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PubMed2000

Hepatocellular carcinoma: screening and therapy.

Treatment of the liver cancer (LC) patient is often problematic as the tumour is identified at an advanced stage: the frequent coexistence of cirrhosis limits the use of surgical resection, there is no efficacious chemotherapy, and in patients treatable with liver transplant, indication is rendered uncertain from the point of view of cost-effectiveness and the high risk of recurrence of the tumour and hepatitis infection. Surgical resection appears to be the treatment of choice in patients with a liver tumour in a ''healthy'' liver. Instead, orthotopic liver transplant is the most valid indication for patients with cirrhosis and tumours of dimensions smaller than 2-3 cm. Nevertheless, due to the lack of organs palliative treatments, like surgical resection, PEI and TACE are the most indicated in patients with advanced neoplastic disease, in practice patients with TNM III and IV; radiotherapy with protons and the coagulation of the tumour by microwaves or laser fibres are also used in the attempt to slow down the progress of the neoplastic process. These methods may increase the possibility of cure in well chosen patients. In some patients the most effective approach may be the combined use of various therapies, such as TACE, PEI and surgery.

Journal Article↗
PubMed2006

Managing breast cancer in the renal transplant patient: a unique dilemma.

Improvements in immunosuppression have increased patient and graft survival in transplant recipients. As a result, there is greater risk of neoplastic processes such as breast cancer. Treatment in this population is complicated by the necessary immunosuppression, vascular accesses, and transplant grafts. General surgeons may expect to encounter more of these complex patients in the community setting. We sought to evaluate the surgical treatment of breast cancer in patients with renal transplants. Hospital and private physician records were queried to identify patients who developed breast cancer after a renal or pancreatic/renal transplantation. These charts were reviewed for demographics, type of breast cancer and treatment, location of dialysis access, and complications. From June 1, 1994, to May 31, 2004, 14 patients were identified. Eight patients had functioning transplants. All patients underwent operative interventions. Ten patients underwent adjuvant treatment. Three had functioning transplants and chose not to risk the graft with cessation of immunotherapy. However, no patient with functioning transplants who underwent chemotherapy developed organ failure. Breast cancer after transplantation poses a unique dilemma. The threat of transplanted organ failure is a major concern to these patients and often supersedes adjuvant therapies.

Adult↗
PubMed2006

[Cyclooxygenase and prostanoids--biological implications].

Arachidonic acid is the main precursor of eikosanoids, which regulate the function of various organs and systems. It is released from cellular membrane phospholipids by phospholipase A2 or indirectly by phospholipases C and D. Prostaglandins, prostacyclin (PGI2), and thromboxane A2 (TAX2) are synthesized from arachidonic acid on a metabolic pathway dependent on prostaglandin H2 synthase activity, also known as cyclooxygenase (COX). Of the 12 prostaglandins, the most potent are PGD2, PGE2, and PGF2. The others are synthesized in a primary step of arachidonic acid transformation (PGG2, PGH2), by degradation of the above-mentioned prostaglandins, or are not presented physiologically and may be chemically generated (PGK2, PGL2). Similar compounds could originate from dihomo-gamma-linolenic, alpha-linoleic, and eicosapentaenoic acids. Three primary COX isoenzymes are distinguished: COX-1 (constitutive), COX-2 (inducible), and COX-3, which is detected mainly in the central nervous system. A number of partial forms of COX-1 and COX-2 are also known, but their biological functions have not been well evaluated. Although they differ in genes, transcription factors, primary protein structure, reactivity to substrates, and drugs which inhibit enzyme activity, the crystal structure is similar for all the izoenzymes. In contrast to the COX-1 gene, whose expression is typical for most of the cells, constant COX-2 expression was detected in the placenta and fetal tissue in late pregnancy. In the postnatal period, COX-2 expression decreases rapidly physiologically, and is observed in kidney, forebrain, spinal cord, as well as some other organs, but to a minor degree. It increases in inflammatory, degenerative, and neoplastic processes.

Animals↗
PubMed1991

Neoplasia associated with feline immunodeficiency virus infection in cats of southern California.

