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PubMed1993

Heritable colorectal cancer and cancer genes: systemic expressions.

Epidemiological studies of heritable cancer have demonstrated that cancer predisposition is a dominant trait; these studies have also predicted the recessive outcome of the neoplastic process. Biochemical studies of dominantly heritable cancer have demonstrated the relevance of systemic effects. The systemic effects are presumably due to a dominant mutation at the "initiator locus." Collectively they define cancer initiation at the cellular level (as described in this review). Molecular biological studies have demonstrated that cancer progression and the appearance of clinical cancer occur through an accumulation of recessive mutations at critical loci. We must continue to try to define not only the inherited and acquired gene defects that initiate the neoplastic state but also the subsequent genetic alterations and biomarkers involved in tumor progression. These genetic defects are already proving useful in diagnosis and prognostication. The hope is that these biomarkers may be useful for designing specific differentiation therapy.

Colorectal Neoplasms↗

PubMed1991

Metastatic and invasive tumours involving the heart in a geriatric population: a necropsy study.

In a series of 744 necropsied subjects with a diffuse malignant process, 57 cases of cardiac involvement were observed (50 metastatic carcinomas and 7 lymphomas or myeloproliferative disorders). The most frequent site of involvement was the pericardium and epicardium in lung or breast carcinoma, suggesting regional lymphatic invasion. Myocardial involvement was rarer and usually associated with cutaneous melanoma and lymphoma, suggesting haematogenic invasion. Endocardial involvement was exceptional. The multiple causes of heart disturbance in the elderly cloud the clinical diagnosis of such cardiac involvement; however, isolated pericardial and/or epicardial abnormalities should heighten suspicion of a neoplastic process.

Aged↗

PubMedDate not supplied

Splenic fine needle aspiration and core biopsy. A review of 49 cases.

OBJECTIVE: To analyze the authors' experience with splenic fine needle aspiration (sFNA) and splenic core biopsy (sCB) and to examine their roles in patients with splenomegaly or splenic mass lesions. STUDY DESIGN: A total of 56 sFNAs and/or sCBs were performed on 49 patients for neoplastic and nonneoplastic indications. Both sFNAs and sCBs were performed in 21 (38%) cases, sFNAs alone in 26 (46%) and sCBs only in 9 (16%). Cytologic findings were evaluated for specimen adequacy, diagnosis and use of ancillary techniques. Cytologic diagnosis was compared with histology on subsequent splenectomy or bone marrow biopsy, when available. RESULTS: There were a total of 33 males and 16 females (aged 30-82 years) in the study. Radiologic findings were single or multiple masses (42), fluid collection (3) or diffuse splenomegaly (4). The cytologic diagnosis was neoplastic process in 12 (25%), nonneoplastic in 32 (65%) and inadequate specimen in 5 (10%). The procedure was adequate for diagnosis in 44 (90%) patients. Cytologic diagnosis correlated with subsequent histology in all cases where tissue diagnosis was available. Major complications occurred in 3 (6%) patients, including hemorrhage, pseudoaneurysm and hypotension. Five other patients (10%) had minor complications. The number of passes, inclusion of sCB and repeat procedures were not associated with an increased risk of complications. CONCLUSION: sFNA and sCB have excellent diagnostic accuracy in both neoplastic and nonneoplastic splenic disorders. While the overall complication rate is significant, major complications of the procedure are uncommon.

Adult↗

PubMed1993

Wild-type but not mutant p53 can repress transcription initiation in vitro by interfering with the binding of basal transcription factors to the TATA motif.

It has previously been shown that excess wild type (wt) p53 can repress the transcriptional activity of a variety of promoters in intact cells. To determine whether this transcriptional repression represented a direct effect of p53, wt and mutant p53 were prepared from E. coli-produced p53 and from insect cells infected with a recombinant baculovirus. When added into an in vitro transcription system, wt p53, but not mutant p53 reduced markedly transcription from the c-myc promoter, as well as from an array of other promoters, with the exception of an MHC class I gene promoter. The presence of wt p53 seemed to affect specifically the formation of the transcription preinitiation complex because preformed initiation complexes were completely refractory to wt p53, as was also the process of transcript elongation. Wild-type but not mutant p53 interfered with the stable binding of TBP and TFIIA to the TATA motif, although both wt and mutant p53 could associate in vitro with purified TBP. We propose that upon binding to TBP, wt but not mutant p53 specifically blocks the ability of TBP to engage in interactions required for efficient transcriptional initiation. This may account, at least in part, for the ability of excess wt p53 to inhibit cell proliferation and to interfere with neoplastic processes.

