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Journal articles on the topic 'Hepatocellular carcinoma'

Author: Grafiati

Published: 4 June 2021

Last updated: 12 April 2025

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1

CHEDID, Marcio F., Cleber R. P. KRUEL, Marcelo A. PINTO, Tomaz J. M. GREZZANA-FILHO, Ian LEIPNITZ, Cleber D. P. KRUEL, Leandro A. SCAFFARO, and Aljamir D. CHEDID. "HEPATOCELLULAR CARCINOMA: DIAGNOSIS AND OPERATIVE MANAGEMENT." ABCD. Arquivos Brasileiros de Cirurgia Digestiva (São Paulo) 30, no. 4 (December 2017): 272–78. http://dx.doi.org/10.1590/0102-6720201700040011.

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ABSTRACT Introduction: Hepatocellular carcinoma is an aggressive malignant tumor with high lethality. Aim: To review diagnosis and management of hepatocellular carcinoma. Methods: Literature review using web databases Medline/PubMed. Results: Hepatocellular carcinoma is a common complication of hepatic cirrhosis. Chronic viral hepatitis B and C also constitute as risk factors for its development. In patients with cirrhosis, hepatocelular carcinoma usually rises upon malignant transformation of a dysplastic regenerative nodule. Differential diagnosis with other liver tumors is obtained through computed tomography scan with intravenous contrast. Magnetic resonance may be helpful in some instances. The only potentially curative treatment for hepatocellular carcinoma is tumor resection, which may be performed through partial liver resection or liver transplantation. Only 15% of all hepatocellular carcinomas are amenable to operative treatment. Patients with Child C liver cirrhosis are not amenable to partial liver resections. The only curative treatment for hepatocellular carcinomas in patients with Child C cirrhosis is liver transplantation. In most countries, only patients with hepatocellular carcinoma under Milan Criteria are considered candidates to a liver transplant. Conclusion: Hepatocellular carcinoma is potentially curable if discovered in its initial stages. Medical staff should be familiar with strategies for early diagnosis and treatment of hepatocellular carcinoma as a way to decrease mortality associated with this malignant neoplasm.

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Hotta, Akihiro, Masaki Ishikawa, Toshihiro Tachikake, Noriaki Matsuura, Naoyuki Toyota, and Kazuo Awai. "Comparison of the effectiveness of celiac versus common hepatic artery injection for the detection of hepatocellular carcinoma and of the feeding artery on cone-beam computed tomographs obtained during hepatic angiography." Acta Radiologica Open 10, no. 2 (February 2021): 205846012199473. http://dx.doi.org/10.1177/2058460121994735.

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Background Cone-beam computed tomography (CBCT) has been widely used during transcatheter arterial chemoembolization for hepatocellular carcinoma. Purpose To evaluate the sensitivity of CBCT for the detection of hepatocellular carcinomas and the tumor feeders by comparing celiac artery (CA) and common hepatic artery (CHA) injection. Material and methods We retrospectively enrolled 30 patients (52 hepatocellular carcinoma lesions) who had undergone CBCT-assisted transcatheter arterial chemoembolization. In 17 procedures (28 hepatocellular carcinomas) we acquired CBCT scans using CA injections (CBCT-CA) and in 18 (24 hepatocellular carcinomas) we used CHA injections (CBCT-CHA). Of the 30 patients, 5 underwent CBCT-CA and CBCT-CHA at different transcatheter arterial chemoembolization procedures. We performed inter-group comparisons of the detectability of hepatocellular carcinoma, the feeding artery, the intrahepatic artery branch order, and the tumor-to-liver contrast. Results CBCT-CA detected all 28 hepatocellular carcinomas and 27 of their feeders (96.4%); CBCT-CHA identified 22 of 24 hepatocellular carcinomas (91.7%) and 21 of their feeders (95.5%). There was no significant inter-group difference in the detectability of hepatocellular carcinoma lesions (p = 0.21) or feeding arteries (p = 0.69). CBCT-CHA was superior for the assessment of the tumor-to-liver contrast and the intrahepatic artery branch order (both: p < 0.01). Conclusion CBCT-CA and CBCT-CHA were equally useful for the detection of hepatocellular carcinoma and of the feeding artery, although CBCT-CHA yields better visualization of hepatocellular carcinoma and the hepatic artery. Thus CA injection seems sufficient for lesion and vessel detection when the insertion of an angiographic catheter into the CHA is difficult.

