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Query: UMLS:C0019204 (hepatocellular carcinoma)
 71,386 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This review first considered some general problems in establishing causal links between a virus and a human cancer and offered some guidelines in the pursuit of this objective. Second, it reviewed the current causal associations for several candidate oncogenic viruses in relation to the tumors with which they are associated. These include Epstein-Barr virus in relation to Burkitt's lymphoma, nasopharyngeal carcinoma, Hodgkin's disease, and non-Hodgkin's lymphoma; hepatitis B and C viruses in relation to hepatocellular carcinoma; human T-cell leukemia/lymphoma virus type 1 and atypical leukemia/lymphoma; and human papilloma viruses in relation to cervical carcinoma. For some, the causal relationship is strong: hepatitis B virus with hepatocellular carcinoma, and human T-cell leukemia/lymphoma virus with adult T-cell leukemia/lymphoma. For one, the causal relationship is moderate: Epstein-Barr virus with African Burkitt's lymphoma. For others it is incomplete or inconclusive: Epstein-Barr virus with Hodgkin's disease and non-Hodgkin's lymphoma, and hepatitis C virus with hepatocellular carcinoma. Current techniques do not permit an answer for some: human papilloma virus with cervical carcinoma.
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PMID:Viruses and cancer. Causal associations. 166 91

The following review considers epidemiological data published from 1990 onwards on oral contraceptives (OCs) and the risk of cancers of the breast, cervix uteri, endometrium, ovary, liver and skin. In several studies, breast cancer risk was seen to be elevated among women who were current users of an OC, or had recently stopped using an OC, whereas there was no residual risk 5 or more years after stopping OC use. No interaction was observed between type of OC, or with any recognised risk factor for breast cancer, or time-factor, except for some potential excess risk for women who started OC use at a young age. Most studies have confirmed that OCs moderately increase the risk of cervical cancer, particularly in human papilloma virus (HPV)-positive women, thus suggesting that OCs may act as a promoter for HPV-induced carcinogenesis. Recent epidemiological studies have confirmed that combined OCs provide substantial protection against endometrial and ovarian cancers, and results suggest that such protection is long-lasting, and may persist for 15 years or more after stopping OC use. Most case-control studies have shown a relationship between OC use and hepatocellular carcinoma. However, data from cohort studies or analysis of vital statistics indicate that the public health impact of such an association is modest, if not negligible. No association was observed between combined OC use and the incidence of skin melanoma, or any other common skin neoplasm. In terms of clinical and public health implications, the most relevant points regarding OC use are: (i) recent data confirm that OCs confer presistent protection against ovarian cancer; and (ii) any increased risk of breast cancer in OC users is moderate and is restricted to current/recent users. This is reassuring for younger women, whose baseline risk of this disease is extremely low.
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PMID:Oral contraceptives and cancer. A review of the evidence. 871 94

Substantial evidence indicates that several common viruses are clearly or probable causal factors in the etiology of specific malignancies. These viruses either normally establish latency or can become persistent infections. Oncogenesis is probably linked to an enhanced level of viral activation in the infected host, reflecting heavy viral dose or compromised immune control. The major virus-malignancy systems include hepatitis B virus (HBV), hepatitis C virus (HCV), and hepatocellular carcinoma; human lymphotropic virus-type 1 (HTLV-1) and adult T-cell leukemia/lymphoma (ATL); Epstein-Barr virus (EBV) and endemic Burkitt's lymphoma, nasopharyngeal carcinoma, and Hodgkin's disease; and human papilloma virus (HPV) and cervical cancer. Of these, a vaccine is available only for HBV. These malignancies tend to occur in early to mid-life and account for a substantial amount of morbidity and person-years lost. They are also likely to occur as "opportunistic malignancies" among individuals infected with human immunodeficiency virus type-1, particularly among those who experience prolonged survival.
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PMID:Overview: viral agents and cancer. 874 95