Between 1988 and 1991, feline immunodeficiency virus (FIV) infection status was evaluated in 1,160 cats examined at an oncology referral and general practice in Los Angeles, California. Twenty-nine (2.5%) cats were FIV positive. Neoplasia was present in 18 of the 29 (62%) cats. Sampling for neoplasia was intentionally biased in the oncology referral group. However, 33% (6/18) of FIV-infected cats with neoplasia originated from the general practice. Three neoplastic processes were observed; myeloproliferative disease (MPD; 5/18), lymphoma (LSA; 5/18), and squamous cell carcinoma (SCC; 7/18). One cat had LSA and SCC. Extranodal sites of LSA were common (66%) in FIV-infected cats. Sites of LSA were submandibular and mesenteric lymph nodes, liver, kidneys, periorbital area, and diffuse (heart, pancreas, bladder). Sites of SCC were sublingual (n = 2), nasal planum (n = 3), nasal planum and eyelids (n = 1), and mandible (n = 2). Feline leukemia virus co-infection was observed in 17% (5/29) of FIV-infected cats. The FIV-infected cats with MPD were young (range, 8 months to 13 years; median, 4 years) and had short survival duration (2, 6, 21, 134, 249 days) even in response to aggressive treatment. The FIV-infected cats with LSA were older (median age, 8 years; range, 4 to 14 years) and survived 60 days if untreated. Cats administered chemotherapy survived 39, 45, 217, and 243 days; the latter 2 cats had partial remission of 2 months' duration. Older FIV-infected cats had SCC (median age, 12 years; remission range, 7 to 16 years) because of more frequent association of both diseases in older cats with outdoor environment.(ABSTRACT TRUNCATED AT 250 WORDS)

Age Factors↗
PubMed1991

[Activity of angiotensin I converting enzyme in serum and bronchoalveolar lavage fluid of patients with sarcoidosis and lung neoplasms].

The lungs have an important role in the synthesis of angiotensin I converting enzyme (ACE). In BAL fluid and serum the ACE activity was determined in 18 patients with sarcoidosis (11 with high intensity and 7 with low intensity alveolitis), 14 patients with lung cancer and 16 with acute bronchitis. The activity of ACE was examined by a reagent set produced by Boehringer Mannheim Biochemica Test-Combination ACE cat. no. 789/011. The ACE activity in the high intensity alveolitis group of sarcoidosis patients was significantly increased in BAL fluid and serum in comparison to other observed patients. On the other hand, in patients with lung cancer the ACE activity was also increased in comparison to acute bronchitis and referred norms, especially in BAL fluid. This findings suggest a role of neoplastic process in ACE secretion in the airways. Very low correlation observed between ACE activity in serum and BAL fluid indicates a separate mechanism of secretion.

Acute Disease↗
PubMed1991

Transgenic models of human cancer.

Transgenic animal technology has been useful for the direct demonstration of the tumorigenic potential of oncogenes in vivo. Over the past eight years a wide variety of oncogenes and proto-oncogenes from viral and cellular sources have been inserted into the germline of mice with subsequent development of neoplasia. Many of the published reports describe similarities between morphologic features of the transgenic mice tumors and those occurring naturally in humans. We discuss the morphologic features of selected transgenic models carrying viral genes and review their applicability to investigations directed toward understanding cancer in general and specifically gastric cancer, neurofibromatosis and leukemia. Examples of the impact of nutrition, interaction with growth factors and initiation with chemical carcinogens are presented. In one of the models functional similarities to the mechanism of oncogenesis in human T-cell leukemia virus type-1 (HTLV-1) lymphoma may exist with activation of cytokine production and subsequent autocrine stimulation. The transgenic model of proximal gastric cancer demonstrates features similar to those seen in carcinogen-induced neoplasia. These studies underscore the vast potential of transgenic models for inquiry into the genetic and epigenetic basis of human carcinogenesis. However, many features of transgenic cancer models differ from cancer in humans and the specific criteria for judging the value of transgenic models remain unclarified. For example, although the tumors arising in the HTLV-1 Tax transgenic mice show numerous similarities to human neurofibromatosis including development of lesions of the iris, the similarities do not necessarily extend to the molecular involvement of neurofibromatosis-1 (NF-1), a gene with structural and functional homology to GTPase activating proteins. Transgenic experiments of the future will ask questions beyond whether a particular gene is capable of initiating the neoplastic process. The ability to construct systems in vivo with a defined starting point that facilitate further controlled manipulation of events resulting in cancer provide great opportunities to dissect the various molecular pathways involved in such a process. Therefore, gene knockout experiments and disruption of gene function will further enhance our ability to understand the multi-factorial process of tumor development.(ABSTRACT TRUNCATED AT 400 WORDS)

Adenovirus E1A Proteins↗
PubMedDate not supplied

[Prognosis of clinical course of primary brain tumours in children in relationship to the duration and characteristic features of initial clinical symptoms].