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Van Treeck, Benjamin J., Taofic Mounajjed, Roger K. Moreira, Mushfig Orujov, Daniela S. Allende, Andrew M. Bellizzi, Stephen M. Lagana, Jaime I. Davila, Erik Jessen, and Rondell P. Graham. "Transcriptomic and Proteomic Analysis of Steatohepatitic Hepatocellular Carcinoma Reveals Novel Distinct Biologic Features." American Journal of Clinical Pathology 155, no. 1 (September 4, 2020): 87–96. http://dx.doi.org/10.1093/ajcp/aqaa114.

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Abstract Objectives Steatohepatitic hepatocellular carcinoma is a distinct variant of hepatocellular carcinoma strongly associated with underlying nonalcoholic steatohepatitis. The molecular biology of steatohepatitic hepatocellular carcinoma is not fully elucidated, and thus we aimed to investigate the molecular underpinnings of this entity. Methods Transcriptomic analysis using RNAseq was performed on eight tumor-nonneoplastic pairs of steatohepatitic hepatocellular carcinoma with comparison to conventional hepatocellular carcinoma transcriptomes curated in The Cancer Genome Atlas. Immunohistochemistry was used to validate key RNA-level findings. Results Steatohepatitic hepatocellular carcinoma demonstrated a distinctive differential gene expression profile compared with The Cancer Genome Atlas curated conventional hepatocellular carcinomas (n = 360 cases), indicating the distinctive steatohepatitic hepatocellular carcinoma morphology is associated with a unique gene expression profile. Pathway analysis comparing tumor-nonneoplastic pairs revealed significant upregulation of the hedgehog pathway based on GLI1 overexpression and significant downregulation of carnitine palmitoyltransferase 2 transcript. Glutamine synthetase transcript was significantly upregulated, and fatty acid binding protein 1 transcript was significantly downregulated and immunohistochemically confirmed, indicating steatohepatitic hepatocellular carcinoma tumor cells display a zone 3 phenotype. Conclusions Steatohepatitic hepatocellular carcinoma demonstrates a distinctive morphology and gene expression profile, phenotype of zone 3 hepatocytes, and activation of the hedgehog pathway and repression of carnitine palmitoyltransferase 2, which may be important in tumorigenesis.

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Takamura, Hiroyuki, Ryousuke Gabata, Yoshinao Obatake, Shinichi Nakanuma, Hironori Hayashi, Kazuto Kozaka, Motoko Sasaki, et al. "Clinical features and diagnostic imaging of cholangiolocellular carcinoma compared with other primary liver cancers: a surgical perspective." Technology in Cancer Research & Treatment 19 (January 1, 2020): 153303382094814. http://dx.doi.org/10.1177/1533033820948141.

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Background and Objectives: Although cholangiolocellular carcinoma is considered a combined hepatocellular and cholangiocarcinoma, we feel that this classification is not appropriate. Therefore, we compared the diagnostic imaging findings, surgical prognosis, and pathological features of cholangiolocellular carcinoma with those of other combined hepatocellular and cholangiocarcinoma subtypes, hepatocellular carcinoma, and cholangiocarcinoma. Methods: The study patients included 7 with classical type combined hepatocellular and cholangiocarcinoma; 8 with stem cell feature, intermediate type combined hepatocellular and cholangiocarcinoma; 13 with cholangiolocellular carcinoma; 58 with cholangiocarcinoma; and 359 with hepatocellular carcinoma. All patients underwent hepatectomy or living-related donor liver transplantation from 2001 to 2014. Results: cholangiolocellular carcinoma could be distinguished from hepatocellular carcinom, other combined hepatocellular and cholangiocarcinoma subtypes, and cholangiocarcinoma by the presence of intratumoral Glisson’s pedicle, hepatic vein penetration, and tumor-staining pattern on angiography-assisted CT. Cholangiolocellular carcinoma was associated with a significantly lower SUV-max than that of cholangiocarcinoma on FDG-PET. Hepatocellular carcinoma, classical type, and cholangiolocellular carcinoma had significantly better prognoses than stem cell feature, intermediate type and cholangiocarcinoma. A cholangiocarcinoma component was detected in cholangiolocellular carcinoma that progressed to the hepatic hilum, and the cholangiocarcinoma component was found in perineural invasion and lymph node metastases. Conclusions: From the viewpoint of surgeon, cholangiolocellular carcinoma should be classified as a good-prognosis subtype of biliary tract carcinoma because of its tendency to differentiate into cholangiocarcinoma during its progression, and its distinctive imaging and few recurrence rates different from other combined hepatocellular and cholangiocarcinoma subtypes.

