experience long-term immunosuppressive therapy are tied to higher risk of developing cancers. Reports concerning about donor-associated cancers are rarely reported, especially for male ovarian cancer. CASE REPORT: Here we report a case of donor-derived ovarian malignancy of a man after 3 years of renal transplantation. This case complied with the Helsinki Congress and the Istanbul Declaration. The donor is the recipient's mother who developed ovarian malignancy 6 months after the transplantation surgery and died 1.5 years later after diagnosis due to tumor progression. The patient devolved into abnormal renal function 3 years after the transplantation. The transplanted kidney lost its function and was subsequently surgically removed. The ovary cancer was confirmed as high-grade serous ovarian cancer by pathology and had potentially metastasized to donor kidney. Then the male patient received regular maintenance and dialysis. Four years after transplantation, he gradually developed the symptoms of coughing and sputum and computed tomography examination revealed a lung space-occupying lesion that was confirmed to be a metastatic tumor with the same pathology as before. Platinum-based combination chemotherapy can effectively control the condition; by the last follow-up evaluation, the progression-free survival of the patient was 23.5 months, and the overall survival was 36 months. CONCLUSIONS: This case demonstrates that donor-derived ovarian tumor can be transferred into the recipient via the transplanted kidney even in the male recipient. This observation provides clinicians with effective treatment options for this rare type of patient population.

Maternal natural killer cell immunoglobulin receptor genes and human leukocyte antigen-C ligands influence recurrent spontaneous abortion in the Han Chinese population.

The underlying mechanism of recurrent spontaneous abortion (RSA) has remained elusive for many years. Several previous studies have suggested that the killer cell immunoglobulin receptor (KIR) gene family is associated with RSA, however, it is not clear exactly how. The present study detected KIR and human leukocyte antigen-C (HLA-C) genes in 110 Han Chinese women with unexplained RSA and 105 Han Chinese healthy females. The aim of the present study was to determine if certain genotypes were more susceptible to the occurrence of miscarriage. The frequency of KIR genes and different KIR haplotypes in the 2 groups demonstrated no statistical differences. However, in women who had miscarried ≥3 times, the frequency of KIR3DL1 was significantly reduced and the BB haplotype frequency was significantly higher compared with the control group. HLA-C2C2 was significantly increased in the KIR AB and KIR BB groups in the RSA groups compared with the control group. The women in the RSA group who had a homozygous HLA-C2C2 had a significantly higher frequency of the 2DS1 gene compared with the control group. The reduction of inhibitory gene and increased activation combinations may induce the activation of uterine natural killer cells, which may reduce the probability of fetal survival. To the best of our knowledge, the present study is the first report demonstrating the association between maternal KIR and HLA-C genes and RSA in women of a Han Chinese ethnicity. The present study revealed that females who miscarry ≥3 times may be used as selection criteria for RSA and so may exhibit higher research value.

Anti-H can trigger apoptosis and down-regulate FUT1 expression in erythroid differentiated K562 cells without complement mediation.

The reason why delayed RBC engraftment and pure red cell aplasia (PRCA) develop only in some but not all recipients of major ABO-incompatible hematopoietic stem cell transplantation (HSCT) remains elusive and the underlying mechanisms are not fully understood. Understanding how incompatible erythroid blood group antibodies (Abs) interact with ABH antigens (Ags) of grafts, and investigating how to induce artificially accommodation of grafts are of obvious importance in transplantation immunology. The effects of anti-H on proliferation, apoptosis, and α-(1,2)-fucosyltransferase gene (FUT1) expression in erythroid differentiated K562 cells were analyzed by the MTT assay, Annexin V/PI staining, and quantitative RT-PCR method. The growth of erythroid differentiated K562 cells was significantly suppressed when anti-H dilution was ≤ 1:8 (P<0.001, as compared with 1:16). Under the complement-free culture conditions, the apoptotic ratio of erythroid differentiated K562 cells was significantly increased when anti-H dilution was ≤ 1:16 (P<0.05, as compared with 1:32). The apoptosis was not only closely associated with anti-H dilution (F=138.991, P<0.001), but also correlated with treated time (F=583.249, P<0.001), which indicated typical dose- and time-dependent effects. Under the complement-free culture conditions, the FUT1 mRNA expression level was also suppressed when anti-H dilution was ≤ 1:16 (P<0.05, as compared with 1:32), which also manifested in typical dose-dependent (F=130.356, P<0.001) and time-dependent (F=1432.00, P<0.001) effects. The results confirm that anti-H can trigger apoptosis and down-regulate FUT1 expression in erythroid differentiated K562 cells without complement mediation. The findings suggest that anti-H could accommodate grafts through triggering apoptosis and down-regulating Fut1 expression to reduce ABH antigens.