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PubMedDate not supplied

US approach to jaundice in infants and children.

High-resolution real-time ultrasonography (US) serves as an important tool for differentiation of obstructive and nonobstructive causes of jaundice in infants and children, independent of liver function. Unconjugated hyperbilirubinemia occurs in approximately 60% of normal term infants and in 80% of preterm infants. Persistence of neonatal jaundice beyond 2 weeks of age demands US evaluation to differentiate between the three most common causes: hepatitis, biliary atresia, and choledochal cyst. In all three conditions, the hepatic echotexture is diffusely coarse and hyperechoic, but this appearance may be seen in a variety of hepatic inflammatory, obstructive, and metabolic processes. Thus, hepatic scintigraphy and at times percutaneous liver biopsy are necessary to narrow the differential diagnosis and to identify patients who require more invasive techniques (eg, intraoperative cholangiography). US is useful for demonstrating inspissated bile and biliary duct stones. In infants, stones are usually secondary to obstructive congenital anomalies of the biliary tract, total parenteral nutrition, furosemide treatment, phototherapy, dehydration, infection, hemolytic anemia, and short-gut syndrome, whereas in older children, stones are usually associated with sickle cell disease, bowel resection, hemolytic anemia, and choledochal cyst. Jaundice in infants and children may also be due to cirrhosis, benign strictures, and neoplastic processes.

Biliary Atresia↗
PubMed2001

The genetic epidemiology of glioma.

With traditional epidemiologic research designs, few environmental risk factors for malignant brain tumors have been revealed, and although syndromes exist where brain tumors occur frequently, these explain a small proportion of the overall incidence. In a similar way, the search for genetic causes has been thwarted by the rarity of families with multiple affected relatives, inhibiting genetic linkage, sib-pair, or even population-based association studies. Molecular genetic studies generally involve searching for candidate proto-oncogenes and tumor suppressor genes by comparing DNA from tumor material with constitutional (germline) DNA. However, it remains difficult to distinguish causative genetic aberrations from chaotic neoplastic processes, and studies so far have not yielded consistent information on the location of such causative genetic lesions. The current literature covering the molecular genetics of glioma is discussed herein and alternative approaches that can be used to identify genetic causes of glioma described.

Adult↗
PubMed1983

Biochemical and quantitative histochemical study of reduced pyridine nucleotide dehydrogenation by human colonic carcinomas.

This study shows a marked increase in the activity of the soluble enzyme DT-diaphorase and of the histochemical activity of the reduced nicotinamide adenine dinucleotide and reduced nicotinamide adenine dinucleotide phosphate nitroblue tetrazolium menadione-mediated reductases in human colonic carcinomas when compared with the enzymatic activities of portions of the colon uninvolved by the carcinomatous process. The activity of the reductases in histological sections was quantitated with a microphotometer. It is believed that the increase in histochemical nitroblue-tetrazolium reductase activity in the histochemical reactions in colonic carcinomas is a real reflection of the activity of the DT-diaphorase, because the increase in the dehydrogenation of reduced nicotinamide adenine dinucleotide equals the dehydrogenation of reduced nicotinamide adenine dinucleotide phosphate when measured biochemically in the soluble fraction, or histochemically, by microspectophotometry in tissue sections; meanwhile, the biochemical dehydrogenation of NAD(P)H by the particulate fractions shows that the enzymatic activities are not altered by the neoplastic process. The biological significance of these changes is discussed in the text.

2,6-Dichloroindophenol↗
PubMed2004

Aberrant nestin expression during ethylnitrosourea-(ENU)-induced neurocarcinogenesis.

Nestin is a unique intermediate filament protein. While it is robustly expressed in developing brain, postnatal expression is limited to the brain's subventricular zone (SVZ) and endothelial cells. Reexpression occurs, however, under several pathological conditions, including injury and neoplasia. We hypothesized that nestin would be a sensitive marker of early neoplasia after transplacental exposure of rats to ethylnitrosourea (ENU). Rats of various ages were administered bromodeoxyuridine (BudR) before sacrifice, and brain sections were examined for proliferative cells and several immunohistochemical markers, including nestin. Additional rats were examined after a stab wound injury to assess the expression of two of these markers, GFAP and nestin, in reactive astrocytes. All ENU-induced brain tumors (n = 9) were classified as gliomas (astrocytomas or oligoastrocytomas) based on their histology and immunophenotype. Nestin expression was noted in all tumors examined and was present in tumor cells as well as endothelial cells. During tumor development, we consistently noted nestin-expressing cells bearing multiple processes distributed throughout brain parenchyma. Both single cells and multiple cell clusters were observed as early as postnatal day 30 in all ENU-exposed brains examined (n = 11). Such distinctive nestin-expressing cells were not seen in nestin-stained control brains or ENU-exposed brains stained for GFAP or vimentin, nor was such a cell seen in a stab wound model used to assess reactive astrocytosis. While the number of these clusters was highly variable among rats, their size increased between 30 and 90 days. The data suggest that these nestin-expressing cells represent an early stage of the neoplastic process. It remains to be determined whether these cells become apparent at 30 days of age due to "dedifferentiation" of a local resident astrocyte or astrocyte precursor cell or migration of a relatively undifferentiated precursor/stem cell from the SVZ.