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Ozaki, I., K. Yamamoto, T. Mizuta, S. Kajihara, N. Fukushima, Y. Setoguchi, F. Morito, and T. Sakai. "Differential expression of laminin receptors in human hepatocellular carcinoma." Gut 43, no. 6 (December 1, 1998): 837–42. http://dx.doi.org/10.1136/gut.43.6.837.

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Background—Laminin receptors are involved in cell-extracellular matrix interactions in malignant cells that show invasion and metastasis. Hepatocellular carcinoma frequently shows early invasion into blood vessels, and intrahepatic and extrahepatic metastases. However, the role of laminin receptors in hepatocellular carcinoma is unknown.Aims—To examine the expression of mRNA for laminin receptors and their isoforms in hepatocellular carcinoma.Methods—The expression of several laminin receptors, including α1 integrin, α6 integrin and its isoforms α6A and α6B, β1 integrin and its isoforms β1A and β1B, and 32kD/67kDa laminin binding protein was examined in human hepatocellular carcinomas and non-cancerous liver tissues using the reverse transcription polymerase chain reaction.Results—α6 Integrin, β1 integrin, and laminin binding protein showed notably increased expression in hepatocellular carcinoma, compared with non-cancerous liver tissue, although the α1 integrin did not show a significant change. Furthermore, β1B integrin, a splicing variant of β1 integrin, was overexpressed in hepatocellular carcinoma while the β1A integrin isoform did not show significant changes between hepatocellular carcinoma and surrounding non-cancerous liver tissue.Conclusions—The differential upregulation of laminin receptors and their splicing isoforms was shown in hepatocellular carcinoma, suggesting that certain laminin receptors and their isoforms may be involved in the development and progression of hepatocellular carcinoma.

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Molina, D. Kimberley, and Philip T. Valente. "Lymphangitic Spread of Hepatocellular Carcinoma." Archives of Pathology & Laboratory Medicine 127, no. 1 (January 1, 2003): e11-e13. http://dx.doi.org/10.5858/2003-127-e11-lsoh.

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Abstract Pulmonary lymphangitic carcinomatosis is a well-documented phenomenon caused by spread of carcinoma to the pulmonary vasculature and lymphatics, often resulting in respiratory failure and cor pulmonale. It has been described in numerous types of carcinoma, most commonly occurring with carcinomas of the breast and stomach and with choriocarcinoma. We report the case of a patient who presented with increasing shortness of breath and dyspnea on exertion. Autopsy findings revealed diffuse pulmonary vascular spread of a hepatocellular carcinoma to the lungs. To our knowledge, this is the first reported case of lymphangitic spread of a hepatocellular carcinoma causing respiratory compromise (lymphangitic carcinomatosis).

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Takeuchi, Tamotsu, Yoshihiro Adachi, and Tomoko Nagayama. "Expression of a Secretory Protein C1qTNF6, a C1qTNF Family Member, in Hepatocellular Carcinoma." Analytical Cellular Pathology 34, no. 3 (2011): 113–21. http://dx.doi.org/10.1155/2011/578097.

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Background: Recent studies have revealed that the adiponectin-associated protein belonging to the C1qTNF family mediates various biological processes. However, the pathobiological property of C1qTNF6 in carcinogenesis remains unclear. Here, we investigated the expression status of C1qTNF6 in human hepatocellular carcinomas and subsequently attempted to determine the role of C1qTNF6 in tumor neovascularization. Methods: Immunohistochemical staining was performed to evaluate the expression of C1qTNF6 in hepatocellular carcinoma tissue specimens. Various eukaryotic recombinant C1qTNF6 proteins were prepared to ask whether C1qTNF6 could activate Akt pathway in human liver sinusoidal microvascular endothelial cells. Xenograft assay was carried out to know the effect of C1qTNF6 on tumor neovascularization. Results: C1qTNF6 was not immunohistochemically detected in any non-cancerous liver tissues but was detected in 21 of 30 hepatocellular carcinoma tissue specimens. C1qTNF6 was not uniformly distributed but rather focally localized in hepatocellular carcinoma cells. Interestingly, it was also localized on the tumor endothelial cells, which were in close proximity of C1qTNF6-expressing hepatocellular carcinoma cells. Eukaryotic recombinant C1qTNF6 increased the level of active phosphorylated Akt molecules in cultured vascular endothelial cells via its C-terminal C1q domain. In the xenograft assay, enforced expression of C1qTNF6 markedly reduced the central hypovascular necrosis areas of the transplanted HepG2 hepatocellular carcinoma cells. Conclusion: These results indicate that C1qTNF6 is overexpressed and possibly contributes to tumor angiogenesis by activating the Akt pathway in many hepatocellular carcinomas.

