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PubMedDate not supplied

Malignant pleural mesothelioma. Multivariate analysis of prognostic factors on 113 patients.

We report on clinical features of 113 cases of pathologically confirmed Malignant Pleural Mesothelioma, observed in Genoa (Italy) between 1979 and 1985. Overall median survival was 10 months. Among the pretreatment variables studied (age, sex, asbestos exposure, pathological type, chest pain and dyspnea at the time of diagnosis), the only one of prognostic value in the univariate analysis was the histological subtype: median survivals were 12, 7 and 4 months for the patients in the epithelial, mixed, and fibrosarcomatous groups, respectively (p = 0.0012). A multivariate analysis confirmed the independent predictive power of the histotype (p = 0.0022). A review of literature data concerning prognostic factors in Malignant Pleural Mesothelioma is presented.

Adult↗

PubMed1997

[Systemic autoimmune diseases with neurocutaneous alterations].

Autoimmune diseases depend on the pathologic activation of cellular clones, potentially harmful, against soft tissues. They can be classified into systemic and organ-specific diseases. In the systemic subtype, in which the abnormal hyperactivity is not as specific, the most remarkable component of the clinical syndrome is frequently the presence of neurological and/or cutaneous manifestations. This article reviews the major pathogenic mechanisms involved in the principal systemic autoimmune conditions including connective tissue diseases (rheumatoid arthritis, systemic lupus erythematosus, polimyositis, dermatomyositis, scleroderma, mixed connective tissue disease, Sjögren's syndrome, overlap syndromes) and vasculitic syndromes (nodous polyarteritis, giant cell arteritis. Wegener's granulomatosis. Behçet disease, microscopic polyarteritis, cryoglobulinemia) as well as their clinical manifestations, focused mainly on neurocutaneous characteristics.

Autoimmune Diseases↗

PubMed2002

Hemangioma of the salivary gland: a study of ten cases of a rarely biopsied/excised lesion.

Hemangioma is a common soft tissue tumor that frequently occurs in the oral and maxillofacial region including salivary glands, but is rarely biopsied and is therefore often unfamiliar to the surgical pathologist. Our study examined the subclassification and histologic features of salivary gland hemangioma (SGH). Consultative cases coded as hemangioma and located in salivary gland from 1970 to 2000 were retrieved from the Registry of Oral and Maxillofacial Pathology of the Armed Forces Institute of Pathology (Washington, DC). Only cases with histologic evidence of salivary gland involvement were included. Slide material and patient history for all cases were reviewed, subclassification assigned, and histologic features were noted. Ten cases coded as hemangioma with slides and history met our inclusion criteria. Seven cases were the "juvenile hemangioma" subtype in the parotid of infants, ranging in age from 3 to 10 months (mean age, 5.3 months) with a male predominance. These SGH had a distinctive histologic appearance of a cellular proliferation of capillary sized vessels around retained salivary gland ducts. Mitoses were easily identified. Three additional cases in females included an arteriovenous hemangioma of a lip minor salivary gland since birth in a 15-month-old infant and two parotid gland lesions: a lobular capillary hemangioma of a 10-year-old and a cavernous hemangioma in a 51-year-old. The latter three cases grew as replacing masses and lacked retained salivary gland ducts within the lesion, despite glandular tissue at the periphery of the tumor. No SGH cases in our series were identified in the submandibular or sublingual glands. Despite its common occurrence, SGH is relatively rare in our surgical pathology files. The parotid gland is the most common location (90%). Salivary gland hemangioma includes usual hemangioma subtypes, mainly in females, and a distinctive infantile subtype of capillary hemangioma (juvenile hemangioma), displaying distinctive histology and found predominately in males. The cellularity, mitotic activity, and retained salivary gland ducts in the latter lesion should not make one consider malignancy.

Biopsy↗

PubMed1987

Cortical neuropathological and neurochemical substrates of Alzheimer's and Parkinson's diseases.

Whilst the neuropathological correlates of Alzheimer type dementia--cortical neurofibrillary tangles and senile plaques--are well defined, the prevalence of these cortical abnormalities in Parkinson's disease and their relation to dementia is unclear. In a series of 46 consecutive cases of clinically and pathologically established Parkinson's disease the prevalence of mild Alzheimer-type pathology (exceeding the normal but not as extensive as in Alzheimer's disease) was increased 2 to 3 fold compared with an age-matched control group, although there was no obvious relation to the presence or severity of dementia. In a subgroup of Parkinsonian cases (both demented and non-demented), examined neurochemically, there were both similarities (decreased choline acetyltransferase, nicotinic and serotonergic S 1 receptor activities) and distinctions (increased muscarinic receptor binding--particularly to the "L" subtype, and normal serotonergic S 2, somatostatin, and D-aspartate binding together with normal levels of an endogenous nicotine binding inhibitor) compared with a group of cases with Alzheimer's disease. Amongst the various pathological and chemical indices examined, only presynaptic cholinergic markers (including the number of Meynert neurons) and S 1 receptor binding were related to dementia in Parkinson's disease. It is suggested that whilst coincidental classical Alzheimer's disease is infrequent in Parkinson's disease (5% in the present series) Alzheimer's disease itself is distinguished from Parkinson's disease by the formation of numerous neocortical neurofibrillary tangles and a reduction in glutamate uptake, serotonergic S 2 receptors and possibly in endogenous nicotine binding inhibitor.