Base Sequence↗

PubMed2001

Immunohistochemical expression of the intracellular component of galectin-8 in squamous cell metaplasia of the bronchial epithelium in neoplastic and benign processes.

Specified galectins are known to play a role in regulating cell proliferation, differentiation, adhesion and migration. Po66, a mouse IgG1 monoclonal antibody produced by immunization against squamous cell cancer, reacts against a carbohydrate-binding protein (Po66-CBP), recently shown to be a member of the galectin family with a strong homology with galectin-8 (PCTA-1), identified as a human tumor-associated antigen. We studied Po66 in squamous metaplasia of the bronchi in order to determine whether it could be specifically involved in neoplastic conditions and if so, if it would be helpful in distinguishing metaplasia at risk of cancer. Twenty-eight formalin-fixed, paraffin-embedded archival tissues of 17 metaplasias with SCC, 3 metaplasia with distant neoplastic disease and 8 metaplasias with an inflammatory process, were immunostained using a streptavidin biotin peroxydase method. The squamous metaplasias were positively stained in non-neoplastic disease as well as in neoplastic processes. Expression was also observed in stromal and normal cells. Po66-CBP was not associated with a pre-neoplastic character. We discussed the expression of this intra-cellular component of galectin-8 according to the functions of galectins in cellular differentiation, host reaction against tumor, and inflammation.

Biomarkers, Tumor↗

PubMed1990

Recent advances in flow cytometric techniques for cancer detection and prognosis.

The application of flow cytometry to cancer diagnosis and the prediction of tumor behavior continues to expand. The ability of flow cytometry to examine multiple parameters of large numbers of individual cells is being exploited increasingly to characterize neoplastic processes better. This will allow closer examination of tumor heterogeneity and identification of subpopulations with different behavioral patterns. Flow cytometry is being used with greater frequency in attempts to predict tumor behavior and response to therapy. Flow cytometry may have the most to offer in this area. Diagnosis of cancer by routine histopathological examination will not be replaced by flow cytometry; flow cytometry will be used in conjunction with morphological descriptions. The detection of proliferation antigens and oncogene products, as well as cell cycling, provides information on neoplastic progression that is not readily obtainable by other methods. In addition, flow cytometry will undoubtedly be used to measure other features of neoplastic cells, such as enzyme levels and ion fluxes, which may better characterize the behavior of the tumor. Advances in flow cytometry instrumentation, light sources, fluorochrome development, and basic aspects of cellular and molecular biology will continue to permit this technology to define neoplastic cells and their behavior better, resulting in both improved patient care and a better understanding of tumor biology.

Antineoplastic Agents↗

PubMed1977

The effect of an aromatase inhibitor, 4-hydroxy-4-androstene-3,17-dione, on estrogen-dependent processes in reproduction and breast cancer.

4-Hydroxy-f-androstene-3,17-dione (4-OH-A) when tested at various concentrations was found to inhibit markedly the conversion of 4-andorstene-3,17-dione to estrogens inhuman placental and rat ovarian microsomes. To obtain evidence that estrogen biosynthesis could also be reduced in vivo with 4-OH-A, rats were treated sc at a dose level of 50 mg/kg body weight. After 3 h the ovarian veins were cannulated and blood collected. Estradiol concentrations in the plasma were reduced by 80% compared to control values during the proestrous surge and on Day 4 of pregnancy. 4-OH-A was also found to be effective in controlling estrogen-dependent reproductive and neoplastic processes. In rats treated from Day 2-7 of pregnancy, implantation of fertilized ova was completely prevented in some rats, while in others either implantation was delayed or the development of implants was retarded. 4-OH-A treatment of rats having estrogen-dependent breast tumors induced by 7,12-dimethylbenz(a)anthracene caused 80% of the tumors to regress significantly in 4 weeks of treatment; 42% of these regressed completely.

9,10-Dimethyl-1,2-benzanthracene↗

PubMed1996

Delineation of antigenic pathways of ethionine-induced liver cancer in the rat.

