Combined downregulation of TGF-β1 and GRP78 is responsible for overcoming acquired sorafenib resistance, which is initiated by rewiring the cell surface CD44-GRP78-IGF-1R signaling circuit.

Previously, we showed that the downregulation of both HSP27 and TGF-β1 decreased the survival of various tumor types. However, we found that HSP27/TGF-β1 downregulation was less effective in acquired sorafenib-resistant HCC cell lines. As an alternative to HSP27/TGF-β1 downregulation to induce acute cell death in sorafenib-resistant cancer, we substituted shGRP78 for shHSP27 as a complement to shTGF-β1.

Enhanced tumor targeting and timely viral release of mesenchymal stem cells/oncolytic virus complex due to GRP78 and inducible E1B55K expressions greatly increase the antitumor effect of systemic treatment.

Systemic delivery of oncolytic viruses has been widely regarded as an impractical option for antitumor treatment. Here, we selected two target genes as leading components, and significant therapeutic effects were obtained by simultaneously reducing the expression of transforming growth factor β 1 (TGF-β1) and heat shock protein 27 (HSP27) in various cancer cell types. Downregulation of HSP27 reduced the cellular levels of tumor progression-related proteins, and the simultaneous downregulation of HSP27 and TGF-β1 increased tumor cell death beyond that observed with TGF-β1 downregulation alone.

Enhanced oncolytic adenoviral production by downregulation of death-domain associated protein and overexpression of precursor terminal protein.

Adequate viral replication in tumor cells is the key to improving the anti-cancer effects of oncolytic adenovirus therapy. In this study, we introduced short hairpin RNAs against death-domain associated protein (Daxx), a repressor of adenoviral replication, and precursor terminal protein (pTP), an initiator of adenoviral genome replication, into adenoviral constructs to determine their contributions to viral replication. Both Daxx downregulation and pTP overexpression increased viral production in variety of human cancer cell lines, and the enhanced production of virus progeny resulted in more cell lysis in vitro, and tumor regression in vivo.

High levels of Daxx due to low cellular levels of HSP25 in murine cancer cells result in inefficient adenovirus replication.

When the adenoviral protein E1B55K binds death domain-associated protein (Daxx), the proteasome-dependent degradation of Daxx is initiated, and adenoviral replication is effectively maintained. Here, we show that the cellular levels of Daxx differ between human and mouse cancer cell lines. Specifically, we observed higher cellular Daxx levels and the diminished replication of oncolytic adenovirus in mouse cancer cell lines, suggesting that cellular Daxx levels limit the replication of oncolytic adenoviruses that lack E1B55K in murine cells.

A case report of angioleiomyoma of uterus.

Angioleiomyoma (AL) is a very rare benign tumor that originates from smooth muscle cells and has thick walled vessels. It may be found throughout the body but more frequently occurs in the lower extremities and rarely develops in the head and other parts of the body. This paper presents a case report of giant AL detected in a 33-year-old woman who complained of severe anemia, menorrhagia, and palpable lower abdominal mass.

Uterine Serous Adenocarcinoma in an Elderly Postmenopausal Woman: Clinically Misdiagnosed as Uterine Cervix Cancer.

Uterine serous adenocarcinoma (USC) is rare and invasive cancer. This cancer is more often reported in the ovary, the fallopian tube, and the endometrium than uterine cervix. No matter where the tumor is located, the tumor exhibits similar histological characteristics.

Sclerosing stromal tumor in an elderly postmenopausal woman.

Sclerosing stromal tumor (SST) of the ovary is a rare tumor derived from the sex cord stroma. This tumor was first described by Chalvaridjian and Scully in 1973. SST of the ovary is prevalence of 1.