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Nguyen, Thuy, Daniel Phillips, Dhanpat Jain, Michael Torbenson, Tsung-Teh Wu, Matthew M. Yeh, and Sanjay Kakar. "Comparison of 5 Immunohistochemical Markers of Hepatocellular Differentiation for the Diagnosis of Hepatocellular Carcinoma." Archives of Pathology & Laboratory Medicine 139, no. 8 (August 1, 2015): 1028–34. http://dx.doi.org/10.5858/arpa.2014-0479-oa.

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Context Several immunohistochemical markers are available to establish the diagnosis of hepatocellular carcinoma. Judicious selection is essential to achieve a reliable diagnosis in limited tissue provided by liver biopsy. Objective To compare the efficacy of 5 hepatocellular markers for the diagnosis of hepatocellular carcinoma across various levels of differentiations. Design Immunohistochemistry for hepatocyte paraffin antigen 1 (Hep Par 1), polyclonal carcinoembryonic antigen (CEA), glypican-3, arginase-1, and bile salt export pump transporter was performed in 79 hepatocellular carcinomas, yielding 93 observations (13 well-differentiated [14%], 41 moderately differentiated [44%], and 39 poorly differentiated [42%] tumors). Results Arginase-1 and Hep Par 1 had the highest sensitivity for well-differentiated hepatocellular carcinoma, whereas arginase-1 and glypican-3 had the highest sensitivity for poorly differentiated hepatocellular carcinoma. When staining of more than 50% of the tumor was considered a positive result, arginase-1 remained the most sensitive marker for all differentiations, whereas sensitivity for Hep Par 1 in poorly differentiated hepatocellular carcinoma dropped to 30% and that of glypican-3 in well-differentiated hepatocellular carcinoma was 15%. The addition of Hep Par 1 and/or polyclonal CEA to arginase-1 did not lead to an increase in sensitivity for any differentiation. The combined use of arginase-1 and glypican-3 yielded 100% sensitivity for poorly differentiated hepatocellular carcinoma. Conclusion Arginase-1 was the most sensitive marker in all differentiations of hepatocellular carcinoma. Glypican-3 had high sensitivity for poorly differentiated cases and its combined use with arginase-1 enabled identification of nearly all cases of poorly differentiated hepatocellular carcinoma. Although bile salt export pump transporter has good overall sensitivity, it has a limited role in establishing hepatocellular differentiation when added to a panel of arginase-1 with either glypican-3 or Hep Par 1.

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Vani, Dayanand, Rao Srijana S.P, Pushpa H.R, and Bharathi M. "Hepatocellular Carcinoma- Sarcomatoid Variant: A Rare Occurence." Indian Journal of Forensic Medicine and Pathology 10, no. 3 (2017): 242–44. http://dx.doi.org/10.21088/ijfmp.0974.3383.10317.13.

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Breder, V. V., K. K. Laktionov, and M. I. Davydov. "PHARMACOLOGICAL THERAPY OF HEPATOCELLULAR CANCER PRACTICAL ISSUES AND SOLUTIONS." Medical Council, no. 14 (November 14, 2017): 11–23. http://dx.doi.org/10.21518/2079-701x-2017-14-11-23.

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Pharmaceutical therapy of hepatocellular carcinoma represents a major clinical issue of debate in modern oncology. Until now, Sorafenib remains the only option for the management of locally advanced and metastatic hepatocellular carcinomas, which increases the overall survival of patients. In the absence of alternative treatment, the oncologist understanding of the place, time, the strategic goal and tactical objectives of the pharmaceutical therapy of hepatocellular carcinoma at different stages of cancer is of great importance. The article considers the practical aspects of the Sorafenib therapy of hepatocellular cancer in various clinical situations, and proposes algorithms of accompanying therapy for the underlying liver pathology. It presents the results of Regorafenib therapy, a new multi-kinase inhibitor, which significantly increases survival in the second line therapy of sorafenib-resistant hepatocellular carcinoma. The options of pharmaceutical therapy for hepatocellular carcinoma using cytotoxic and molecular-directed medicines, prospects of modern immunotherapy are discussed.

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Yadav, Krohit, Kanupriya Agrawal, Manu Solanki, Nikita Jindal, Venkata Raviteja, and Reddy Gayam. "Synchronous Renal Cell Carcinoma and Hepatocellular Carcinoma - A Rare Case Report." International Journal of Science and Research (IJSR) 11, no. 2 (February 5, 2022): 1025–27. http://dx.doi.org/10.21275/sr22221170303.