Adult↗

PubMedDate not supplied

[The role of the selective blocking of angiotensin II receptors in the treatment of cardiovascular diseases].

Angiotensin II plays an important role in blood pressure control and in water and salt homeosthasis. It is involved in the pathogenesis of hypertension and structural alterations of the vasculature, kidney, and heart, including nephrosclerosis, post infarction remodelling and left ventricular hypertrophy. At least two subtypes of receptors have been identified, angiotensin type 1 (AT1) and type 2 (AT2). The AT1 receptor is responsible for all the known effects of Ang II on blood pressure, osmoregulation, and cell growth and consequently for the contribution to cardiovascular and renal pathology. Research has indicated that the AT1 receptor modulates cardiac and vascular hypertrophy, cellular growth and ventricular remodelling. Evidence suggests that, on the other hand, the AT2 receptor is involved in growth inhibition, inhibits cell proliferation, induces vasodilatation and reverses the AT1 induced hypertrophy. The accumulating evidence appears to demonstrate therefore that the function of these receptor subtypes may exerts opposite effects while stimulated by AngII. The angiotensin receptor antagonists are able to inhibit the renin angiotensin system by blocking selectively the AT1 receptor. It is supposed that AT1 receptor antagonists may provide end organ protection by blocking angiotensin II effects via the AT1 receptor leaving the AT2 receptor unopposed: it is conceivable that the stimulation of AT2 receptors may prevent the hypertropic effects seen in conditions such as LVH, hypertrophy, postinfarction remodeling and repair after injury. For this, the AT1/AT2 selectivity associated to these drugs may be important for their effects and to differentiate them from ACE inhibitors.

Angiotensin I↗

PubMed2004

Epithelial lesions associated with invasive penile squamous cell carcinoma: a pathologic study of 288 cases.

A heterogeneous spectrum of epithelial alterations and atypical lesions affect the squamous epithelium of penile mucosal anatomical compartments. Analogous to other genital sites, the terminology utilized to define the lesions is variable. The few pathologic studies of penile precancerous lesions are mostly related to carcinoma in situ and human papilloma virus (HPV), and the information on low-grade atypical lesions is limited. The objective of this study was to comprehensively describe the morphologic features of all epithelial alterations, benign and atypical, low grade and high grade, associated with invasive squamous cell carcinoma of the penis and to investigate their relation with each other and with subtypes of invasive carcinoma. We also propose herein a simple and reproducible nomenclature for penile precancerous abnormalities until more biological, molecular, or epidemiologic information on the lesions is available. Two hundred and eighty-eight penectomy and circumcision specimens with invasive squamous cell carcinoma were pathologically evaluated. Carcinomas were classified as usual, verrucous, papillary not otherwise specified, warty (condylomatous), basaloid, and mixed. Associated lesions were classified as squamous hyperplasia and squamous intraepithelial lesions of low and high grade (LGSIL and HGSIL). In LGSIL, atypia was confined to the lower third, and in HGSIL, atypical cells affected at least two thirds of the squamous epithelium. Subtypes of SIL were squamous, warty, basaloid, warty-basaloid, and papillary. Squamous hyperplasia, the most common lesion, was found in 83% of the cases, followed by LGSIL (59%) and HGSIL (44%). In 62% of the cases more than 1 associated lesion was present per specimen. A sequence from squamous hyperplasia to low-grade to high-grade SIL was seen frequently. Squamous hyperplasia was more commonly associated with usual squamous, papillary, and verrucous than with warty and basaloid invasive carcinomas. LGSIL was associated with all types of squamous cell carcinoma but was rarely present adjacent to basaloid or verrucous tumors. HGSIL was present in two thirds of invasive warty, basaloid, and mixed warty-basaloid tumors, in about half of usual squamous cell carcinomas, and was absent in papillary and verrucous carcinomas. Correlation of special types of invasive carcinomas with subtypes of SIL revealed morphologic correspondence of invasive tumor and the associated intraepithelial lesion. Squamous LGSIL was preferentially associated with verrucous, papillary, and usual squamous cell carcinomas; warty LGSIL, with invasive warty and mixed warty-basaloid carcinomas. High-grade SIL of the squamous type was frequently found in squamous cell carcinoma of usual type but was rarely present with warty or basaloid carcinomas. Basaloid HGSIL was associated with basaloid carcinoma, and HGSIL of warty type, with either warty or mixed warty-basaloid carcinomas. The high frequency of squamous hyperplasia and LGSIL and preferential association with usual, verrucous, and papillary carcinomas plus the subtle morphologic differences of the 2 lesions suggest that, despite its benign appearance, squamous hyperplasia is a precursor of the aforementioned carcinomas. The association and histologic similarities between high-grade SIL of the basaloid, warty, or mixed forms with their invasive counterparts indicate these lesions are their likely precursors.

