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Background: Human endogenous retrovirus (HERV)-K is a type of retrovirus that is present in the human genome, and its expression is usually silenced in healthy tissues. The precise mechanism by which HERV-K env influences cancer stemness is not fully understood, but it has been suggested that HERV-K env may activate various signaling pathways that promote stemness traits in cancer cells. Objective: To establish the connection between HERV-K env expression and cancer stemness in ovarian cancer cells, we carried out correlation analyses between HERV-K env and the cancer stem cell (CSC) marker known as the cluster of differentiation 133 (CD133) gene in SKOV3 ovarian cancer cells. Method: To perform correlation analysis between HERV-K env and CSCs, ovarian cancer cells were cultured in a medium designed for cancer stem cell induction. The expression of HERV-K env and CD133 genes was verified using quantitative real-time polymerase chain reaction (RT-qPCR) and Western blot analyses. Additionally, the expression of stemness-related markers, such as OCT-4 and Nanog, was also confirmed using RT-qPCR. Results: In the stem cell induction medium, the number of tumorsphere-type SKOV3 cells increased, and the expression of CD133 and HERV-K env genes was up-regulated. Additionally, other stemness-related markers like OCT-4 and Nanog also exhibited increased expression when cultured in the cancer stem cell induction medium. However, when HERV-K env knockout (KO) SKOV3 cells were cultured in the same cancer stem cell induction medium, there was a significant decrease in the number of tumorsphere-type cells compared to mock SKOV3 cells subjected to the same conditions. Furthermore, the expression of CD133, Nanog, and OCT-4 did not show a significant increase in HERV-K env KO SKOV3 cells compared to mock SKOV3 cells cultured in the same cancer stem cell induction medium. Conclusion: These findings indicate that the expression of HERV-K env increased in SKOV3 cells when cultured in cancer stem cell induction media, and cancer stem cell induction was inhibited by KO of HERV-K env in SKOV3 cells. These results suggest a strong association between HERV-K env and stemness in SKOV3 ovarian cancer cells. [ABSTRACT FROM AUTHOR]

Colorectal cancer (CRC) ranks among the world’s most prevalent cancers, annually claiming tens of thousands of lives. Early detection of tumor DNA in serum/plasma before metastasis can significantly enhance patient outcomes post-tumor removal. Recent advances in detecting tumor DNA in serum/plasma have catalyzed many new research directions and opportunities for molecular diagnostics. This article synthesizes data from approximately 45 research and review papers, representing the latest findings in this field. Specifically, 30 research articles from databases such as PubMed, Web of Science, Scopus, and Google Scholar were reviewed to investigate the diagnostic significance of Oct-4 in CRC. These articles focused on tissue samples from CRC and adjacent non-tumor tissues.Oct-4, an octamer-binding transcription factor, is crucial for developing embryonic stem and germ cells. Moreover, it plays a vital role in preserving cancer stem-like characteristics in specific tumor types, making it a pivotal biomarker for cancer stem cells. Our study indicates a strong association between Oct-4 expression and CRC. Primary CRC tissues, matched non-tumor tissues, and benign polyp tissues, each representing different carcinogenesis stages, were analyzed to substantiate this claim. Oct-4 expression was quantified through reverse transcription polymerase chain reaction, flow cytometry, and immunohistochemistry analyses.Furthermore, medical records of CRC patients were examined, and clinical pathology analyses were conducted to assess the correlation between Oct-4 expression and specific clinical pathology features. Findings reveal a progressive increase in Oct- 4 transcription and translation from non-tumor tissues to benign polyp tissues and from benign polyps to CRC tissues. These observations suggest that aberrant Oct-4 expression may significantly contribute to the development of CRC.