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Torbenson, Michael. "Fibrolamellar Carcinoma: 2012 Update." Scientifica 2012 (2012): 1–15. http://dx.doi.org/10.6064/2012/743790.

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Fibrolamellar carcinomas are a unique type of primary liver cancer. They occur most commonly in children and young adults. Their etiology remains a mystery, as they are not associated with chronic liver disease. Fibrolamellar carcinomas are not indolent tumors, but have an overall better prognosis than typical hepatocellular carcinomas, in part because of the younger age at presentation and the lack of cirrhosis. The most important prognostic feature is whether the tumor is resectable. Histologically, the tumor is made up of large cells that contain abundant mitochondria. The nuclei of the tumor cells have prominent nucleoli. The tumor cells induce the formation of extensive intratumoral fibrosis, which often grows in parallel, or lamellar bands. The tumor cells clearly show hepatocellular features but are also unique in showing both biliary and neuroendocrine differentiation. The uniqueness of fibrolamellar carcinoma extends to their molecular findings. While the genetic abnormalities that lead to fibrolamellar carcinomas are not yet known, studies have shown that they lack mutations in the genes most commonly mutated in typical hepatocellular carcinoma (TP53andCTNNB1). In this paper, the clinical, pathological, and basic science literature on fibrolamellar carcinoma is comprehensively reviewed. Key areas of needed research are also discussed.

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Reis, Marcio Augusto Correia Rodrigues dos, and Ronaldo Hueb Baroni. "Liver-specific magnetic resonance contrast medium in the evaluation of chronic liver disease." Einstein (São Paulo) 13, no. 2 (June 2015): 326–29. http://dx.doi.org/10.1590/s1679-45082015rw3159.

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ABSTRACT The hepatobiliary-specific contrast medium (gadoxetic acid – Primovist®) is primarily used to improve detection and characterization of focal hepatic lesions, such as in chronic liver disease patients with suspected hepatocellular carcinoma. Since the contrast medium is selectively taken up by functioning hepatocytes in the late hepatobiliary phase, it helps to detect typical hepatocellular carcinoma, which show low signal intensity on this phase. This imaging feature also assists in differentiating regenerative/dysplastic nodules from early hepatocellular carcinomas (with over 90% accuracy), as well as hypervascular hepatocellular carcinomas from arterial pseudo-enhancement foci. Future perspectives include its use in quantification of hepatic function and fibrosis.

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Ulmer, Scott C. "Hepatocellular carcinoma." Postgraduate Medicine 107, no. 5 (January 2000): 117–24. http://dx.doi.org/10.3810/pgm.2000.5.1.1062.

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OBARA, Yuki, Miho HAGIOITA, Michihiro SHIMIZU, Kohji YOSHIDA, and Shunichi SASOU. "Hepatocellular carcinoma." Journal of the Japanese Society of Clinical Cytology 57, no. 5 (2018): 259–66. http://dx.doi.org/10.5795/jjscc.57.259.

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Shirato, Kazuhito, Manabu Morimoto, Naohiko Tomita, Atsushi Kokawa, Kazuya Sugimori, Toshifumi Saito, Kazushi Numata, Hisahiko Sekihara, and Katsuaki Tanaka. "Hepatocellular Carcinoma." Journal of Ultrasound in Medicine 21, no. 9 (September 2002): 1015–22. http://dx.doi.org/10.7863/jum.2002.21.9.1015.

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Kim, Kyoung Won, Byung Ihn Choi, Seong Ho Park, Hyo-Cheol Kim, Min Woo Lee, Se Hyung Kim, Kyoung Ho Lee, et al. "Hepatocellular Carcinoma." Journal of Ultrasound in Medicine 22, no. 9 (September 2003): 887–96. http://dx.doi.org/10.7863/jum.2003.22.9.887.

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Gonzalez, Karen B., and Misty Woodall. "HEPATOCELLULAR CARCINOMA." Nursing Clinics of North America 36, no. 3 (September 2001): 593–602. http://dx.doi.org/10.1016/s0029-6465(22)02581-6.

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Parikh, PM, R. Bhagwat, G. Biswas, and L. Goyal. "Hepatocellular Carcinoma." Indian Journal of Medical and Paediatric Oncology 26, no. 04 (October 2005): 43–57. http://dx.doi.org/10.1055/s-0041-1733134.

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Rehman, Khalil ur, Dr Muhammad Samiullah, Sidra Sharif, and Saira Farhat. "HEPATOCELLULAR CARCINOMA." Professional Medical Journal 23, no. 02 (February 10, 2016): 209–12. http://dx.doi.org/10.29309/tpmj/2016.23.02.1072.