UNLABELLED: Primary tumours of the central nervous system belong to the most frequently occurring neoplastic diseases in paediatric patients. During the initial phase of disease development, the clinical symptoms of brain tumours might suggest disorders of other organs and their diagnosis is frequently delayed in relation to therapeutic possibilities. The aim of the study was to analyse the characteristic features and duration of preliminary symptoms arising due to brain tumours in paediatric patients treated in a single centre and to try to assess their prognostic significance for recurrence and death. MATERIAL AND METHODS: We performed a retrospective assessment of the characteristic features of preliminary symptoms of brain tumours in 81 paediatric patients (45 female, 35 male) in the age range of 1.5 month - 17.2 years. Those characteristic features included the duration of symptoms until diagnosis (Pre-Diagnostic Symptoms Interval, PSI) and their correlation with the tumour type, its localization and size at the moment of diagnosis. RESULTS: The mean duration of symptoms in the studied group was 3 months. In nearly 45% of patients PSI was longer then 3 months and in 17,5% it was over 6 months. The predominant preliminary disease symptoms were the symptoms of increased intracranial pressure (n=56, 69,1%) The longer PSI correlated with the disease recurrence rate (p=0.024) and death rate (p=0.04). When PSI was longer then 6 months, all the tumours diagnosed were larger then 30 mnm, however no relationship was found between PSI duration and the tumor size (p=0.35). There was no correlation between the tumour size and the frequency of death (p=0.8), but in patients with tumours smaller then 30 mm in their greatest dimension, the recurrence of the neoplastic process was more frequent. CONCLUSIONS: Duration of preliminary symptoms may have an effect on the tumour recurrence and on the rate of death in paediatric patients with brain tumours. Early diagnosis plays an evident role in prognosis.

Adolescent↗
PubMed2006

[Adenomatoid tumor].

Adenomatoid tumour is a neoplastic process of discussed origin, but the immunohistochemical phenotype leads a mesothelial derivation. The preferential site of origin is the genital apparatus of both sexes, however extragenital cases have been described. The histological pattern varies from tubular formation, to solid growth, to cystic areas. In the present report we described a case of Adenomatoid tumour of the uterus body in a 46 years old patient.

Actins↗
PubMed2006

Enhancing the pathologist's role at hospital tumor boards.

Recommendations are proposed to enhance the role of the pathologist in the hospital-based tumor conference (tumor board). The modifications focus on two components integral to the conference: the presentation of salient pathologic features of each tumor selected for discussion within the time constraints allotted, and the pathologist's role as a principal institutional educator with respect to neoplastic processes. Opportunities to utilize conference presentations as a resource in other educational settings are also considered.

Neoplasms↗
PubMed2006

[Interleukin-10 in laryngeal cancer patients treated by surgery or radiotherapy].

INTRODUCTION: The early detection and right monitoring of the laryngeal cancer make a better chance of recovery. Therefore factors that might be showing the presence of neoplastic process are constantly being looked for. The detection of correlation between incidence of cancer and immunity system disorders makes us look for and try to answer an important question: are there any factors that might be cancer markers in immunity system? Cytokines are molecules that regulate the process of differentiation and proliferation. They are also the mediators of immunological and inflammatory reactions. Interleukina-10 (IL-10) is a cytokine that has various important functions stimulating immunity processes. IL-10 is a factor stimulating killer cells/cytoxic lymphocytes/ and is able to kill cancer cells growth spontaneously. It has been detected that some cancer cells can produce some IL-10, too. The aim of the study was to evaluate the serum level concentration of IL-10 in the laryngeal cancer patients before any medical treatment and its denotation after surgery or radiotherapy. MATERIAL AND METHODS: A group of 43 male patients with laryngeal cancer was considered for the purpose of this study. 22 patients were treated by surgery and 21 by radiotherapy. In all the cases the serum concentration of IL-10 before the treatment, in the first and 30th days after therapy was evaluated. The results were compared with the group of 20 healthy volunteers. RESULTS: The mean value of IL-10 concentration in laryngeal cancer patients treated by surgery was 14.0 pg/ml before treatment, 12.8 pg/ml in the 1 day and 14.4 pg/ml 30 days after the therapy. IL-10 concentrations in patients treated by radiotherapy were respectively: 15.4, 14.4 and 15.9 pg/ml. The mean value of IL-10 in the control group was 4.9 pg/ml. The serum concentrations of IL-10 in the laryngeal cancer patients were significantly higher than in the control group. These IL-10 concentrations didn't change significantly after the surgery or radiotherapy. CONCLUSION: The serum concentration of IL-10 in the laryngeal cancer patients is significantly higher than in the healthy control group. The changes of serum concentrations after the surgery or radiotherapy of laryngeal cancer patients are not significant and characteristic.