Objective: To establish the connection between human endogenous retrovirus (HERV)-K env expression and cancer stemness in ovarian cancer cells, we carried out correlation analyses between HERV-K env and the cancer stem cell (CSC) marker known as the cluster of differentiation 133 (CD133) gene in SKOV3 ovarian cancer cells. Methods: To perform correlation analysis between HERV-K env and CSCs, ovarian cancer cells were cultured in a medium designed for CSC induction. The expression of HERV-K env and CD133 genes was verified using quantitative real-time polymerase chain reaction (RT-qPCR) and Western blot analyses. Additionally, the expression of stemness-related markers, such as OCT-4 and Nanog, was also confirmed using RT-qPCR. Results: In the stem cell induction medium, the number of tumorsphere-type SKOV3 cells increased, and the expression of CD133 and HERV-K env genes was up-regulated. Additionally, other stemness-related markers like OCT-4 and Nanog also exhibited increased expression when cultured in the CSC induction medium. However, when HERV-K env knockout (KO) SKOV3 cells were cultured in the same CSC induction medium, there was a significant decrease in the number of tumorspheretype cells compared to mock SKOV3 cells subjected to the same conditions. Furthermore, the expression of CD133, Nanog, and OCT-4 did not show a significant increase in HERV-K env KO SKOV3 cells compared to mock SKOV3 cells cultured in the same CSC induction medium. Conclusion: These results suggest a strong association between HERV-K env and stemness in SKOV3 ovarian cancer cells. [ABSTRACT FROM AUTHOR]

Objetivo: Describir las características clínico-patológicas de pacientes con Astrocitoma de Células Gigantes Subependimario (SEGA), en el INNN (2013-2022) y evaluar el perfil de expresión de nuevos marcadores mediante inmunohistoquímica (IHQ). Antecedentes: El SEGA es un tumor benigno de bajo grado, generalmente asociado al complejo de esclerosis tuberosa (TSC), un síndrome hereditario autosómico dominante, por mutación en los genes TSC1 o TSC2. Métodos: Realizamos un estudio descriptivo, retrospectivo y comparativo, bajo el protocolo 36/23, que incluyó a todos los pacientes con diagnóstico de SEGA que fueron sometidos a cirugía entre enero de 2013 y diciembre de 2022. Se obtuvieron datos clínicos y paraclínicos de expedientes. Se aplicó panel de IHQ (NF, GFAP, hamartina, tuberina, Ki67, nestina, OCT-4, INI1, STAT-6, CKAE1/AE3). Se realizó análisis estadístico de los datos recolectados. Resultados: Se incluyeron 4 pacientes, dos de los cuales (23 y 25 años) tenían diagnóstico previo de TSC (10 y 12 años) y dos (18 y 46 años) no presentaban datos clínico-radiológicos de TSC. Un caso de TSC experimentó recidiva y fue sometido a reintervención. Todos los casos fueron positivos para NF, GFAP y nestina en células tumorales, con Ki67 (-). Uno de los casos sin TSC y uno con, no expresaron tuberina ni hamartina, mientras que el otro caso sin TSC, mostró (+) homogénea citoplásmica para hamartina y en mosaico (tinción positiva y negativa) para tuberina. El paciente con TSC ostentó hamartina (+), pero tuberina (-). Para OCT-4, la positividad citoplasmica intensa se observó en las células tumorales de los 2 casos con TSC; en los otros, uno no expresó y en el otro, la tinción fue en células endoteliales, pericitos y escasos astrocitos en contacto con células neoplásicas. Todos los casos fueron positivo (citoplasma y en procesos) para STAT-6 y CK. Para INI1, los casos con TSC mostraron tinción nuclear intensa y tenue tinción citoplásmica; en los casos sin TSC, uno tuvo tinción nuclear y otro, solo citoplásmica. Conclusiones: SEGA expresa marcadores de células madre neuroepiteliales, lo que explica su naturaleza dual, y la capacidad, como se demostró, de expresar CK, un marcador epitelial. El estudio de IHQ mostró perfiles diferentes en SEGA asociado a TSC de los "esporádicos", se demostró por primera vez, positividad en OCT-4, STAT-6 e INI1 en estos tumores. La expresión de la proteina salvaje harmatina y tuberina fue variable. La expresión de OCT-4 que se sabe modula la via mTOR, puede ser un blanco terapéutico adicional, asociado a inhibidores de esta vía. [ABSTRACT FROM AUTHOR]