Recent studies have demonstrated that angiogenesis and suppressed cell-mediated immunity (CMI) play a central role in the pathogenesis of malignant disease facilitating tumour growth, invasion and metastasis. In the majority of tumours, the malignant process is preceded by a pathological condition or exposure to an irritant which itself is associated with the induction of angiogenesis and/or suppressed CMI. These include: cigarette smoking, chronic bronchitis and lung cancer; chronic oesophagitis and oesophageal cancer; chronic viral infections such as human papilloma virus and ano-genital cancers, chronic hepatitis B and C and hepatocellular carcinoma, and Epstein-Barr virus (EBV) and lymphomas; chronic inflammatory conditions such as Crohn's disease and ulcerative colitis and colorectal cancer; asbestos exposure and mesothelioma and excessive sunlight exposure/sunburn and malignant melanoma. Chronic exposure to growth factors (insulin-like growth factor-I in acromegaly), mutations in tumour suppressor genes (TP53 in Li Fraumeni syndrome) and long-term exposure to immunosuppressive agents (cyclosporin A) may also give rise to similar environments and are associated with the development of a range of solid tumours. The increased blood supply would facilitate the development and proliferation of an abnormal clone or clones of cells arising as the result of: (a) an inherited genetic abnormality; and/or (b) acquired somatic mutations, the latter due to local production and/or enhanced delivery of carcinogens and mutagenic growth factors. With progressive detrimental mutations and growth-induced tumour hypoxia, the transformed cell, to a lesser or greater extent, may amplify the angiogenic process and CMI suppression, thereby facilitating further tumour growth and metastasis. There is accumulating evidence that long-term treatment with cyclo-oxygenase inhibitors (aspirin and indomethacin), cytokines such as interferon-alpha, anti-oestrogens (tamoxifen and raloxifene) and captopril significantly reduces the incidence of solid tumours such as breast and colorectal cancer. These agents are anti-angiogenic and, in the case of aspirin, indomethacin and interferon-alpha have proven immunomodulatory effects. Collectively these observations indicate that angiogenesis and suppressed CMI play a central role in the development and progression of malignant disease.
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PMID:The relationship between angiogenesis and the immune response in carcinogenesis and the progression of malignant disease. 1074 Dec 73

Most up-to-date information on oral contraceptives (OCs) and breast cancer risk comes from a collaborative re-analysis of individual data on 53297 cases and 100239 controls. It is now established that there is a moderately increased breast cancer risk among current OC users, which tends to level off in the few years after stopping use. With regard to cervical cancer, OC use has been found to be associated with increased risk in human papilloma virus-positive women. With reference to the well known protective effects of OCs against endometrial carcinogenesis, additional information has suggested a consistent protection across types of OCs used. Further data on ovarian cancer confirm that the protection of OCs is long lasting, and may well be observed 15 to 20 years after stopping use. Several studies have suggested an inverse relationship between use of OCs and risk of colorectal cancer, and in a meta-analysis of published data the pooled relative risk of colorectal cancer for DC ever-use was 0.82 (95% confidence interval 0.74 to 0.97). There was no association with duration of use. The increased risk for hepatocellular carcinoma in the absence of hepatitis B viruses is the only established evidence of a direct association between OC use and cancer risk, which led an International Agency for Research on Cancer Working Group to classify OCs as carcinogenic to humans in 1998.
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PMID:Oral contraceptives and cancer: an update. 1167 2

It is estimated that 15% of all cancers are etiologically linked to viral infection. Specific cancers including adult T-cell leukemia, hepatocellular carcinoma, and uterine cervical cancer are associated with infection by human T-cell leukemia virus type I, hepatitis B virus, and high-risk human papilloma virus, respectively. In these cancers, genomic instability, a hallmark of multistep cancers, has been explicitly linked to the expression of oncoproteins encoded by these viruses. This review discusses mechanisms utilized by these viral oncoproteins, Tax, HBx, and E6/E7, to mediate genomic instability and cellular transformation.
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PMID:Impact of transforming viruses on cellular mutagenesis, genome stability, and cellular transformation. 1564 40

Given the fact that infectious agents contribute to around 18% of human cancers worldwide, it would seem prudent to explore their role in neoplasms of the ocular adnexa: primary malignancies of the conjunctiva, lacrimal glands, eyelids, and orbit. By elucidating the mechanisms by which infectious agents contribute to oncogenesis, the management, treatment, and prevention of these neoplasms may one day parallel what is already in place for cancers such as cervical cancer, hepatocellular carcinoma, gastric mucosa-associated lymphoid tissue lymphoma and gastric adenocarcinoma. Antibiotic treatment and vaccines against infectious agents may herald a future with a curtailed role for traditional therapies of surgery, radiation, and chemotherapy. Unlike other malignancies for which large epidemiological studies are available, analyzing ocular adnexal neoplasms is challenging as they are relatively rare. Additionally, putative infectious agents seemingly display an immense geographic variation that has led to much debate regarding the relative importance of one organism versus another. This review discusses the pathogenetic role of several microorganisms in different ocular adnexal malignancies, including human papilloma virus in conjunctival papilloma and squamous cell carcinoma, human immunodeficiency virus in conjunctival squamous carcinoma, Kaposi sarcoma-associated herpes virus or human herpes simplex virus-8 (KSHV/HHV-8) in conjunctival Kaposi sarcoma, Helicobacter pylori (H. pylori,), Chlamydia, and hepatitis C virus in ocular adnexal mucosa-associated lymphoid tissue lymphomas. Unlike cervical cancer where a single infectious agent, human papilloma virus, is found in greater than 99% of lesions, multiple organisms may play a role in the etiology of certain ocular adnexal neoplasms by acting through similar mechanisms of oncogenesis, including chronic antigenic stimulation and the action of infectious oncogenes. However, similar to other human malignancies, ultimately the role of infectious agents in ocular adnexal neoplasms is most likely as a cofactor to genetic and environmental risk factors.
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PMID:The role of infectious agents in the etiology of ocular adnexal neoplasia. 1857 51