Adult↗
PubMed2006

The mismatch repair gene hPMS2 is mutated in primary breast cancer.

Mismatch repair (MMR) genes play a fundamental role in the correction of replication errors and their mutation leads to cancer development. In the present study we have analyzed the hPMS2 MMR gene for mutation using 20 primary breast cancers and seven breast tissues obtained from areas adjacent to breast cancer. For this purpose we have used cDNA sequence analysis and Western blotting using the specific antibody against the amino-terminal domain E-19. In primary breast cancers we found that the hPMS2 gene had 9 missense mutations [codons: 513 (by change of Ser x Asp) in 14 tumors, 520 (Ala x Val) in 8 tumors, 573 (by change of Thr x Ser in 19 tumors), 578 (by change of Arg x Leu in 9 tumors), 587 (by change of Ser x Asp in 7 tumors), 590 (by change of Ile x Leu in 12 tumors), 598 (by change of Gln x His in 5 tumors), 601 (by change of Ser x Leu in 13 tumors), 608 (by change of Ala x Ser in 9 tumors. Nine out of 20 breast cancers had a non-sense mutation in nucleotide 1862 by changing Adenine by Thymine (AAG x TAG), which corresponded with a change in codon 613 by a change of Lys by stop codon. This non-sense mutation is responsible for the premature truncation of the protein hPMS2, which is reflected in the Western blotting by two bands, one corresponding with the wild-type form (100 kDa) and a lower one (75 kDa) corresponding with the truncated form of the hPMS2 MMR protein. This truncated protein and the mutations in the hPMS2 gene were also detected in two samples of normal-appearing tissue adjacent to their corresponding cancerous lesion. Altogether the present report demonstrates that primary breast cancers harbor mutations in this MMR gene and that normal-appearing breast tissue adjacent to the primary lesion also harbors the same mutations before the neoplastic process is manifested.

Adenosine Triphosphatases↗
PubMed1990

[Cancers of the prostate and cyproterone acetate. Value of blood testosterone and PSA levels for treatment surveillance].

On the basis of a retrospective series of 74 patients with adenocarcinoma of the prostate, the authors study the survival of these patients according to the clinical stage of the lesion when treated with cyproterone acetate. Biologically speaking, the authors have studied the evolution of the blood testosterone level, as well as of PSA and PAPs. Their conclusion is that the PSA is an excellent indicator of the efficacy of the cyproterone acetate treatment. Its fast decrease proves treatment efficacy, while a new rise indicates the resumption of evolution of the neoplastic process and must lead to change the therapeutic approach.

Adenocarcinoma↗
PubMed1991

[Acute pancreatitis in primary and metastatic tumors of the pancreas].

Malignant tumours both of the pancreatoduodenal zone and of other organs situated close to or remote from it occupy a certain place among various etiopathogenetic factors of acute pancreatitis. Complication of the neoplastic process of these organs by acute carcinogenic pancreatitis (ACP) has an effect on the clinical picture of the disease as well as on the therapeutic tactics and the outcomes of the treatment. According to the authors' data (30 patients), ACP occurs in primary carcinoma of the pancreas and in its secondary involvement (metastases and growth of tumours of other organs into the pancreatic tissue). The article discusses the causative factors and clinical forms of ACP, the specific features of their diagnosis and therapeutic tactics. Purposeful nonoperative and operative treatment of ACP makes it possible to reduce the mortality in malignant diseases and prolong the patients' survival.

Acute Disease↗
PubMed1991

Immortalization by human papillomavirus type 16 alters retinoid regulation of human ectocervical epithelial cell differentiation.