Although oval cell proliferation is observed prior to the appearance of hepatic nodules and hepatocellular carcinomas during ethionine-induced liver carcinogenesis in the rat, the role of these presumptive hepatic stem cells during the neoplastic process remains controversial. In order to investigate this question, we have used a panel of monoclonal antibodies against antigens associated with normal hepatocytes, oval cells and transplantable hepatocellular carcinomas (THC) to trace antigenic pathways leading to liver cancer. Male ACI rats were fed a choline-deficient diet containing 0.1% DL-ethionine for 4, 16 or 30 weeks. Immunocytochemical analysis of frozen liver sections revealed a subpopulation of hepatic nodules (7/52), carcinomas (8/15) and lung metastases (3/5) containing populations of cells expressing both oval cell, hepatocyte and neoplastic markers. Carcinomas expressing oval cell markers often appeared as a mosaic of well-defined patches composed of phenotypically distinct cells. Many of the phenotypes expressed closely mimicked patterns of expression observed in fetal and neonatal liver. THC derived from primary tumors positive for oval cell antigens (4/5) continued to express these markers. Northern blot analysis and immunocytochemical analysis revealed that 4/5 primary hepatocellular carcinomas (PHC) and THC expressed alpha-fetoprotein (AFP) and albumin transcripts and contained subpopulations expressing AFP together with hepatocyte and oval antigens. In contrast, a well-differentiated PHC and its corresponding THC lacked AFP mRNA and oval cell antigens but showed strong expression of both hepatocyte and neoplastic markers. These results demonstrate that a subpopulation of malignant and metastatic hepatocellular carcinomas are comprised of cells expressing multiple oval cell markers in this model system.

Animals↗

PubMed2001

Immunosenescence and cancer: a review.

The human neoplastic pathologies are age-dependent. The increased occurrence of tumors observed with advancing age may be determined by the accumulation of certain phenomena promoting different phases of neoplastic processes. In these events, important roles can be attributed to mutations of the genome that accumulate during aging and to the immunosenescence. It may be hypothesized that certain tumors controlled by the immune system may become more frequent in the elderly as a consequence of the decreased functionality of this important defense system of the organism. Nevertheless, the problems of the interrelationships between the immunosenescence and tumors are seriously contradictory. Therefore, on the one hand, one has to establish how much the immunodeficit of the elderly patient may be responsible for the neoplastic pathology, while on the other hand, one cannot neglect important environmental and pathophysiological factors in these cases.

Journal Article↗

PubMed1995

Disruption of the architectural factor HMGI-C: DNA-binding AT hook motifs fused in lipomas to distinct transcriptional regulatory domains.

Lipomas are one of the most common mesenchymal neoplasms in humans. They are characterized by consistent cytogenetic aberrations involving chromosome 12 in bands q14-15. Interestingly, this region is also the site of rearrangement for other mesenchymally derived tumors. This study demonstrates that HMGI-C, an architectural factor that functions in transcriptional regulation, has been disrupted by rearrangement at the 12q14-15 chromosomal breakpoint in lipomas. Chimeric transcripts were isolated from two lipomas in which HMGI-C DNA-binding domains (AT hook motifs) are fused to either a LIM or an acidic transactivation domain. These results, identifying a gene rearranged in a benign neoplastic process that does not proceed to a malignancy, suggest a role for HMGI-C in adipogenesis and mesenchyme differentiation.

Amino Acid Sequence↗

PubMedDate not supplied

[Nf-kB transcription factor: role in the pathogenesis of inflammatory, autoimmune, and neoplastic diseases and therapy implications].

PURPOSE: Description of the involvement of the transcription factor NF-kB in inflammatory, autoimmune and neoplastic processes. Clinical implications from basic research. DESIGN: Review of the most significant data reported in the literature and personal publications. RESULTS: NF-kB is an ubiquitous transcription factor member of the proto-oncogene family rel. NF-kB regulates the expression of several genes involved in inflammatory and immune responses. The classical activated form of NF-kB consists of the p50/p65 heterodimer, different dimers may be formed with members of rel, AP1, steroid hormones receptors family. Many studies suggest that NF-kB should be considered as an important mechanisms of inflammatory processes and autoimmune diseases. Many important anti-inflammatory drugs and immunosuppressants inhibit NF-kB. Several observations have suggested a role of the inappropriate activation of NF-kB in cell proliferation, transformation, and tumor development, mainly lymphomas. Conversely, it has been proposed that the activation of NF-kB in immune cells may contribute to anti-tumor immunity. CONCLUSIONS: NF-kB is an optimal target of anti-inflammatory and immunosuppresant therapies. Molecular studies on NF-kB are very important to understand the pathogenesis of inflammatory, autoimmune and neoplastic diseases, and to identify new drugs that inhibit NF-kB activation.