The occurrence of de novo malignant neoplasias has been shown in postransplant patients under imunosuppression. It is the second leading cause of late death in liver transplant recipients. The greatest incidence is seen in cancers associated with chronic infection by human papilloma virus, skin cancers, oropharyngeal, and gastrointestinal (GI) malignancies. GI stromal tumors (GISTs) are the most common mesenchymal tumors of the GI tract. Rare cases are identified outside the GI tract are collectively known as extragastrointestinal stromal tumors (EGISTs). We present an EGIST case in a liver transplantation patient. A 64-year-old man underwent liver transplantation because of cirrhosis (hepatitis B virus and alcoholism) and hepatocellular carcinoma. Histopathologic findings revealed 2 trabecular hepatocellular carcinomas: a 3.5-cm-diameter lesion located at segment VIII and another 2-cm one at segment V. Seven months later, he noticed a hardened, mobile, painless, 3-cm subcutaneous nodule in the perineum localized in the right lateral quadrant 2 cm distant from the anus. A surgical resection with 1 cm margin yielded a histopathology report of a 5.0 x 3.0 cm spindle cell stromal tumor. The immunohistochemical profile was compatible with a GIST, with 5 mitosis per 50 high-powered fields. This tumor is extremely rare after liver transplantation but has shown a good outcome up to now.
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PMID:Extragastrointestinal stromal tumor and liver transplantation: case report and review. 1910 Apr 89

Chronic inflammation caused by persistent infection is closely related to a number of cancers; these include hepatitis B (HBV) or C and hepatoma, human papilloma virus and cervical cancer, and Helicobacter pylori and gastric cancer. The first evidence of cancer prevention by vaccination in humans was provided by HBV vaccination in infants. Chronic HBV is related to approximately 60%-90% of hepatocellular carcinomas (HCC) in adults and nearly 100% of childhood HCC in areas endemic for HBV infection. The first universal HBV vaccination program was launched in Taiwan and has continued for more than 20 years. Three or four doses of HBV vaccine were given to all infants starting from the first week of life. In addition, infants of high-risk mothers (with positive hepatitis B e antigen or high HBsAg titers) were given hepatitis B immunoglobulin within 24 h after birth. At 20 years after the launch of the HBV vaccination program in Taiwan, chronic HBV infection (HBsAg seropositive) rates in the general population below 20 years of age have revealed a remarkable reduction from 10%-17% before the vaccination program to 0.7%-1.7% after the program. HCC incidence rate in children 6-14 years old also fell from 0.52-0.54 to 0.13-0.20 per 100,000 (R.R. = 0.25-0.36). HCC prevention failure is mainly related to vaccine failure to prevent chronic HBV infection. The causes of vaccine failure have included intrauterine infection, vaccine escape mutants, genetic hyporesponsiveness, and poor compliance. Future efforts to reduce vaccine failure will improve the efficacy of liver cancer prevention by HBV vaccination. The experience of HCC prevention by HBV immunization may be applied to the prevention of other infection-related cancers.
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PMID:Cancer prevention by vaccination against hepatitis B. 1921 61

The natural history of HIV infection has been greatly changed by the introduction of highly active antiretroviral therapy (HAART). As a consequence of improved immune function, the incidence of AIDS-defining cancers (ADCs), such as Kaposi's sarcoma, non-Hodgkin's lymphoma (NHL) and invasive cervical cancer, has significantly declined. On the contrary, non-AIDS-defining cancers (NADCs), such as hepatocellular carcinoma, anal cancer, lung cancer, colorectal cancer and Hodgkin's lymphoma, have gradually emerged as a major fraction of the overall cancer burden. The reasons are still partially unknown. Some of the increased risk may be explained by a high prevalence of cancer risk factors, such as smoking, alcohol consumption, human papilloma virus (HPV) infection and HCV infection among HIV-infected people. The role of immunosuppression in the development of NADCs is controversial, as several studies have not found a clear-cut evidence of an association between the degree of immunosuppression and the development of NADCs. Analogously, the impact of HAART is still not well defined. Future research should focus on the etiology of NADCs, in order to shed light on the pathogenesis of cancer and ultimately to work for prevention; moreover, additional studies should evaluate the best therapeutic approaches to NADCs and the impact of cancer screening interventions among HIV-infected people, in an effort to diagnose cancer at an earlier stage.
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PMID:Non-AIDS-defining cancers among HIV-infected people. 2310 54


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