Background: In the global scenario of public health, cervical cancer poses a major threat with high mortality rates, especially in women. New incidence cases and prevalence vary across different regions, as recently shown by GLOBOCAN data. The development of cervical cancer is primarily due to persistent infection by high-risk genotypes of human papillomavirus (HPV), which is a multifaceted process that is influenced by genetic, environmental, and lifestyle factors. Purpose: The goal of this study is to thoroughly investigate cervical cancer, including its etiology, molecular mechanisms, progression, diagnosis strategies, and current therapies. This review further highlights the transformative power of HPV vaccination and screening programs in curbing the disease’s burden and potentially promising novel approaches like immunotherapy and targeted therapy. Research Design: This is a narrative review article that summarizes previous literatures regarding cervical cancer in terms of molecular mechanism, etiology, clinical developments, and prevention. Study Sample: The review encompassed studies from diverse sources, including experimental, observational, and clinical research published between 1992 and 2025. Data Collection and/or Analysis: Data were collected through comprehensive literature searches using databases such as PubMed, Scopus, and the Cochrane Library with defined inclusion and exclusion criteria. Results: Nonetheless, there are gaps in research and controversies regarding vaccine coverage, screening practices, and treatment accessibility for poor populations. Precision medicine trends are emerging along with new biomarkers for early detection and personalized treatment, which also form part of this discussion. Key findings include the critical role of prevention measures in controlling the global impact of cervical cancer. Conclusions: The paper synthesizes the existing knowledge and identifies gaps that require further research, which is significant in augmenting prevention, diagnosis, and treatment of cervical cancer towards addressing its public health implications worldwide.

Jeong JH, et al. J Korean Med Sci. 2013 Jul;28(7):1005-1014. https://doi.org/10.3346/jkms.2013.28.7.1005

Oncolytic viruses are a promising class of anti-tumor agents; however, concerns regarding uncontrolled viral replication have led to the development of a replication-controllable oncolytic vaccinia virus (OVV). The engineering involves replacing the native thymidine kinase (VV-tk) gene, in a Wyeth strain vaccinia backbone, with the herpes simplex virus thymidine kinase (HSV-tk) gene, which allows for viral replication control via ganciclovir (GCV, an antiviral/cytotoxic pro-drug). Adding the wild-type HSV-tk gene might disrupt the tumor selectivity of VV-tk deleted OVVs; therefore, only engineered viruses that lacked tk activity were selected as candidates. Ultimately, OTS-412, which is an OVV containing a mutant HSV-tk, was chosen for characterization regarding tumor selectivity, sensitivity to GCV, and the influence of GCV on OTS-412 anti-tumor effects. OTS-412 demonstrated comparable replication and cytotoxicity to VV^tk- (control, a VV-tk deleted OVV) in multiple cancer cell lines. In HCT 116 mouse models, OTS-412 replication in tumors was reduced by >50% by GCV (p = 0.004); additionally, combination use of GCV did not compromise the anti-tumor effects of OTS-412. This is the first report of OTS-412, a VV-tk deleted OVV containing a mutant HSV-tk transgene, which demonstrates tumor selectivity and sensitivity to GCV. The HSV-tk/GCV combination provides a safety mechanism for future clinical applications of OTS-412.

The bone is a common site for metastasis in hepatocellular carcinoma (HCC). However, bone marrow metastasis from HCC is rarely reported, and its frequency is unclear. Here we report a rare case of bone marrow metastasis that presented as bicytopenia originating from HCC without bone metastasis. A 58-year-old man was admitted for investigation of a liver mass with extensive lymph node enlargement that was detected when examining his general weakness and weight loss. Laboratory findings revealed anemia, thrombocytopenia, mild elevated liver enzymes, normal prothrombin time percentage and high levels of tumor markers (α-fetoprotein and des-γ-carboxyprothrombin). Abdominal computed tomography showed multiple enhanced masses in the liver and multiple enlarged lymph nodes in the abdomen. A bone marrow biopsy revealed only a few normal hematopoietic cells and abundant tumor cells. Despite its rarity, bone marrow metastasis should always be suspected in HCC patients even if accompanied by cirrhosis.

Glioblastoma is an aggressive primary brain tumor that poses many therapeutic difficulties because of the high rate of proliferation, genetic variability, and its immunosuppressive microenvironment. The theory of cancer immunoediting, which includes the phases of elimination, equilibrium, and escape, offers a paradigm for comprehending interactions between the immune system and glioblastoma. Immunoediting indicates the process by which immune cells initially suppress tumor development, but thereafter select for immune-resistant versions leading to tumor escape and progression. The tumor microenvironment (TME) in glioblastoma is particularly immunosuppressive, with regulatory T cells and myeloid-derived suppressor cells being involved in immune escape. To achieve an efficient immunotherapy for glioblastoma, it is crucial to understand these mechanisms within the TME. Existing immunotherapeutic modalities such as chimeric antigen receptor T cells and immune checkpoint inhibitors have been met with some level of resistance because of the heterogeneous nature of the immune response to glioblastoma. Solving these issues is critical to develop novel strategies capable of modulating the TME and re-establishing normal immune monitoring. Further studies should be conducted to identify the molecular and cellular events that underlie the immunosuppressive tumor microenvironment in glioblastoma. Comprehending and modifying the stages of immunoediting in glioblastoma could facilitate the development of more potent and long-lasting therapies.

Autophagy is an ancient conserved and catabolic process required to maintain cellular homeostasis through sequestration and lysosomal degradation of cytosolic dysfunctional contents. The bulk degradation of cytosolic material through autophagy provides the necessary nutrients that cells utilize under starvation. Autophagy can play a mixed role in both the growth and survival of cancer cells. As a damaged cellular content-clearing mechanism, autophagy is involved in the early stage of tumor regression. Subsequently, in a mature tumor cell microenvironment, autophagy protects tumor cells from cellular stress, immune evasion, and therapeutic resistance. Therapeutic resistance mediated by autophagic regulators can make anticancer therapy less effective. This review discusses the molecular mechanism of mammalian autophagy, evaluates the dynamic role of autophagy in cancer, highlights autophagy-mediated therapeutic resistance, and suggests the use of biomarkers. In cancer therapy, the addition of biomarkers can provide specific identification, and the conjugation of biomarkers with chemo-drugs can reduce the side effects and ensure normal cell integrity.