Autoimmune Diseases↗

PubMed2003

Epigenetic gene silencing in cancer initiation and progression.

Hypermethylation of CpG islands, an epigenetic event that is not accompanied by changes in DNA sequence, represents an alternative mechanism to deletions or mutations to inactivate tumor suppressor genes. Recent evidence supports the notion that CpG island hypermethylation, by silencing key cancer-related genes, plays a major causal role in cancer. However, a long-standing issue in the field is the sequence of molecular events leading to epigenetic gene silencing. A new model has been proposed that chromatin remodeling, as a result of histone deacetylation and methylation, is the primary event in abrogating transcriptional initiation; subsequently, CpG island hypermethylation establishes a permanent state of gene silencing. Accumulating evidence indicates that CpG island hypermethylation is an early event in cancer development and, in some cases, may precede the neoplastic process. Because of their heritable nature, hypermethylated CpG islands leave 'molecular footprints' in evolving cancer cells and can be used as molecular markers to reconstruct epigenetic progression during tumorigenesis. Furthermore, hypermethylated CpG islands are proving to be useful for molecular classification of different cancer types.

CpG Islands↗

PubMedDate not supplied

Inflammatory myofibroblastic tumor of the gastroesophageal junction in childhood.

We report a unusual case of an inflammatory myofibroblastic tumor arising at the gastroesophageal junction in a 14-year-old girl. The bland histologic appearance with concurrent infiltration into adjacent structures made diagnostic interpretation difficult, but suggested a neoplastic process. A literature review was undertaken to address diagnostic and management issues raised in this case. Although the anatomic location was unusual, clinical, grass, histopathologic, and immunohistochemical data substantiated the diagnosis of inflammatory myofibroblastic tumor. The bland histologic appearance was consistent with the most widely accepted view of inflammatory myofibroblastic tumor as a low-grade neoplasm. Wide surgical excision was performed. This is considered the preferred treatment given the potential risk of recurrence and aggressive behavior, most frequently noted with extrapulmonary disease. Although inflammatory myofibroblastic tumor represents an heterologous spectrum of benign to malignant neoplastic proliferations, the prognosis is good in casts with benign histologic features.

Adolescent↗

PubMed2000

Bile acid secretion during rat liver carcinogenesis.

Retro-differentiation of liver parenchyma during neoplastic processes is characterized by the expression of tumor antigens, such as alpha-fetoprotein and the placental isoenzyme of glutathione-S-transferase (GST-P). To investigate whether this may also affect a typical liver function such as bile acid secretion was the aim of this work. Rat hepatocarcinogenesis was induced by diethylnitrosamine (i.p., 200 mg/Kg body weight at day 0) and promoted by two-thirds partial hepatectomy (at day 21) plus 2-acetamidofluorene administration (50 mg/Kg body weight, subcutaneously, twice a week from day 14 to day 35). In order to carry out planimetric measurements of neoplastic tissue after immunohistochemical staining, a novel monoclonal antibody (MAb 14.1.3) against GST-P with no cross-reactivity against the major liver isoform of GST (GST-H) was raised. Analysis of total biliary bile acid output using the 3alpha-hydroxysteroid dehydrogenase method indicated that a significant reduction (-26%) occurred during the formation of GST-P-positive foci (12 wk). This was restored to normal values during adenoma formation (16-20 wk), but decreased again during carcinoma transformation (32 wk). These changes were not parallel to that observed in bile flow, which was progressively but slightly decreased throughout the whole period under study. HPLC analysis of bile samples collected for 1 h at different time points during hepatocarcinogenesis revealed that in contrast to what happens during cholestatic disease, a continuous and progressive increase in the cholic acid-to-chenodeoxycholic acid ratio (from 4.4+/-0.5 in control animals to 15.1+/-1.9 in rats with hepatocellular carcinoma) occurs. A significant and transient increase at 16 wk (+120%) in the proportion of bile acids amidated with glycine as compared to those conjugated with taurine was also observed. These results indicate that the mechanisms accounting for the secretion of major bile acids are modified differently at various steps of rat liver tumor development.

2-Acetylaminofluorene↗

PubMed1999

Combined morphological and interphase fluorescence in situ hybridization study in multiple myeloma of Chinese patients.

