Kelpikov* and Marion Howard
DOI: 10.37421/1948-5956.2023.15.596
Ilham Khalfaoui
Cholestatic jaundice as the initial symptom in patients with metastatic prostate cancer is extremely rare. Few cases only of paraneoplasic cholestatic jaundice associated with prostate cancer have been reported in the literature. We present a case of 57 years old patient who presented cholestatic jaundice revealing an underlying metastatic prostate cancer after detailed examinations including Computed Tomography (CT), Magnetic Resonance Imaging (MRI), Positon Emission Tomography (PET), and Endoscopic Retrograde Cholangiopancreatography (ERCP). Cholestatic jaundice may be brought on by malignancies via identified pathways (e.g., bile duct obstruction or widespread hepatic infiltration). Through an unknown pathogenetic mechanism, paraneoplastic syndromes connected to malignancy, particularly renal cell carcinoma (Stauffer's syndrome) and malignant lymphoproliferative disorders, can cause a reversible form of cholestasis. There have been two cases documented in the medical literature of prostate cancer that originally manifested as cholestatic jaundice without any clear reason (i.e., blockage or invasion). We describe a patient who had pruritus and cholestatic jaundice when they first arrived. The diagnosis of prostate cancer was made throughout the diagnostic process. Conjugated bilirubin and alkaline phosphatase levels significantly rose, but transaminase and glutamyltranspeptidase levels only slightly increased. No signs of extrahepatic biliary blockage or hepatic metastases were found, according to the findings of the necessary studies carried out while the patient was hospitalised.
Cheryl Anandas, Shobhit Srivastava* and Himani Sharma
According to the NICPR in the year 2010, the average estimated prevalence of cancer was 25 lakhs and incidence was about 07 lakhs in India, there were 5.56 lakh deaths due to cancer. The study is based on data from NFHS (2015-16). Univariate and Bivariate analysis and Poisson regression models were used to establish an association between all independent predictors and outcome variable. Among both women and men, asthma and diabetes emerged as the main determinants for cancer prevalence. Women who smoke tobacco are 1.76 times significantly more likely to get cancer whereas in case of men who smoke are 2.65 times significantly more likely to get cancer. Among both women and men, non-vegetarian diet emerged to be important determinants for cancer prevalence i.e. (IRR=1.58, P<0.05) for women and (IRR=3.17, P<0.05) for men. Among women who are exposed to arsenic through groundwater are 1.81 times significantly more likely to get cancer. From the study, it has been found that asthma and diabetes among biological factors; tobacco and alcohol consumption, consumption of non-vegetarian food and arsenic exposure (only among women) among behavioral factors are the main determinants of cancer prevalence among both men and women in India.
Musadiq Ali*
There are many genes that have been explored in relation with cancer. But 50 percent of cancers occur due to mutation in P53. In the beginning, there was a thought that P53 act as an oncogenic protein instead of suppressing cancers. Now we have reached on conclusion that mutant P53 instead of wild type, act as an oncogenic protein. Through research carried out in the past, it has been concluded that gain of function mutation in the P53 has early onset of cancer as compared to mutant P53 with loss of function. A number of hotspots for mutation in P53 such as R175, G245, R248, R249, R273 and R282 have been identified in the past. Mutant P53 interact and inhibit proteins normal functioning such as p63, MRE11, Rad51-NSB complex, p73 and Sp-1. Mutant P53 also lead to enhance functioning of protein such as SREBP, NF-Y, VDR, ETS2 and NRF2. For proper folding of wild type P53 Zn+2 is necessary. There are microRNAs which are under the control of mutant P53. Mostly, PRIMA-1 analog has been used to reactivate the mutant P53 to wild type.
Albert Rikz*
DOI: 10.37421/1948-5956.2022.14.554
Brian Carr*, Vito Guerra, Ümit Karaoğullarından, Hikmet Akkiz, Volkan Ince, Burak Isik and Sezai Yilmaz
Introduction: Survival in patients with Hepatocellular Carcinoma (HCC) has been previously found to be worse with increase in tumor size, but also with increase in inflammation. To examine these issues separately, we aimed to study the influences on survival of various liver inflammation parameters in the whole cohort, and separately in patients with HCCs of defined Maximum Tumor Diameter (MTD).
Methods: A prospectively collected large database of Turkish HCC patients with documented survival was interrogated. Patients had baseline liver function tests and CT scans for tumor characteristics. Liver function and inflammation parameters included blood tests for levels of albumin, AST, GGT, ALKP, CRP, ESR and WBC.
Results: Survival was worse for patients with larger HCCs, including those with low or high serum AFP levels. Highest hazard ratios were found for patients with abnormal blood albumin (low) or AST (high) levels, regardless of AFP status. When patients were separately examined according to tumor size, only albumin and AST were significant for survival in patients with small <3cm tumors; whereas albumin, AST and ALKP were significant in patients with >3cm HCCs. Abnormal albumin or AST levels in different HCC size cohorts significantly related to percent patients with PVT, higher AFP or increased tumor focality, regardless of tumor size.
Results: Survival was worse for patients with larger HCCs, including those with low or high serum AFP levels. Highest hazard ratios were found for patients with abnormal blood albumin (low) or AST (high) levels, regardless of AFP status. When patients were separately examined according to tumor size, only albumin and AST were significant for survival in patients with small <3cm tumors; whereas albumin, AST and ALKP were significant in patients with >3cm HCCs. Abnormal albumin or AST levels in different HCC size cohorts significantly related to percent patients with PVT, higher AFP or increased tumor focality, regardless of tumor size.
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