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Background: Hepatocellular carcinoma (HCC) also known as malignanthepatoma, accounts for most of the liver cancers. Alpha fetoprotein (AFP) has been undoubtedlywidely used as a marker for the detection and monitoring of HCC. This study aimed to find thecorrelation of serum alpha fetoprotein and tumor size in HCC in the tertiary care hospital. StudyDesign: This cross sectional descriptive study. Setting: Pathology Department of Allama IqbalMedical College, Lahore (AIMC). Materials and Methods: The study was carried out on 45HCC patients (13 females and 32 males) came to Jinnah Hospital Lahore. Five ml of venousblood was drawn aseptically from anterior cubital vein of patients and added into plain vial toclot. The samples were centrifuged, to get the plasma separated from blood cells. Serum AFPwas measured by using Enzyme linked Immunosorbent Assay technique (ELISA). Results:There were 10 (22.2%), 19 (42.2%), 16 (35.6) cases in AFP group 1,2,3 respectively. While10 (22.2%), 13 (28.8%), 22 (48.8%) cases in tumor size groups A,B,C. Group C with largetumor size got 48.8% raised AFP levels as compared to group B (28.8%) and group A (10%).Conclusion: This study shows there is significant correlation between serum AFP and tumorsize in HCC (r=0.668). Serum AFP progressively increases with tumor size especially in largersize. Although AFP have suboptimal sensitivity but it is still proves a beneficial in early diagnosisand screening of HCC, when used in combination of USG/Imaging technique.

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Fahim, Amin, Mohammad Ahmed Azmi, Muhammad Hanif, and Anila Qureshi. "HEPATOCELLULAR CARCINOMA." Professional Medical Journal 23, no. 04 (April 10, 2016): 415–21. http://dx.doi.org/10.29309/tpmj/2016.23.04.1499.

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Objectives: To determine the expression of miR-92-1 in HCC patients and correlatethem with clinicopathological data. Study Design: A Cross sectional study. Place of Study:Samples were collected from Jinnah Postgraduate Medical Center Karachi, Civil HospitalKarachi and Asian Institute of Medical Sciences Hyderabad. Duration of Study: January2014 to December 2014. Materials and Methods: 150 patients of hepatocellular carcinomawere divided into two groups on the basis of etiologic agent. HCC patients with chronic viralhepatitis B were labeled as group-I, whereas those with chronic viral hepatitis C in group-II,compared with 75 healthy control individuals in group-III. Results: The results showed thatmiR-92-1 expression was decreased in patients with HCC when compared with controls. Downregulation was seen more pronounced in HCC cases with chronic viral hepatitis C. A significantcorrelation was found between the expression of miR-92-1 and AFP level 20-200 ng/ml andChild Pugh score B. However no correlation was found between the expression of miR-92-1and age, gender, fibro scan, tumor distribution, tumor size, tumor metastasis and BCLC stage.Conclusion: miR-92-1 is down regulated in HCC patients with significant correlation with serumAFP level between 20-200 ng/ml.

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Kalhoro, Muhammad Amjad, Irfan Murtaza Shahwani, Mashooque Ali Dasti, Syed Zulfiquar Ali Shah, Faisal Shahab, and Zulfiqar Ali Qutrio Baloch. "HEPATOCELLULAR CARCINOMA;." Professional Medical Journal 21, no. 06 (December 10, 2014): 1222–26. http://dx.doi.org/10.29309/tpmj/2014.21.06.2671.

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Objective: To determine the frequency of hepatocellular carcinoma in different Child-Pugh classes based on Alfa fetoprotein level. Study design: Case series study. Period: Six months Setting: Medical Unit-I of Liaquat University Hospital, Hyderabad Sindh Pakistan. Patients & Methods: A total of 100 patients admitted (inpatients) in Medical Unit I with the diagnosis of cirrhosis were enrolled in the study. Patients with cirrhosis of liver (more than six month duration) of either gender were included. If patients had metastatic lesion of the liver, liver abscess, or acute liver failure then they were excluded. Child-Pugh score was calculated which included ascites, encephalopathy, prothrombin time, albumin and serum bilirubin. The levels of α-fetoprotein were measured and HCC was diagnosed. The primary outcome variable was presence of HCC in cirrhotic patients. Results: The proportion of males (53%) was higher as compared to females (47%). The mean age of the study patients was 40.47 years with a standard deviation of 11.5. At the beginning patients were categorized according to Child Pugh Classes (A= up to 6, B=7-9 and C=10-11), age groups (15-30 years, 31-50 years and 51-70 years respectively). The mean Child Pugh score was 6.83 with ± 1.8 S.D. The majority of the cases of HCC (75.61%) occurred in the Child Class A, whereas 21.95% occurred in Child Class B and finally only one case of HCC (2.44%) was present in Child Class C. Conclusions: This study comprehensively demonstrated that hepatocellular carcinoma (HCC) is far more common in compensated cirrhosis (Child Pugh Class A) vs. decompensated cirrhosis (Child Pugh Class B and C).

