Someone said that Topotecan worked better when combined with thalidomide -- don't know much more about it than that, although when I have chemo again (when the Arimidex doesn't hold my counts steady anymore) they are threatening me with topotecan next.
an individual gets priority on the liver transplant list if the tumor is 2 cms in size or greater. the chance of locoregional therapy to cure HCC is small, but the cure rate is greater when the lesion is smaller. if the liver function is compromised and you need a transplant from that perspective it is reasonable, but if the HCC would be the only inidcation for transplantation, early locoregional therapy can be considered to obviate the potential need for transplantation.
AFP is a blood marker for liver cancer. HCC. But, it is NOT an accurate predictor of HCC. If you mean will the blood level go down after treatment I don't know. Maybe someone else knows.
If you have HCC, treatment will not cure the cancer. HCC is particuliar fast and fatal illness. If you are a cirrhotic, with Stage 4 liver disease, you should have a scan (CT triple phase is what I have had done) done every 6 months to monitor for HCC.
Some long-term studies found that even most potent NA (TDF) could not cut risk of HCC. Especially, when we have had this virus for a long time and it already integrated in our genome.
HCC is very complicated if cure (cccDNA - & anti-hbs +) could not achieve, the risk of HCC remains higher.
The current work was designed to determine the level of prothrombin induced by vitamin K absence-II (PIVKA-II) in sera of patients suffering from HCC and hepatitis C virus (HCV) patients being the most common predisposing factor for HCC. Our ultimate goal is diagnosis of HCC at its early stage. The current study was carried out on 83 individuals within three groups; Normal control, HCV and HCC groups. Patients were subdivided into cirrhotic and non-cirrhotic.
HCC is almost always diagnosed using MRI or sometimes CT with and without contrast.which reveals the blood flow characteristics of HCC. All HCC grows, like all cancers. So anything that stays the same size is not cancer. That is the vary definition of cancer. That is why when someone has HCC their AFP while continually rise into the hundreds or thousands.
Hemangioma is the most common benign lesion found in the liver. It is a bundle of blood vessels. It can NEVER turn into cancer.
The finding turns conventional thinking on its head as it is generally stated that successful use of oral nucleso(t)ide analogues (NUCs) decreases HCC risk, the authors from the Sungkyunkwan University School of Medicine in Seoul said.
Involving over 2300 CHB patients, the study showed 7.7% of those started on NUC therapy had developed HCC within 42 months compared with just 1.1% in the inactive CHB group.
If you didn’t have cirrhosis it would be very rare for you to develop HCC now. If you did have cirrhosis than being SVR does reduce the chances of developing HCC, but does not reduce it to the level of risk that a person who never had cirrhosis has. So there always is a possibility if a person had cirrhosis in the past at any time they can develop HCC. That is why HCC surveillance is recommended for patients even if they are now SVR.
Let me make a few assumptions here to save time.
Does anyone know what are the success rates of multifocal HCC also in the liver portal , liver in good shape, Cirrhosis stage A, with systemic Immunotherapy?
Significant clinical variations exist among patients with the most common type of liver cancer called hepatocellular carcinoma (HCC), depending on the viral cause of the disease -hepatitis B virus (HBV) or hepatitis C virus (HCV). These differences suggest that hepatitis status should be considered when developing treatment plans for newly diagnosed patients, according to researchers at The University of Texas MD Anderson Cancer Center.
my question is inactive carrier at first must be active diseas (high level ALT) and then develop cirrohs and hcc or no they can develop hcc in inactive state with normal ALT???
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