https://www.emcdda.europa.eu/attachements.cfm/att_231442_EN_INT17_easl-recommendations-on-treatment-of-hepatitis-C.pdf

EASL Recommendations on Treatment of Hepatitis C

https://aasldpubs.onlinelibrary.wiley.com/doi/pdf/10.1002/hep.23527

The Incidence and Risk Factors of Hepatocellular Carcinoma in Patients with Nonalcoholic Steatohepatitis

https://www.liver.theclinics.com/article/S1089-3261(04)00130-8/pdf

Epidemiology of hepatocellular carcinoma.

https://aasldpubs.onlinelibrary.wiley.com/doi/pdf/10.1002/hep.22898

The natural history of chronic hepatitis B virus infection.

Hepatitis C and hepatocellular carcinoma

https://www.gastrojournal.org/article/S0016-5085(97)70233-6/pdf

The relative roles of hepatitis B and C viruses in the etiology of hepatocellular carcinoma in Southern African blacks

Does hepatitis GB virus‐C infection cause hepatocellular carcinoma in black Africans?

(1) Background: Glioblastoma multiforme (GBM) is the most common and malignant intracranial tumor in adults. At present, temozolomide (TMZ) is recognized as the preferred chemotherapeutic drug for GBM, but some patients have low sensitivity to TMZ or chemotherapy resistance to TMZ. Our previous study found that GBM patients with EGFRvIII (+) have low sensitivity to TMZ. However, the reasons and possible mechanisms of the chemoradiotherapy resistance in GBM patients with EGFRvIII (+) are not clear. (2) Methods: In this study, tissue samples of patients with GBM, GBM cell lines, glioma stem cell lines, and NSG mice were used to explore the causes and possible mechanisms of low sensitivity to TMZ in patients with EGFRvIII (+)-GBM. (3) Results: The study found that EGFRvIII promoted the proneural–mesenchymal transition of GBM and reduced its sensitivity to TMZ, and EGFRvIII regulated of the expression of ALDH1A3. (4) Conclusions: EGFRvIII activated the NF-κB pathway and further regulated the expression of ALDH1A3 to promote the proneural–mesenchymal transition of GBM and reduce its sensitivity to TMZ, which will provide an experimental basis for the selection of clinical drugs for GBM patients with EGFRvIII (+).

/pdf/egfrviii-promotes-the-proneural-mesenchymal-transition-of-2un4wwvp.pdf

EGFRvIII Promotes the Proneural–Mesenchymal Transition of Glioblastoma Multiforme and Reduces Its Sensitivity to Temozolomide by Regulating the NF-κB/ALDH1A3 Axis

MC Yu

Papers

The relative roles of hepatitis B and C viruses in the etiology of hepatocellular carcinoma in Southern African blacks

Does hepatitis GB virus‐C infection cause hepatocellular carcinoma in black Africans?

EGFRvIII Promotes the Proneural–Mesenchymal Transition of Glioblastoma Multiforme and Reduces Its Sensitivity to Temozolomide by Regulating the NF-κB/ALDH1A3 Axis

Immunological profiles of human oligodendrogliomas define two distinct molecular subtypes