Carcinoma in Situ↗

PubMed2003

Prostanoids in immunity: roles revealed by mice deficient in their receptors.

Prostanoids including prostaglandins (PGs) and thromboxanes (TX) are a group of lipid mediators formed and released in response to various, often noxious, stimuli. While the roles of prostanoids in acute inflammatory responses are well known and have been extensively studied, it is generally believed that they play very little in immunity. This is partly because non-steroidal anti-inflammatory drugs that inhibit prostanoid synthesis have little effects on immune processes in vivo. Prostanoids exert their actions by acting on a family of G-protein-coupled receptors. They include PGD receptor, EP1, EP2, EP3 and EP4 subtypes of PGE receptor, PGF receptor, PGI receptor and TX receptor. We generated mice deficient in each of these prostanoid receptors individually, and examined their roles under various pathological conditions. These studies have revealed that prostanoids works at various sites or levels of immune responses and exert many, often opposing, actions. For example, using EP4-deficient mice, we found that stimulation of the PGE(2)-EP4 signaling in dendritic cells facilitates their migration and maturation, while the stimulation of the same pathway in T cells potently suppresses their activation and proliferation. The latter action is evident in PGE(2)-mediated suppression of T cell proliferation in the gut of mice subjected to dextran sodium sulfate-induced colitis, a model of inflammatory bowel disease. Here I summarize our findings obtained by these and other studies. These findings suggest that selective manipulation of the prostanoid receptors may be beneficial in treatment of certain immunological disorders.

Adjuvants, Immunologic↗

PubMed2004

[Prognosis of post-irradiation soft-tissue sarcoma: case-control study].

PURPOSE: We describe clinical and pathological aspects and survival of 12 recent of radio-induced soft tissue sarcoma. METHOD: We performed a single center case-control study, with 23 control matched by grade (according to Federation nationale des centres de lutte contre le cancer Grading) and by location. Survival comparison used Log Rank test. RESULTS: The development of these 12 cases was a result of 12 previous cancer treatment (including 4 breast cancers and 2 cervix cancers) with radiotherapy (median dose of 58 Grays). The median latency period was 10 years. There were nine women and three men. The median age was 68.5 years. The main location was chest wall (5 cases). The two main histologic subtypes were malignant histiocytofibromas (6 cases) and angiosarcomas (3 cases). Five cases were high grade. Treatments were performed with curative intent in 9 cases, including complete resection in six cases. Clinical and pathological aspects and treatments of controls were similar, but postoperative radiotherapy was most frequent and malignant histiocytofibroma was less common. Median overall survival (47 months vs. 30 months, P = 0.6), median metastatic disease-free survival (37 vs. 15 m., P = 0.6) and median locoregional disease-free survival (14 vs. 24 m., P = 0.07) were similar for cases and control. CONCLUSION: This study suggests that prognosis of radio-induced soft-tissue sarcomas is similar as other soft tissue sarcoma of same grade and same location.

Adult↗

PubMed2006

Brain neuronal nicotinic receptors as new targets for drug discovery.

Neuronal nicotinic receptors (nAChRs) are a heterogeneous family of ion channels differently expressed in the nervous system where, by responding to the endogenous neurotransmitter acetylcholine, they contribute to a wide range of brain activities and influence a number of physiological functions. Over recent years, the application of newly developed molecular and cellular biological techniques has made it possible to correlate the subunit composition of nAChRs with specific nicotine-elicited behaviours, and refine some of the in vivo physiological functions of nAChR subtypes. The major new findings are the widespread expression of nAChRs, outside the nervous system, their specific and complex organisation, and their relevance to normal brain function. Moreover, the combination of clinical and basic research has better defined the involvement of nAChRs in a growing number of nervous pathologies other than degenerative diseases. However, there are still only a limited number of nicotinic-specific drugs and, although some nicotinic agonists have an interesting pharmacology, their clinical use is limited by undesirable side effects. Some selective nicotinic ligands have recently been developed and used to explore the complexity of nAChR subtype structure and function in the expectation that they will become rational therapeutic alternatives in a number of neurodegenerative, neuropsychiatric and neurological disorders. In this review, we will discuss the molecular basis of brain nAChR structural and functional diversity mainly in pharmacological and biochemical terms, and summarise current knowledge concerning the newly discovered drugs used to classify the numerous receptor subtypes and treat the brain diseases in which nAChRs are involved.

