A clinicopathological review of 100 cases of primary malignant tumours of the liver

Macsween, R. N. M.

doi:10.1136/jcp.27.8.669

Cited by 58 publications

(19 citation statements)

References 37 publications

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“…For example, Stone et al (1968) found 86 %, Parker (1957) 88 %, andMacSween (1974) 92% males, and our figure agrees with these. The reasons for this must remain speculative but there is considerable evidence that in animals testosterone increases the evidence of, and castration affords protection against, spontaneous and chemically-induced hepatic tumour (Agnew and Gardner, 1952;Reuber, 1969).…”

Section: Discussionsupporting

confidence: 91%

Hepatocellular carcinoma in Great Britain: influence of age, sex, HBsAg status, and aetiology of underlying cirrhosis.

Johnson¹,

Krasner²,

Portmann³

et al. 1978

Gut

121

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SUMMARY An analysis of 294 patients who died with cirrhosis showed that 24% had developed hepatocellular carcinoma. Haemochromatosis and HBsAg positive chronic active hepatitis were high risk groups (36% and 42% respectively) and the frequency was lowest in primary biliary cirrhosis and HBsAg negative chronic active hepatitis (3 % and 11 % respectively). Those with hepatocellular carcinoma showed a striking male preponderance (11:1) and further analysis has shown that the proportion developing this tumour in each group was closely related to the proportion of males in that group (r=0-97). Age was the only other significant factor, malignant change occurring more commonly in those over the age of 50 years than those below (30 % and 7 % respectively, P < 0.005). The influence of HBsAg was largely accounted for by the known predisposition of males to carry HBsAg. The group of patients who had developed this tumour without cirrhosis were younger (mean age 39 years) and had a lower male to female ratio of 1-1:1 and the place of contraceptive-related tumour within this group is discussed.It is well recognised that hepatocellular carcinoma may develop in longstanding cirrhosis (Stewart, 1931;Berman, 1951;Gall, 1960), though the reported frequency varies both from country to country (Doll et al., 1966) and with the underlying aetiology (Powell et al., 1971). In parts of Africa and the Far East where the incidence is high, environmental factors, such as aflatoxin and the hepatitis B virus, may be important (Vogel et al., 1970;Alpert et al., 1971). Indeed, in these populations up to 80% of patients have HBsAg present in their serum and the most widely held view is that the tumour has developed from a cirrhosis related to the hepatitis B infection (Tong et al., 1971 Davis et al., 1975;Christopherson and Mays, 1976), and males ingesting androgenic sterReceived for publication 8 June 1978 oids (Johnson et al., 1972;Farrell et al., 1975), both of which suggest the additional influence ofhormonal factors.In this paper we analyse the influence of age, sex, HBsAg status, and aetiology of underlying cirrhosis on the frequency of hepatocellular carcinoma development in 294 British patients dying of cirrhosis and the relative importance of these factors in 25 other patients in whom no evidence of an underlying cirrhosis was found. MethodsThe case notes of all British patients seen at King's College Hospital who were recorded as dying with hepatocellular carcinoma, or as a result of cirrhosis, between 1967 and 1975 were analysed. These comprised 294 patients with cirrhosis, in 71 (24%) of whom hepatocellular carcinoma had been detected either during life or at necropsy, and 25 who had developed carcinoma in an otherwise normal liver. In all cases the diagnosis of cirrhosis and the presence of hepatocellular carcinoma were confirmed by histological examination of liver biopsy tissue. Other types of primary liver tumour, such as cholangiocarcinoma and heamangiosarcoma, were ex-

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Section: Discussionsupporting

confidence: 91%

Hepatocellular carcinoma in Great Britain: influence of age, sex, HBsAg status, and aetiology of underlying cirrhosis.

Johnson¹,

Krasner²,

Portmann³

et al. 1978

Gut

121

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show abstract

“…This is a rather higher percentage than in other series reported from this country (MacSween, 1974), and may reflect a bias in referral to the Liver Unit of the more unusual cases. It has, however, allowed us to determine whether a true relationship exists between serum AFP and survival.…”

Section: Discussioncontrasting

confidence: 66%

Relationship between serum alpha-foetoprotein, cirrhosis and survival in hepatocellular carcinoma

Johnson¹,

Melia²,

Palmer³

et al. 1981

Br J Cancer

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Summary.-An analysis of survival time of 57 West European patients with hepatocellular carcinoma was carried out to define which of several possible factors (age, sex, cirrhosis and raised serum a-foetoprotein (AFP)) influenced survival. Although survival was significantly longer in younger patients (P<0-02) and in patients with normal serum AFP (P< 001), multivariate analysis showed that significant variation in survival time is better explained by the single factor, the presence of cirrhosis, than by AFP level. This does not seem to apply for patients with this tumour in Africa and the Far East, and there may be a fundamental difference in the natural history of the tumour between high-and low-incidence areas.

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“…We have shown that several manipulations, including partial hepatectomy, iron injections and choline deficiency, enhanced the carcinogenicity of aflatoxin for rat liver (Table 2) and the presence of the cirrhotic liver appears to have a unique effect on the induction of liver carcinoma. This, of course, is similar to the observations in human populations where cirrhosis and hepatocellular carcinoma are often concomitants (20)(21)(22)(23)(24)(25).…”

Section: Table L-composition Of Dietssupporting

confidence: 74%

Choline Deficiency, Partial Hepatectomy, and Liver Tumors in Rats and Mice

1982

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Choline deficiency (CD) increases susceptability of the rat liver to a number of~epatocellular carcinogens with a wide diversity of structure and potency. While severe CD results in micronodular cirrhosis and enhanced tumor induction, even a mild deficiency, without cirrhosis is sufficient to result in the increased carcinogenic response. The effects of CD are in part mediated via modulation of microsomal and, possibly, cytosolic enzymes responsible for activation/deactivation of carcinogens.. The 86C3F1 hybrid mouse is remarkably sensitive to initiation/promotion of liver tumors by many substances or conditions. Choline deficiency or partial hepatectomy alone, or in concert, markedly enhances liver tumor induction in the absence of any known carcinogen. These data indicate that the liver of this strain of mouse is "initiated" at or shortly after birth and can be promoted by non-carcinogenic substances or conditions.

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A clinicopathological review of 100 cases of primary malignant tumours of the liver

Cited by 58 publications

References 37 publications

Hepatocellular carcinoma in Great Britain: influence of age, sex, HBsAg status, and aetiology of underlying cirrhosis.

Hepatocellular carcinoma in Great Britain: influence of age, sex, HBsAg status, and aetiology of underlying cirrhosis.

Relationship between serum alpha-foetoprotein, cirrhosis and survival in hepatocellular carcinoma

Choline Deficiency, Partial Hepatectomy, and Liver Tumors in Rats and Mice

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