Animals↗
PubMed2006

Tissue evidence of the testosterone role on the abnormal growth and aging effects reversion in the gerbil (Meriones unguiculatus) prostate.

Prostate differentiation during embryogenesis and its further homeostatic state maintenance during adult life depend on androgens. Abundant biological data suggest that androgens play an important role in the development of the prostate cancer and other prostatic diseases. The objective of this work was to evaluate the effects of the testosterone supplementation in gerbil (a new experimental model) at different ages. Tissues from experimental animals were studied by histological and histochemistry procedures, androgen receptor immunohistochemistry assay, morphometric-stereological analysis, and transmission electron microscopy (TEM). After the treatment were observed increase of prostate weight and epithelium height in all ages studied. In some adult and aged treated animals, hyperplasic and dysplastic process were observed, including prostatic intraepithelial neoplasias and adenocarcinomas. Increase of the thickness of the smooth muscle cell (SMC) layer was observed in pubescent and adult animals and TEM revealed apparent SMC hypertrophy. An apparent increase in the frequency of blood vessels distributed by the subepithelial stroma in the treated animals was noticed. Reversion of the natural effects of aging on the prostate was observed in the aged treated animals in some acini of the gland. These data demonstrate that the gerbil prostate is susceptible to androgenic action at the studied ages and it can serve, for example, as experimental model to studies of prostate neoplastic process induction and hormonal therapy in aged animals.

Age Factors↗
PubMed1988

Analysis of hepatocyte plasma membrane polarity during rat azo dye hepatocarcinogenesis using monoclonal antibodies directed against domain-associated antigens.

While carcinogenesis is known to induce various alterations in epithelial cell polarity, little information is available about the fate of plasma membrane polarity during the neoplastic process. Using three monoclonal antibody-defined antigens as markers of the three plasma membrane domains of rat hepatocytes, the sinusoidal, the lateral, and the canalicular, we demonstrated by immunohistochemical techniques that changes in hepatocyte plasma membrane polarity occur at every stage of 3'-methyldimethylaminoazobenzene-induced hepatocarcinogenesis. At the preneoplastic stage, the division of hepatocyte plasma membrane into three distinct domains was retained despite rearrangements in hepatocytic architecture, characterized by the disorganization of hepatocytic plates and the formation of pseudoacinar structures. The most striking change was the distribution of the canalicular-associated antigen over the entire plasma membrane in disorganized plates. At the neoplastic stage, changes in plasma membrane polarity depended on the degree of morphological differentiation of neoplastic cells. Poorly differentiated cells inconstantly expressed the monoclonal antibody-defined antigens and showed no evidence of plasma membrane polarization. Differentiated cells constantly expressed the three antigens, and their plasma membrane was divided into antigenically distinct domains. The changes in hepatocyte plasma membrane polarity demonstrated in situ during 3'-methyldimethylaminoazobenzene hepatocarcinogenesis may therefore be compared with situations known to occur in vitro, in cultured epithelial cells presenting varying degrees of polarization. Our observations suggest that these alterations are of relevance to the in vivo biology of cancer.

Animals↗
PubMed2001

Clinical significance of atypical glandular cells of undetermined significance in postmenopausal women.