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AMER, WASIM, MUHAMMAD ASHRAF MAJROOH, and MUHAMMAD AKRAM. "HEPATOCELLULAR CARCINOMA." Professional Medical Journal 16, no. 03 (September 10, 2009): 364–69. http://dx.doi.org/10.29309/tpmj/2009.16.03.2793.

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Introduction: Hepatocellular carcinoma (HCC) is the commonest primary malignant cancer of the liver in the world.Characteristics of our population suffering from HCC are not known, this study aims to present epidemiological, clinical and laboratorycharacteristics of HCC patients..Design: A retrospective study. Setting: At Jinnah hospital, Lahore. Period: 36 months. Material & m e t h o dsHCC was diagnosed according to the guide lines given by EASL-2000. The data was later analyzed by SPSS13. Results. A total of 34 patientswere included in the study. Majority patients were male 21(80%) and belonged to urban setting (21). Pain abdomen 21(61.8%) and Ascites22(64.7%) were the commonest presentations. 15(44%) patients were suffering from HCV and 12 (35.3%) were negative for both HCV & HBV,while 9 out of these were also not alcoholic. Most of the patients had symptoms present for 1 -6 (76%) months and majority presented in eitherstage III or IV (91 %), none of the patient presented in stage I. Most the patients 25(73.5%) had tumor size larger than 5 cm at presentation andsimilarly 20 (59%) had more than one lesions at presentation, stage of tumor was positively associated (p <0.02) with number of tumor lesions.Conclusion. HCC does occur in a cirrhotic background but a good number of patients were not cirrhotic and need to be investigated furtherfor other possible dietary risk factors. Pain and abdominal distension in a cirrhotic patient should be addressed to immediately so as to diagnoseHCC at an earlier stage.

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Blendis, Laurie, and Morris Sherman. "Hepatocellular Carcinoma." American Journal of Cancer 3, no. 6 (2004): 349–68. http://dx.doi.org/10.2165/00024669-200403060-00003.

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DI BISCEGLIE, ADRIAN M. "Hepatocellular Carcinoma." Annals of Internal Medicine 108, no. 3 (March 1, 1988): 390. http://dx.doi.org/10.7326/0003-4819-108-3-390.

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Giovannini, M., D. Elias, G. Monges, J. L. Raoul, and P. Rougier. "Hepatocellular carcinoma." British Journal of Cancer 84, s2 (2001): 74–77. http://dx.doi.org/10.1054/bjoc.2001.1769.

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Bergsland, Emily K., and Alan P. Venook. "Hepatocellular carcinoma." Current Opinion in Oncology 12, no. 4 (July 2000): 357–61. http://dx.doi.org/10.1097/00001622-200007000-00013.

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Ohtomo, Kuni, Yuji Itai, Yujiro Matuoka, Manabu Minami, Yoshitaka Okada, Nobuo Kawauchi, Masahiro Iio, Ikuo Nagashima, and Jungi Shiga. "Hepatocellular Carcinoma." Journal of Computer Assisted Tomography 14, no. 4 (July 1990): 650–52. http://dx.doi.org/10.1097/00004728-199007000-00026.

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El-Serag, Hashem B. "Hepatocellular Carcinoma." New England Journal of Medicine 365, no. 12 (September 22, 2011): 1118–27. http://dx.doi.org/10.1056/nejmra1001683.

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Villanueva, Augusto. "Hepatocellular Carcinoma." New England Journal of Medicine 380, no. 15 (April 11, 2019): 1450–62. http://dx.doi.org/10.1056/nejmra1713263.

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Hesketh, Richard L., Andrew X. Zhu, and Rahmi Oklu. "Hepatocellular Carcinoma." American Journal of Clinical Oncology 38, no. 4 (August 2015): 431–36. http://dx.doi.org/10.1097/coc.0000000000000123.

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32

Smith, C. Scott, and Douglas S. Paauw. "Hepatocellular carcinoma." Postgraduate Medicine 94, no. 8 (December 1993): 71–74. http://dx.doi.org/10.1080/00325481.1993.11945770.

