Spontaneous regression of hepatocellular carcinoma

Halteren, H.K. van; Salemans, Johannes M.J.I.; Peters, H. M.; Vreugdenhil, Gerard; Driessen, W. M. M.

doi:10.1016/s0168-8278(97)80304-2

Cited by 35 publications

(23 citation statements)

References 10 publications

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“…Nineteen cases of spontaneous HCC regression have been reported in the English-language literature, [1][2][3][4][7][8][9][10][11][12][13][14][15][16][17][18][19] and it is speculated that necrosis, caused by an ischemic disorder, and tumor immune activation are important causal factors. When we evaluated the causes of spontaneous regression in the 19 patients reported, 5 involved necrosis, 1,2,7-9 and 8 involved immunity.…”

Section: Discussionmentioning

confidence: 99%

Spontaneous regression of recurrent hepatocellular carcinoma after TAE: possible mechanisms of immune mediation

Nakai¹,

Shimomura²,

Hirokawa³

2001

Int J Clin Oncol

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We report findings in a 76-year-old man who underwent a lateral segmentectomy of the liver for hepatocellular carcinoma in July 1996. In July 1997, transarterial embolization (TAE) was performed for recurrent tumors in the remnant liver. Augmentation of the tumors and an increase in protein induced by vitamin K absence or antagonist (PIVKA)-II level were noted in October 1997, and, although we recommended TAE again, the patient and his family refused further treatment. Subsequently, the patient was only observed, and, except for a small lesion that was probably a scar, no tumors were noted on image examinations in November 1998, and the PIVKA-II level had returned to a normal value at this time. Two years after the regression, the tumors appeared to be in complete spontaneous remission. This patient had no history indicative of ischemic necrosis, and levels of cellular surface markers for natural killer (NK) cells and NK cell activity showed high values, which suggested that tumor immunity was activated by some, unknown, mechanism.

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Section: Discussionmentioning

confidence: 99%

Spontaneous regression of recurrent hepatocellular carcinoma after TAE: possible mechanisms of immune mediation

Nakai¹,

Shimomura²,

Hirokawa³

2001

Int J Clin Oncol

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“…In the analysis of published cases between 1900 and 1964 by Everson and Cole, HCC is not mentioned [33,35], although HCC has a high prevalence and an increasing incidence in the world [1]. Since 1982, spontaneous regression of HCC has been described in more than 20 cases [11,[13][14][15][16][17][18][19][20][21][22][23][24][25][26][27][28][29][30][31][32]. Most of the patients are male, and the period of observation ranged from 1 year to 20 years.…”

Section: Discussionmentioning

confidence: 99%

“…In only one patient was the HCC smaller than 2 cm [20], while in all other cases registered the tumor measured at least 5 cm in diameter. In six cases HCC was multicentric [13,14,17,18,21,32]. Mostly tumors were well differentiated (trabecular [11,13,14,17,18]; moderately differentiated [22,23,27,[30][31][32]; acinous [14,23]; pseudo-acinous [22]).…”

Section: Discussionmentioning

confidence: 99%

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Spontaneous regression of hepatocellular carcinoma confirmed by surgical specimen: report of two cases and review of the literature

Stoelben

Koch

Hanke

et al. 1998

Langenbeck's Archives of Surgery

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Two cases with spontaneous regression of a histologically confirmed hepatocellular carcinoma (HCC) are presented. This rarely seen phenomenon of a spontaneous tumor involution is discussed and compared with the current literature. The clinical symptoms were very similar to that of a liver abscess. A 56-year-old male suffered from a multicentric, highly differentiated, trabecular HCC. First symptoms were epigastric pain, septic fever and arthritis. The tumor marker AFP was constantly normal and no hepatitis could be verified. A resection of the tumor was performed. In patient 2, a 74-year-old male, a multicentric, clear cell HCC was found. The patient had completely recovered from hepatitis type B and within the liver tissue no viruses could be identified. Clinical symptoms were mainly characterized by upper abdominal pain and septic fever. AFP was excessively elevated (3850 ng/ml) but returned to normal preoperatively. In both cases, the specimen showed a subtotal necrotic HCC with insignificant amounts of vital tumor cells. Neither patient had a liver cirrhosis macroscopically, however patient 2 had local periportal fibrosis histologically. After 24 and 41 months of follow-up, respectively, both patients are in good health

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“…At initial evolutionary stages, the tumor is well differentiated and the progression to more advanced stages with loss of differentiation and appearance of an invasive phenotype may require months or even years (5,6). Interestingly, in a minority of patients, HCC can regress or even disappear because of unknown mechanisms (7). Tumor progression is achieved by the sequential accumulation of molecular alterations that bring the cells into a more transformed stage characterized by an increased proliferation.…”

Section: Introductionmentioning

confidence: 99%

Orthotopic Implantation of Human Hepatocellular Carcinoma in Mice

Armengol

Tarafa

Boix

et al. 2004

Clinical Cancer Research

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Purpose: To allow the longitudinal investigation of molecular events associated with the progression of human hepatocellular carcinoma (HCC), we sought to develop a murine model by orthotopic implantation of tumor fragments obtained from patients diagnosed at early stage.Experimental Design: Tumor pieces (2 ؋ 2 mm) were implanted on the liver surface of nu/nu mice. After xenograft growing, subsequent passages were performed to achieve long-term implant viability. Isolation of tumoral hepatocytes was done to establish new cell lines. HCC characteristics, proliferation rate, apoptotic index (terminal deoxynucleotidyl transferase-mediated nick end labeling), and expression of cell-cycle regulators (cyclins E and A, p21Cip1 , p27 Kip1 , p16 INK4a , pRb, and p53) were assessed by Western Blot and immunohistochemistry, to correlate them with tumor progression.Results: Five (50%) of the 10 primary HCCs resulted in small slow-growing liver implants. Three of them are viable after 48 months, whereas the remaining two survived for 15 and 13 months. Xenografts throughout passages exhibited a more aggressive phenotype with a poorer degree of differentiation, intense proliferation, moderate apoptosis, cellcycle deregulation, p53 alterations, microvascular invasion, and dissemination. In one single passage, we observed critical growth delay, which was associated with significant p27 kip1 overexpression. We established the anchor-free growing BCLC-9 cell line from one xenograft. This has gains of chromosomes 7, 5p, 6q, and 9q, is hepatitis B virus-DNA positive, does not secrete ␣-fetoprotein, and has TP53 missense mutations in codons 192 and 242.Conclusions: The orthotopic implantation of early HCC fragments in nude mice provides a useful model to investigate the mechanisms of human HCC evolution and to establish new cell lines.

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Spontaneous regression of hepatocellular carcinoma

Cited by 35 publications

References 10 publications

Spontaneous regression of recurrent hepatocellular carcinoma after TAE: possible mechanisms of immune mediation

Spontaneous regression of recurrent hepatocellular carcinoma after TAE: possible mechanisms of immune mediation

Spontaneous regression of hepatocellular carcinoma confirmed by surgical specimen: report of two cases and review of the literature

Orthotopic Implantation of Human Hepatocellular Carcinoma in Mice

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