BACKGROUND: Glandular atypia in Papanicolaou (Pap) smears from postmenopausal women is encountered frequently. This finding can be the result of artifactual alterations such as drying artifacts and inflammatory changes or may represent a squamous or glandular, preneoplastic or neoplastic process. Therefore, it is important to determine the clinical implication of a diagnosis of atypical glandular cells of undetermined significance (AGUS) in postmenopausal patients. METHODS: A total of 30,036 Pap smears were obtained from postmenopausal women between 1995 and 1997. Among these smears, 154 (0.51%) had a diagnosis of AGUS. Follow-up was available for 133 patients (86.4%); 110 patients (82.7%) had histologic follow-up (including cervical biopsy, endocervical [EC] curettage, and/or endometrial [EM] biopsy) and 23 patients (17.3%) had repeat smears. RESULTS: Thirty-six of 110 patients (32.7%) were found to have a clinically significant lesion (defined as a preneoplastic or neoplastic, glandular or squamous lesion) on subsequent histologic follow-up. Nineteen patients (53%) had glandular lesions (15 EM adenocarcinoma [ACA] cases, 2 EC ACA cases, 1 EC adenocarcinoma is situ case, and 1 EM hyperplasia case). Seventeen patients (47%) had a squamous intraepithelial lesion (SIL) (6 cases of low-grade SIL, 9 cases of high-grade [HGIL], and 2 cases of squamous cell carcinoma). Among those patients with repeat Pap smears, five patients had persistent AGUS/atypical squamous cells of undetermined significance and one patient had an SIL. CONCLUSIONS: The incidence of AGUS among postmenopausal patients was similar to that of the general population (0.51% vs. 0.56%; P > 0.05). A significant percentage of these patients were found to have a clinically significant lesion on subsequent follow-up. Furthermore, a majority of these lesions were ACA (53%) or HGSIL (26%). The findings of the current study strongly suggest the need for the close follow-up of postmenopausal patients with a diagnosis of AGUS. Cancer (Cancer Cytopathol)

Adult↗
PubMed1996

Increased cytosine DNA-methyltransferase activity is target-cell-specific and an early event in lung cancer.

The association between increased DNA-methyltransferase (DNA-MTase) activity and tumor development suggest a fundamental role for this enzyme in the initiation and progression of cancer. A true functional role for DNA-MTase in the neoplastic process would be further substantiated if the target cells affected by the initiating carcinogen exhibit changes in enzyme activity. This hypothesis was addressed by examining DNA-MTase activity in alveolar type II (target) and Clara (nontarget) cells from A/J and C3H mice that exhibit high and low susceptibility, respectively, for lung tumor formation. Increased DNA-MTase activity was found only in the target alveolar type II cells of the susceptible A/J mouse and caused a marked increase in overall DNA methylation in these cells. Both DNA-MTase and DNA methylation changes were detected 7 days after carcinogen exposure and, thus, were early events in neoplastic evolution. Increased gene expression was also detected by RNA in situ hybridization in hypertrophic alveolar type II cells of carcinogen-treated A/J mice, indicating that elevated levels of expression may be a biomarker for premalignancy. Enzyme activity increased incrementally during lung cancer progression and coincided with increased expression of the DNA-MTase activity are strongly associated with neoplastic development and constitute a key step in carcinogenesis. The detection of premalignant lung disease through increased DNA-MTase expression and the possibility of blocking the deleterious effects of this change with specific inhibitors will offer new intervention strategies for lung cancer.

Animals↗
PubMed2001

Exclusive radical surgery for esophageal adenocarcinoma.

BACKGROUND: Because very poor survival rates were reported after exclusive nonradical surgery, the current opinion in the medical community is that very few esophageal adenocarcinoma patients can anticipate long-term survival after esophagectomy. In the current study the ability of exclusive radical surgery including very extended lymph node dissection to provide a substantial percentage of patients with long-term survival was examined. METHODS: Radical esophagectomy (including removal of the esophageal tube, excision of the potentially involved locoregional lymph nodes, and skeletization of the nonresectable vital organs in the mediastinum and upper abdomen) was attempted in 183 consecutive patients with either Barrett (n = 77) or non-Barrett (n = 106) adenocarcinoma of the esophagus or cardia. Esophagectomy was subtotal (neck anastomosis) or distal (chest anastomosis) in 103 patients and 80 patients, respectively. RESULTS: Radical esophagectomy (Ro resection) was feasible in 137 patients (75%) whereas 46 patients (25%) in whom a part of the neoplastic process was not resectable (R1 or R2 resection) underwent a palliative esophagectomy. The 5-year survival, including in-hospital deaths (4.3%), was 35.3% for the whole series, 48% after Ro resection, and 0% after R1 or R2 resection. The 5-year survival rate after any R resection was 57.2% in patients with Barrett adenocarcinoma compared with 20% in patients with non-Barrett adenocarcinoma (P < 0.0001) because of a higher prevalence of nontransmural tumors (Tis through T2, N0) in the former group (56.5%) compared with the latter group (6.6%) (P < 0.0001). The 5-year survival was related closely to the magnitude of both wall penetration and extraesophageal neoplastic spread (Ro, Tis-T1-T2, N0 = 83.5% vs. Ro, T3, N0 = 44.4% vs. Ro, any T, N1 < 5 metastatic lymph nodes = 37% vs. Ro, any T, N1 > or = 5 metastastic lymph nodes = 6.8% vs. R1, R2 = 0%; P < 0.0001). CONCLUSIONS: Exclusive radical esophagectomy provides a chance of long-term survival in 35% of esophageal adenocarcinoma patients in whom it is attempted and nearly 50% of those patients in whom it is feasible. The presence of a small number of metastatic lymph nodes does not appear to preclude a long-term favorable outcome.

