Synchronous uterine serous carcinoma and ovarian sex cord stromal tumor (thecoma)-A rare first case report.

Synchronous endometrial and ovarian carcinoma is a rare instance and it accounts for 50 to 70% of all synchronous female genital tract tumors. However, it is very rare to find synchronous endometrial carcinoma and ovarian sex cord-stromal tumor (thecoma). The present case is a 75-year-old woman with a complaint of post-menopausal vaginal bleeding. Radiologically, the magnetic resonance imaging (MRI) pelvis revealed altered signal intensity mass in the uterus. Frozen section and routine histopathological examination were done on radical hysterectomy. Microscopically, serous carcinoma involving uterine corpus and left Fallopian tube was identified along with the unusual finding of contralateral ovarian sex cord-stromal tumor (thecoma), which was confirmed on immunohistochemical examination. It is a very rare association and is first reported in the present study after a thorough search of the published literature. Their relationship based on a high level of estrogen produced by the hyperactive ovary is controversial as serous carcinomas are less hormone-dependent.

Anti-P30-52 monoclonal antibody cross-reacted to Env V3 and inhibited the viral multiplication of HIV-1-infected MT-4 cells.

It is well known that the anti-p17 antibody titer decreases with the disease progression among human immunodeficiency virus type 1 (HIV-1) carriers. We previously established several murine anti-p17 monoclonal antibodies (MAbs) to investigate the immunological role of p17, and to further characterize these MAbs, we examined the anti-p17 antibody titer in serum of a patient who was a long-term nonprogressor with hemophilia, and found that the antibody for the p17-derivative peptide from amino acid residues 30 to 52 (P30-52) cross-reacted to the third variable region of the envelope glycoprotein of HIV-1, Env V3. In the present study, we primed mice with P30-52 to establish anti-P30-52 MAbs (P30-52 MAbs), and examined their affinity and whether they suppressed the viral multiplication of HIV-1-infected MT-4 (HTLV-1-transformed CD4+ T-cell line) cells, in a TCID50 assay. At the same time, an anti-Env V3 MAb (Env V3 MAb) was also established and examined as above. The IgM-type P30-52 MAb and Env V3 MAb showed heteroclitic binding, and the IgM-type P30-52 MAb inhibited the viral multiplication. We also found that an increase of fragmented DNA of HIV-1-infected MT-4 cells co-cultured with P30-52 MAbs. Because DNA fragmentation is one of the features of programmed cell death, the viral multiplication may be suppressed by the apoptosis of HIV-1-infected MT-4 cells co-cultured with P30-52 MAbs. Though the relationship between cross-reactivity and the inhibition mechanism of multiplication of HIV-1 is unclear, P30-52 of p17 may well be a useful region of viral proteins for the development of therapeutic and vaccination strategies.