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Subject: search.filters.subject.hepatocellular carcinoma

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    Prevalence of K-Ras mutations in hepatocellular carcinoma: A Turkish Oncology Group pilot study
    (SPANDIDOS PUBL LTD, 2015-01-01) Turhal, Nazi Serdar; Savas, Berna; Coskun, Oznur; Bas, Emine; Karabulut, Bulent; Nart, Deniz; Korkmaz, Taner; Yavuzer, Dilek; Demir, Gokhan; Dogusoy, Gulen; Artac, Mehmet
    Hepatocellular carcinoma (HCC) is the fifth most common male-predominant type of cancer worldwide. There is no effective treatment regimen available for advanced-stage disease and chemotherapy is generally ineffective in these patients. The number of studies on the prevalence of K-Ras mutations in HCC patients is currently limited. A total of 58 patients from 6 comprehensive cancer centers in 4 metropolitan cities of Turkey were enrolled in this study. Each center committed to enroll approximately 10 random patients whose formalin-fixed paraffin-embedded tumor tissues were available for K-Ras, exon 2 genotyping. Two methods were applied based on the availability of adequate amounts of tumor DNA. In the first method, the samples were processed using TheraScreen. The genomic DNA was further used to detect the 7 most frequent somatic mutations (35G>A
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    Differential expression of full-length and NH2 terminally truncated FAM134B isoforms in normal physiology and cancer
    (AMER PHYSIOLOGICAL SOC, 2020-01-01) Keles, Umur; Iscan, Evin; Yilmaz, Huriye Erbak; Karakulah, Gokhan; Suner, Asli; Bal, Erhan; Tasdemir, Nilgun; Cavga, Ayse Derya; Ekin, Umut; Mutlu, Zeynep; Kahyaoglu, Sila; Serdar, Muhittin A.; Atabey, Nese; Ozturk, Mehmet
    Selective autophagy of the endoplasmic reticulum (ER), namely ER-phagy, is mediated by ER-localized receptors, which are recognized and sequestered by GABARAP/LC3B-decorated phagophores and transferred to lysosomes for degradation. Being one such receptor, FAM134B plays critical roles in cellular processes such as protein quality control and neuronal survival. FAM134B has also been associated with different cancers, although its exact role remains elusive. We report here that the FAM134B gene encodes not one but at least two different protein isoforms: the full-length and the NH2 terminally truncated forms. Their relative expression shows extreme variation, both within normal tissues and among cancer types. Expression of full-length FAM134B is restricted to the brain, testis, spleen, and prostate. In contrast, NH2 terminally truncated FAM134B is dominant in the heart, skeletal muscle, kidney, pancreas, and liver. We compared wild-type and knockout mice to study the role of the Fam134b gene in starvation. NH2 terminally truncated FAM134B-2 was induced in the liver, skeletal muscle, and heart but not in the pancreas and stomach following starvation. Upon starvation, Fam134b(-/-) mice differed from wild-type mice by less weight loss and less hyperaminoacidemic and hypocalcemic response but increased levels of serum albumin, total serum proteins, and a-amylase. Interestingly, either NH2 terminally truncated FAM134B or both isoforms were downregulated in liver, lung, and colon cancers. In contrast, upregulation was observed in stomach and chromophobe kidney cancers. NEW \& NOTEWORTHY We reported tissues expressing FAM134B2 such as the kidney, muscle, heart, and pancreas, some of which exhibit stimulated expression upon nutrient starvation. We also demonstrated the effect of Fam134b deletion during ad libitum and starvation conditions. Resistance to weight loss and hypocalcemia, accompanied by an increase in serum albumin and alpha-amylase levels, indicate critical roles of Fam134b in physiology. Furthermore, the differential expression of FAM134B isoforms was shown to be significantly dysregulated in human cancers.
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    Long-term Kinetics of Alpha-fetoprotein in Chronic Hepatitis C Patients Treated with Direct-acting Antivirals and Possible Predictive Role of AFP Response to Treatment on Development of Hepatocellular Carcinoma
    (GALENOS YAYINCILIK, 2021-01-01) Ulasoglu, Celal; Senates, Banu Erkalma; Yapali, Suna; Dumanoglu, Betul; Enc, Feruze; Colak, Yasar; Senates, Ebubekir
    Objectives: To evaluate the post-treatment upto fourth-year kinetics of alpha-fetoprotein (AFP) in patients with chronic hepatitis C (CHC) treated with direct-acting antiviral (DAA) drugs. Materials and Methods: In this retrospective, single-center study, 182 patients (124 female, 58 male) with CHC treated with DAA were included in the study. Biochemistry and AFP were recruited from the hospital database. The data at pre-treatment, 3rd and 48th month after the end of treatment were evaluated. Results: Of the 182 patients, mean age was 58 +/- 12 (28-76), and forty-nine (27\%) had cirrhosis. At month 3, the average decline of AFP was 35.6\% (0.4-97.0). Early decline of AFP <8.7\% was found to be a predictor for HCC development. Mean AFP was 7.7 +/- 9.2 ng/mL at pre-treatment and 3.8 +/- 2.7 at third month (p<0.001). The decline persisted at 48th month (3.6 +/- 2.4 ng/mL). Conclusion: Early decline of AFP and persistence at fourth-year after DAA treatment was observed, except five cases developing HCC. Inadequate decline in AFP level found to be a possible predictor for HCC development. However, these results needs to be confirmed in large-scale multicenter cohorts. This study highlights the importance of AFP response to DAA treatment in identifying HCC risk, especially in patients with cirrhosis.
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    Lack of hotspot mutations other than TP53 R249S in aflatoxin B1 associated hepatocellular carcinoma
    (WALTER DE GRUYTER GMBH, 2020-01-01) Akyerli, Cemaliye B.; Yuksel, Sirin K.; Yakicier, M. Cengiz
    Objective: Despite the recent advances in diagnosis and treatment of hepatocellular carcinoma (HCC), it is still a major health problem. Therefore, understanding the molecular mechanism is very important. Our aim is to investigate the molecular basis of aflatoxin B1 (AFB1) induced HCC other than the hotspot TP53 p.Arg249Ser (c.747G>T) (R249S) mutation. Methods: 525 genes previously reported to be involved in carcinogenesis with mutations in different cancer types were analyzed by next generation sequencing for 525 cancer-gene panel (Roche/NimbleGen) in one tumor sample (T29) and one cell line (MAHLAVU) carrying TP53 R249S mutation. Additionally, ARID2 and BCORL1 genes were analyzed by Sanger sequencing for MAHLAVU and Primary Liver Carcinoma/Poliomyelitis Research Foundation/5 (PLC/PRF/5) cell lines. Results: No other common gene mutations were found in the analyzed T29 and MAHLAVU samples and also no genetic variation possibly associated with AFB1 was detected in PLC/PRF/5 cell line and 68 COSMIC HCC samples. Likewise, no pathogenic mutation was detected in ARID2 and BCORL1 genes of MAHLAVU and PLC/PRF/5 cell lines. Conclusion: No fingerprint mutations were detected in the analyzed genes. To the best of our knowledge, other hotspot mutations appear to be absent if not at a very low frequency in HCC carrying TP53 R249S mutation.