Adenocarcinoma↗
PubMed1999

Atypical presentations of actinomycosis.

BACKGROUND: Actinomycotic infections of the cervicofacial region are uncommon. Most major medical centers report approximately one case per year. Presenting clinical manifestations are confusing because they often mimic other disease processes. Diagnosis may be difficult due to a general lack of familiarity with the disease and the fastidious nature of the organism in culture. The cervicofacial manifestations of actinomycosis are varied, and a high index of suspicion is required to make an accurate and timely diagnosis. METHODS: Retrospective chart review with the presentation of four unusual cases of actinomycosis were performed. RESULTS: Two patients were initially seen with dysphagia from a tongue base mass. The third patient was initially seen with a 3-week history of worsening hoarseness and stridor. Examination revealed an ulcerative lesion of the left hemilarynx and pyriform sinus. All three patients were thought to have a neoplastic process. Diagnosis was made on histologic examination of a tissue biopsy. The fourth patient was initially seen with a buccal space mass that was draining externally. Culture of the purulent drainage revealed Actinomyces. In all four cases, symptoms resolved after appropriate antimicrobial therapy. CONCLUSIONS: Actinomycosis of the head and neck, although rare, is an important entity to the otolaryngologist. A confusing clinical presentation combined with the fastidious nature of the organism make for a difficult diagnosis. A high index of suspicion is required to make an accurate diagnosis and institute the appropriate antibiotic therapy.

Actinomycosis, Cervicofacial↗
PubMed2000

Pancreatic mucinous cystic neoplasms with sarcomatous stroma: molecular evidence for monoclonal origin with subsequent divergence of the epithelial and sarcomatous components.

Neoplasms with mixed carcinomatous and sarcomatous growth patterns occur in many organs and tissues. The pathogenesis of these cancers is thought to be either the result of two independent neoplastic processes merging to form a single tumor, or a neoplasm of monoclonal origin that develops phenotypic diversity. To address this issue, we characterized molecular alterations in separately microdissected epithelial and sarcomatous areas in three cases of pancreatic mucinous cystic neoplasms with sarcomatous stroma. Using microsatellite markers for six chromosomal loci commonly deleted in infiltrating ductal adenocarcinomas of the pancreas, we found genetic alterations to be virtually identical between the sarcomatous and epithelial components of two of the three neoplasms. In the third neoplasm, we found allelic losses and retentions to be identical at five of the six chromosomal loci, but at a single locus, we noted allelic loss in the neoplastic epithelial component but not the sarcomatous component. The same neoplasms were also analyzed for activating point mutations in codon 12 of the K-ras gene by using mutant-enriched polymerase chain reaction and allele-specific oligonucleotide hybridization. A K-ras mutation was identified in the epithelial component of one of the three neoplasms (the same tumor with an additional allelic loss in the neoplastic epithelial cells), but the sarcomatous component of this tumor was wild-type at codon 12 of K-ras, as were both components of the other two neoplasms. Overall, these results suggest a monoclonal origin with subsequent divergence of the neoplastic epithelial and sarcomatous portions of these neoplasms.

Adenocarcinoma, Mucinous↗
PubMed1986

[Papilloma viruses: group-specific antigens within lesions of the oral mucosa].

The present study was undertaken with purpose to investigate the relationships between intraepithelial proliferations of malpighian mucosa and the presence of group specific papilloma virus antigens. The investigations allowing to give viral types or subtypes, the hybridization technics, are very heavy and not disponible in routine practice. The detection of widely distributed genus specific HPV antigen using PAP immunohistochemical labeling in different lesions and their association with displastic or neoplastic processes is presented. Only few studies were performed on oral mucosal proliferations, showing the association of these viral proteins with papillomatous or condylomatous lesions. Our work is directed towards the identification of the HPV antigens in more advanced lesions and in the mucosal epithelium surrounding and perhaps preexistent with the buccal cancer.