Human cervical cells are a primary site of papillomavirus infection and 90% of all cervical tumors are positive for human papillomavirus (HPV) DNA. Over one-half million cases of HPV-associated cervical, vulvar, and penile cancers are reported per year. Yet, in spite of the magnitude of this problem, the effects of HPV infection on cervical cell growth and differentiation are not well characterized. To study these effects we have developed a clonal cell line of HPV-16-immortalized ectocervical epithelial cells, ECE16-1. In the present study we demonstrate that under normal growth conditions the cytokeratin content of ECE16-1 cells is dramatically altered compared to normal cervical cells; the level of K5, K6, K14, K16, and K17 is reduced and the level of K7, K8, and K19 is increased. We demonstrate that this change is largely due to a difference in the response of the cells to retinoids, as growth in retinoid-free medium produces a complete normalization of cytokeratin levels. Upon addition of natural and synthetic retinoids, the levels of cytokeratins K5, K6, K14, K16, and K17 are reduced, while the levels of cytokeratins K19, K7, and K8 are increased. Cytokeratin K13 levels are only slightly altered. The level of involucrin, a precursor of the cervical cell envelope (superficial cell), is not changed by immortalization nor is it regulated by retinoids. Transglutaminase activity is also not appreciably altered by immortalization; however, ECE16-1 cells make fewer envelopes than normal ECE cells. Our results clearly indicate that natural and synthetic retinoids suppress the differentiation of HPV transformed cervical cells. In early, low grade, cervical intraepithelial neoplasia, transcription of the HPV16 E6/E7 oncogenes is confined to the suprabasal layers. Our results suggest that retinoids, because they inhibit the differentiation of HPV16 immortalized cervical cells, may reduce the extent of viral oncogene transcription and thus be useful in slowing the neoplastic process.

Cell Differentiation↗
PubMed1992

Chest manifestations of AIDS.

Chest radiographs, computed tomography and gallium scanning are useful in diagnosing the pulmonary manifestations of acquired immunodeficiency syndrome. Most opportunistic infections in patients with AIDS affect the lung as the primary target organ. Bilateral perihilar or basilar interstitial infiltrates, which may progress to the ground-glass appearance of adult respiratory distress syndrome, are commonly seen in cases of Pneumocystis carinii pneumonia. Unilateral or miliary infiltrates and cavitary lesions may be atypical presentations. Diffuse interstitial infiltrates are also seen in mycobacterial, fungal and cytomegalovirus infections. Mycobacterium tuberculosis infection in AIDS patients resembles primary tuberculosis infection rather than secondary tuberculosis reactivation. Intrathoracic adenopathy in AIDS patients suggests neoplastic processes, such as lymphoma and Kaposi's sarcoma, and opportunistic infections such as M. tuberculosis, Mycobacterium avium-intracellulare and fungal infections. Bronchoscopy with bronchoalveolar lavage and transbronchial biopsy are usually necessary for identification of the etiologic agent.

Acquired Immunodeficiency Syndrome↗
PubMed1992

Mobile encapsulated lipomas.

Mobile encapsulated lipomas are a benign neoplastic process with pronounced mobility in the subcutaneous plane. Characteristic clinical and histologic features differentiate this distinctive entity from similar reactive adipose processes.

Aged↗
PubMed1975

Influence of carbon tetrachloride or riboflavin on liver carcinogenesis with a single dose of aflatoxin b1.

Liver carcinogenesis with a single dose of aflatoxin B1 (7 mg/kg body weight) has been investigated in a group of female Wistar strain rats by repeated biopsies and necropsies. Another group received a subsequent intoxication with carbon tetrachloride by inhalation (approximately 200 doses) and another one was overloaded with riboflavin (25 parts/10(6) in drinking water). The frequency of hepatomata was almost equal in the aflatoxin and aflatoxin-carbon tetrachloride group. It was lowere in the riboflavin-aflatoxin group. In these 3 groups cirrhosis was never present in neoplastic livers. Megalocytosis was the first lesion observed. All tumoral livers had previous or concomitant megalocytosis. This modification was about as frequent, intense and widespread in aflatoxin-CCl4 and aflatoxin groups but appeared much earlier, as did the first hepatoma, in the aflatoxin-CCl4 group. It was less frequent, less intense and less widespread in the riboflavin-aflatoxin group than in the aflatoxin group. There was also a lower frequency of hepatomata in the riboflavin-aflatoxin group, but the difference was not significant due to the too small number of animals involved. The facts are not a proof of the existence of an obligatory link between megalocytosis and carcinogenesis since a slight megalocytosis was observed in the riboflavin group not affected by the neoplastic process. However, the simplest explanation of our results would be to consider that the potential tumour cells are located among the megalocytic cells, without admitting that every megalocyte is obligatorily a precancerous cell. CCl4 seems to act in shortening the time of appearance of megalocytosis. The protective effect of riboflavine should be regarded with more caution.

Aflatoxins↗