To gain insight into the real incidence of the numeric chromosomal aberrations and the cell lineage involvement of the neoplastic process in multiple myeloma (MM), we examined 18 Chinese MM patients by May-Grunwald-Giemsa (MGG) staining and fluorescence in situ hybridization using three DNA centromeric probes specific for chromosomes 3, 7, and 9. In this investigation, cytogenetic abnormalities were detected in plasma cells (PCs), myeloid cells (MCs), and lymphoid cells (LCs) in all of the MM patients studied. This is the first demonstration of the cytogenetic aberration involved in the myeloid series. Furthermore, the MCs and PCs of 16 MM patients had the same aneuploidies in one or more of the chromosomes analyzed. These data suggest that the neoplastic transformation of MM may occur early in the hematopoietic development. Chromosomal aberrations involving mainly subclones and considerable cellular heterogeneity with gain of a variety of copy numbers of the same chromosome were demonstrated within PCs, which may possibly be the result of an underlying defect of PCs in the control of their number of chromosomes. Whereas PCs showed evidence suggestive of increased polyploidization, MCs and LCs, which exhibited similar chromosomal patterns as the former, rarely did. Thus, the clonal evolution from LC to PC, if that happens in MM, is characterized by chromosomal instability favoring growth of tumor cells with polysomies and polyploidies.

Adult↗

PubMed1996

Magnetic resonance imaging (MRI) of the knee: a pattern approach for evaluating bone marrow edema.

The applications of magnetic resonance imaging (MRI) have become numerous for the assessment of disorders involving the knee. Once a technique used nearly exclusively in the evaluation of internal derangement of this joint, it now plays an important role in the diagnosis of processes that affect the bone marrow, including those that occur as a result of trauma, infection, tumor, and rheumatologic disorders. Signal alterations in the bone marrow frequently are present in association with these pathological processes. When the signal is of low intensity on T1-weighted images and becomes heterogeneously increased in intensity on T2-weighted images, it indicates the presence of edema in the bone marrow. Two types of marrow edema are presented in this review: posttraumatic and reactive. In many situations, the area of altered signal intensity is radiographically occult. The distribution of marrow edema often reflects the mechanism of injury in trauma and may correlate with additional injuries to the surrounding soft tissues. Reactive marrow edema occurs either in response to an inflammatory focus in the bone and/or joint or a neoplastic process in or adjacent to the bone.

Adolescent↗

PubMed1999

[Cerebral ischemia as initial manifestation of neoplastic low-malignancy changes. 2 case reports and review of the literatures].

Thrombembolic events as paraneoplastic complications in malignant disease account for severe morbidity and mortality in these patients. In some cases disturbance in hemostasis is the first manifestation of a neoplastic process. We report the cases of two patients with cerebral and extracerebral vessel occlusions, in whom epithelial tumors of low malignant potential (borderline-tumors) of ovary and peritoneum were diagnosed later on. In one case the removal of the tumor stopped the coagulation problems. The second patient died a few days after the first symptoms with devastating multiple vessel occlusion. In stroke of unknown aetiology a paraneoplastic process should be kept in mind. The diagnosis is more probable with recurrent thrombembolism in different body regions and when warfarin therapy was ineffective. Thoughtful coagulation studies and a tumor search program is recommended in these cases.

Adult↗

PubMed1976

Bone marrow necrosis.

The clinical findings of bone marrow necrosis in 13 patients undergoing bone marrow examination to investigate a peripheral blood cytopenia or leukoerythroblastic blood smear were reviewed and compared to those in the literature. Excluding sickle cell disease, all cases of bone marrow necrosis diagnosed during life were associated with a neoplastic process involving the marrow. A myeloproliferative disorder was found in five patients, metastatic carcinoma in five patients, a lymphoma in two patients, and both a myeloproliferative disorder and metastatic carcinoma in one patient. Marrow necrosis was found to involve the marrow at multiple sites in a piecemeal fashion with areas of necrotic marrow and structurally intact marrow adjacent to each other. Severe bone pain without roentgenographic abnormality was the major symptom in 85% of the patients. Marrow and fat emboli, hypercalcemia and peripheral blood cytopenias were identified as direct complications of marrow necrosis. The prognosis of patients with marrow necrosis secondary to neoplastic disease was found to be extremely poor with a median survival of less than one month. However, one patient responded to antineoplastic chemotherapy and showed healing of the bone marrow.

Adenocarcinoma↗