Adult↗
PubMed2004

The future of gastric cancer prevention.

Despite advances in surgical treatment and chemotherapy, gastric cancer remains a major global health burden. The most recent estimates show that it is the fourth most common cancer and the second most common cause of cancer deaths worldwide. Various etiologic factors have been linked with the disease. It is widely accepted that Helicobacter pylori infection and high salt intake are positively associated with this neoplastic process. Controversial associations have been found with smoking or drinking habits. In contrast, there is convincing evidence that the adequate consumption of fresh fruits and vegetables reduces the risk of gastric cancer. Prevention intervention trials involving antioxidant supplements and anti- H. pylori treatment have shown beneficial effects in preventing the progression of pathologic changes in the gastric mucosa. On the other hand, recent advances related to differences in the genotypes of the bacteria and in human cytokine polymorphisms would allow the design and implementation of large-scale screening programs to identify subjects at the highest risk of gastric cancer. Curing the infection in such subjects and supplying adequate amounts of antioxidants should prevent a neoplastic outcome, and this intervention should be monitored by endoscopic surveillance.

Antioxidants↗
PubMed2004

Mammalian target of rapamycin (mTOR) inhibitors as anti-cancer agents.

Highly specific signal transduction inhibitors are being developed as anti-cancer agents against an array of molecular targets, with the promise of increased selectivity and lower toxicity than classic cytotoxic chemotherapy agents. Rapamycin and its analogues are a promising class of novel therapeutics that specifically inhibit signaling from the serine-threonine kinase, mammalian target of rapamycin (mTOR). mTOR is a key intermediary in multiple mitogenic signaling pathways and plays a central role in modulating proliferation and angiogenesis in normal tissues and neoplastic processes. Rapamycin potently inhibits T-cell proliferation, and is approved for clinical use as an immuno-suppressant following kidney transplantation. Hyperactivation of mTOR signaling has been implicated in tumorigenesis, and promising pre-clinical studies in several tumor types suggest that the anti-proliferative and anti-angiogenic properties of rapamycin may be useful in cancer therapy. These studies have led to several clinical trials evaluating the safety and efficacy of rapamycin analogs in cancer therapy. The goal of this article is to review the mechanism of action of rapamycin as an anti-cancer agent, and to review the clinical experience with rapamycin and rapamycin analogs as immunosuppressive and anti-neoplastic therapeutic agents.

Animals↗
PubMed1998

The leukocyte semaphorin CD100 is expressed in most T-cell, but few B-cell, non-Hodgkin's lymphomas.

The 150-kd transmembrane protein CD100 is the first semaphorin protein shown to be expressed in lymphoid tissue. CD100 is present in the interfollicular T cell zones and is also expressed by B cells in the germinal centers of secondary lymphoid follicles, but not in the mantle zones. The CD100 molecule was recently cloned, and CD100 transfectants were shown to induce homotypic aggregation of human B cells and improve their viability in vitro, suggesting that CD100 may play a role in lymphocyte aggregation and germinal center formation. We studied the expression of CD100 in 138 clinical cases representing a range of lymphoproliferative disorders, to determine whether this molecule is expressed in these neoplastic processes. In general, we found CD100 expression to be common in peripheral T-cell non-Hodgkin's lymphomas but rare in B-cell non-Hodgkin's lymphomas. CD100 expression was not detectable in low-grade B-cell non-Hodgkin's lymphomas, including cases of small lymphocytic lymphoma (18 cases), marginal zone lymphoma (10 cases), and mantle cell lymphoma (10 cases), as might be expected for these neoplasms that are not of follicular center cell origin. Surprisingly, we found that the vast majority of follicular lymphomas (37 of 40 cases) as well as diffuse large-cell lymphomas of B-cell type (35 cases) did not express CD100. The neoplastic cells in 3 of 11 cases of predominantly large-cell-type follicular lymphoma did express CD100. In contrast, all five cases of high-grade, small non-cleaved (Burkitt-like) B-cell lymphoma were immunoreactive for CD100 expression, as were 18 of 20 cases (90%) of malignant T cell neoplasms. Northern blot analysis of CD100 expression correlated with immunohistochemical findings. Absence of expression of CD100 by neoplastic follicular center B cells is a common feature in follicular lymphomas, but expression of CD100 by T cells is maintained in T-cell lymphoproliferative disorders.