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Mitchell, Kisha A. "Hepatocellular Carcinoma." Journal of Clinical Gastroenterology 47 (July 2013): S20—S26. http://dx.doi.org/10.1097/mcg.0b013e318291f237.

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Stein, Stacey M. "Hepatocellular Carcinoma." Journal of Clinical Gastroenterology 47 (July 2013): S47—S49. http://dx.doi.org/10.1097/mcg.0b013e3182932e6f.

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Pinato, David J., Alessia Dalla Pria, Rohini Sharma, and Mark Bower. "Hepatocellular carcinoma." AIDS 31, no. 5 (March 2017): 603–11. http://dx.doi.org/10.1097/qad.0000000000001422.

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Choi, Byung Ihn, Ah Young Kim, Jae Young Lee, Kyoung Won Kim, Kyoung Ho Lee, Tae Kyoung Kim, and Joon Koo Han. "Hepatocellular Carcinoma." Journal of Ultrasound in Medicine 21, no. 1 (January 2002): 77–84. http://dx.doi.org/10.7863/jum.2002.21.1.77.

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Macdonald, Graeme A. "Hepatocellular carcinoma." Current Opinion in Gastroenterology 13, no. 3 (May 1997): 257–62. http://dx.doi.org/10.1097/00001574-199705000-00012.

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Macdonald, Graeme A. "Hepatocellular carcinoma." Current Opinion in Gastroenterology 14, no. 3 (May 1998): 250–55. http://dx.doi.org/10.1097/00001574-199805000-00011.

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Macdonald, Graeme A. "Hepatocellular carcinoma." Current Opinion in Gastroenterology 15, no. 3 (May 1999): 253–59. http://dx.doi.org/10.1097/00001574-199905000-00011.

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Edwards, John T., and Graeme A. Macdonald. "Hepatocellular carcinoma." Current Opinion in Gastroenterology 16, no. 3 (May 2000): 275–81. http://dx.doi.org/10.1097/00001574-200005000-00011.

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Chokshi, Manish M., and Jorge A. Marrero. "Hepatocellular carcinoma." Current Opinion in Gastroenterology 17, no. 3 (May 2001): 276–80. http://dx.doi.org/10.1097/00001574-200105000-00011.

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Huang, Mary Ann, and Jorge A. Marrero. "Hepatocellular carcinoma." Current Opinion in Gastroenterology 18, no. 3 (May 2002): 345–50. http://dx.doi.org/10.1097/00001574-200205000-00008.

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Marrero, Jorge A. "Hepatocellular carcinoma." Current Opinion in Gastroenterology 19, no. 3 (May 2003): 243–49. http://dx.doi.org/10.1097/00001574-200305000-00007.

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Lopez, Luis J., and Jorge A. Marrero. "Hepatocellular carcinoma." Current Opinion in Gastroenterology 20, no. 3 (May 2004): 248–53. http://dx.doi.org/10.1097/00001574-200405000-00009.

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Marrero, Jorge A. "Hepatocellular carcinoma." Current Opinion in Internal Medicine 2, no. 3 (June 2003): 222–28. http://dx.doi.org/10.1097/00132980-200302030-00002.

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Scheirhauer, W., and M. Hejna. "Hepatocellular Carcinoma." Oncology Research and Treatment 18, no. 4 (1995): 327–32. http://dx.doi.org/10.1159/000218612.

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Buendia, M. A., and C. Neuveut. "Hepatocellular Carcinoma." Cold Spring Harbor Perspectives in Medicine 5, no. 2 (February 1, 2015): a021444. http://dx.doi.org/10.1101/cshperspect.a021444.

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Falkson, G., S. Lipsitz, E. Borden, I. Simson, and D. Haller. "Hepatocellular Carcinoma." American Journal of Clinical Oncology 18, no. 4 (August 1995): 287–92. http://dx.doi.org/10.1097/00000421-199508000-00003.

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Kokudo, Takashi, Kiyoshi Hasegawa, Norihiro Kokudo, Takashi Kokudo, Emilie Uldry, Nicolas Demartines, and Nermin Halkic. "Hepatocellular Carcinoma." Annals of Surgery 267, no. 2 (February 2018): e27-e28. http://dx.doi.org/10.1097/sla.0000000000001960.

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El-Serag, Hashem B. "Hepatocellular Carcinoma." Journal of Clinical Gastroenterology 35 (November 2002): S72—S78. http://dx.doi.org/10.1097/00004836-200211002-00002.

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