Surgical smoke is the gaseous by-product produced by heat generating devices in various surgical operations including laser conization and loop electrosurgical procedures that often are performed by gynecologists. Surgical smoke contains chemicals, blood and tissue particles, bacteria, and viruses, which has been shown to exhibit potential risks for surgeons, nurses, anesthesiologists, and technicians in the operation room due to long term exposure of smoke. In this review, we describe the detailed information of the components of surgical smoke. Moreover, we highlight the effects of surgical smoke on carcinogenesis, mutagenesis, and infection in gynecologists. Furthermore, we discussed how to prevent the surgical smoke via using high-filtration masks and smoke evacuation systems as well as legal guidelines for protection measures among the gynecologists.

The nuclear speckle-type pox virus and zinc finger (POZ) protein (SPOP), a representative substrate-recognition subunit of the cullin-RING E3 ligase, has been characterized to play a dual role in tumorigenesis and cancer progression. Numerous studies have determined that SPOP suppresses tumorigenesis in a variety of human malignancies such as prostate, lung, colon, gastric, and liver cancers. However, several studies revealed that SPOP exhibited oncogenic function in kidney cancer, suggesting that SPOP could exert its biological function in a cancer type-specific manner. The role of SPOP in thyroid, cervical, ovarian, bone and neurologic cancers has yet to be determined. In this review article, we describe the structure and regulation of SPOP in human cancer. Moreover, we highlight the critical role of SPOP in tumorigenesis based on three major categories: physiological evidence (animal models), pathological evidence (human cancer specimens) and biochemical evidence (downstream ubiquitin substrates). Furthermore, we note that SPOP could be a promising therapeutic target for cancer treatment.

E-cadherin plays a pivotal role in cancer progression, including the epithelial-mesenchymal transition (EMT) process and tumor metastasis. Loss of E-cadherin contributes to enhanced invasion and metastasis in human cancers. Therefore, restoring E-cadherin could be a potential approach for cancer therapy. Multiple natural compounds have been shown to possess anti-tumor activities through the regulation of key molecules in signaling pathways, including E-cadherin. In this review, we describe the numerous compounds that restore the expression of E-cadherin in genital and urinary malignancies. We further discuss the potential anti-tumor molecular mechanisms of these agents as the activators of E-cadherin in genital and urinary cancers. Although these compounds exhibit their potential to inhibit the development and progression of cancers, there are several challenges to developing them as therapeutic drugs for cancer patients. Poor bioavailability in vivo is the main disadvantage of these compounds. Modification of compound structures has produced actual improvements in bioavailability. Nanoparticle-based delivery systems could be useful to deliver the agents to targeted organs. These compounds could be new promising therapeutic agents for the treatment of human genital and urinary cancers. Further investigations are required to determine the safety and side effects of natural compounds using animal models prior to clinical trials.

Accumulated evidence has demonstrated that WNT1 inducible signaling pathway protein (WISP) genes, which belong to members of the CCN growth factor family, play a pivotal role in tumorigenesis and progression of a broad spectrum of human cancers. Mounting studies have identified that WISP proteins (WISP1-3) exert different biological functions in various human malignancies. Emerging evidence indicates that WISP proteins are critically involved in cell proliferation, apoptosis, invasion and metastasis in cancers. Because the understanding of a direct function of WISP proteins in cancer development and progression has begun to emerge, in this review article, we describe the physiological function of WISP proteins in a variety of human cancers. Moreover, we highlight the current understanding of how the WISP protein is involved in tumorigenesis and cancer progression. Furthermore, we discuss that targeting WISP proteins could be a promising strategy for the treatment of human cancers. Hence, the regulation of WISP proteins could improve treatments for cancer patients.