Antigens, CD↗
PubMedDate not supplied

[Hypertrophic cranial and spinal pachymeningitis. A description of four new cases and a review of the literature].

INTRODUCTION: Hypertrophic pachymeningitis is an infrequent disease that is characterised by inflammatory hypertrophy of the dura mater. There are cranial, spinal and craniospinal forms of the disease. They may be due to underlying infectious, autoimmune or neoplastic processes, although most of the cases reported in recent years have no base pathology and are known as idiopathic hypertrophic pachymeningitis. The ideal treatment is unknown, but most cases usually respond well to therapy with corticoids. CASE REPORTS: We report two cases of cranial forms, one idiopathic with typical clinical features consisting in cranial polyneuropathy and good response to corticoids, and another case secondary to rheumatoid arthritis that began with epileptic seizures. Both had a parenchymatous oedema. The two forms of spinal pachymeningitis presented as progressive paraparesis that evolved well after surgical removal of the lesion. CONCLUSIONS: On observing pachymeningitis in neuroimaging tests it becomes necessary to conduct a comprehensive aetiological study in search of infectious, autoimmune and neoplastic diseases. In the cranial forms there may be parenchymatous oedema, which would explain the epileptic seizures and the cognitive deterioration of our patients. Response to corticoids is spectacular, although it is often necessary to continue to administer them for prolonged periods of time.

Aged↗
PubMed2000

DNA ploidy status and proliferative activity as markers of malignant potential in Barrett's esophagus: flow cytometric study using routinely paraffin-embedded tissue.

Regular endoscopic surveillance is recommended for patients with Barrett's esophagus to detect dysplasia and to diagnose carcinoma while it is in an early and possibly treatable stage. However, there are numerous unknown aspects regarding the natural history of dysplasia in this disease, and there is still a need for more accurate markers of risk of a malignant change. The aim of this study was to investigate the usefulness of DNA flow cytometry in Barrett's esophagus to define subgroups of patients showing similar histologic findings but with a different malignancy potential. Routinely formalin-fixed and paraffin-embedded tissues of 43 patients with Barrett's esophagus were processed for flow cytometric measurements (ploidy, proliferative index) and the results were compared with the histologic evolution observed in these patients. Only in the group of patients with "indefinite" dysplasia did we find statistically significant differences between the samples from patients with and without progression to more severe lesions (mean proliferative index of stable patients: 5.2% versus 8.3% in patients with progression, p = 0.001, Student's t-test). The presence in the flow cytometric analysis of a DNA aneuploid cell line is closely related to the presence of severe histologic alterations (i.e., high-grade dysplasia: p < 0.001, Fisher's exact test). Our results suggest that this procedure is at least capable of distinguishing between a real, although incipient, neoplastic process and morphologic changes of a reactive or reparative type. The increment in the tissue proliferative index could be an indicator of an early genomic instability which, with time, will develop into lesions with a more altered DNA content: aneuploidy.

Adenocarcinoma↗
PubMed1996

Random suppression of T cells that bear specific T cell receptor V beta sequences in adult T cell leukemia/lymphoma (ATLL) patients at each clinical stage: carrier, smoldering, chronic, and acute.

Human T cell leukemia virus type I (HTLV-I) is associated with adult T cell leukemia/lymphoma (ATLL), which is well known as a T cell malignancy. In order to clarify whether HTLV-I plays a role as a virus-encoded superantigen in the neoplastic process, we examined the TCR V beta families in the peripheral blood at four different clinical stages: carrier, smoldering leukemia, chronic leukemia, and acute leukemia. An increased number of CD4 T cells was found in each of the four clinical stages. However, we found neither uniform specific losses nor uniform clonal expansion of particular TCR V beta gene families in any case from the four clinical stages. However, a suppression of the random TCR V beta families was found. Our data did not therefore directly suggest the existence of a common superantigen model of HTLV-I which induces an increase in CD4 T cells. The random suppression in the TCR V beta repertoire is most likely caused by the influence of HTLV-I neoplastic pathogenesis rather than by virus-encoded superantigens. In the patients with acute leukemia, one or two families of the V beta repertoires were very strongly expressed, while in chronic leukemia, no such repertoire of strong expression was observed. The immunological reaction of the hosts might thus be different between the above described groups.

Acute Disease↗