Animals↗

PubMed2003

Small Bowel Lymphoma.

Treatment of small bowel lymphoma requires the expertise of medical and surgical subspecialists. The two most important factors that determine the optimal treatment are histology and staging of small bowel lymphoma. Other factors that may affect treatment include age, multiple areas of involvement, tumor size, and perforation. At present, the best treatment for gastrointestinal lymphoma (stage IE disease) is limited resection of the tumor, followed by postoperative radiotherapy. The cure rate is approximately 75% for stage IE patients, even for those with aggressive histologic types. Chemotherapy is reserved for advanced-staged tumors. In patients with regional nodal involvement or extranodal involvement confined to one side of the diaphragm (pathologic stage IIE disease), chemotherapy should be combined with radiation therapy. The best chemotherapy regimen depends on the histology of the tumor. For diffuse large B-cell lymphoma, the most frequently diagnosed subtype of non-Hodgkin's lymphoma (NHL), the CHOP regimen (cyclophosphamide, doxorubicin, vincristine, and prednisone) is still the gold standard. Clinical trials have been conducted evaluating the new monoclonal antibody rituximab, along with the CHOP regimen for primary NHL. Results have been promising. The use of rituximab in the treatment of extranodal lymphoma is still being evaluated. Low-grade lymphomas have a more indolent course and do not respond as well to combination chemotherapy agents as the high-grade tumors. Fludarabine alone or in combination with cyclophosphamide is effective as a first-line agent for patients with low-grade NHL. It has also been used to treat relapsed or refractory low-grade NHL. Some promising results have been reported using the chemoimmunotherapy agent rituximab alone or in combination with fludarabine for the treatment of low-grade NHL. However, clinical trials are still needed. In patients with nodal involvement on both sides of the diaphragm or other extranodal involvement such as bone marrow or liver (pathologic stages IIIE and IVE), the disease is managed primarily with combination chemotherapy. Radiation therapy is reserved for treatment of initially bulky tumor sites, treatment of residual disease following chemotherapy, or serious local problems. The disease can be controlled in 25% to 40% of patients with stage IIIE or IVE disease. As with stage IIE disease, the optimal chemotherapy regimen depends on the histologic subtype of NHL.

Journal Article↗

PubMed1997

Correlation between mutations in p53 gene and protein expression in human lymphomas.

A discordance between p53 protein overexpression and the presence of mutations in the gene has been observed in many types of tumors, including human lymphomas. To probe this finding, we have studied a large series of 94 lymphomas of different pathologic types and histologic differentiation. Analyzing exons 5-9, we have found mutations in the p53 gene in 7 of 94 cases distributed in different subtypes: 4/12 (33%) high-grade B-cell non-Hodgkin's lymphomas (B-NHLs), in 1 of 5 (20%) high-grade mucosa-associated lymphomas (MALT), in 1 of 22 (4.5%) anaplastic large cell lymphoma (ALCL), and in 1 of 24 (4%) T-cell NHLs. Immunostaining with anti-p53 antibody DO-7 was possible in 87 lymphomas, and overexpression of p53 protein was observed in 16 cases (18%). A discrepancy between the results of SSCP and immunostaining was detected on 18 tumor samples. Two cases with mutations in the gene showed no altered protein expression and 16 cases overexpressed p53 protein had no point mutations. In these cases, the possibility that mutations occur outside the exons studied has been tested and the entire coding sequence analyzed. Only one case showed a mutation in exon 10, and we found two cases carrying a polymorphism in exon 4 and in intron 10. We conclude that mutations in p53 occur mainly in high-grade B-cell NHLs. Although not limited to a specific subtype of lymphoma, they may be rare in Hodgkin's disease and in low-grade lymphomas. The discrepancies between overexpression and presence of mutations suggest (1) the existence of another mechanism to stabilize the p53 protein, and (2) that the immunohistochemistry cannot be used to predict mutations in the gene.

Antibodies, Monoclonal↗

PubMed2005

Phenotypes of the N88S Berardinelli-Seip congenital lipodystrophy 2 mutation.

Recently, two missense mutations (N88S, S90L) in the Berardinelli-Seip congenital lipodystrophy gene have been identified in autosomal dominant distal hereditary motor neuropathy and Silver syndrome. We report the phenotypic consequences of the N88S mutation in 90 patients of 1 large Austrian family and two unrelated German families. Variation in the clinical and electrophysiological phenotype enabled us to distinguish six subtypes. In 4.4%, the disorder was not penetrant. Twenty percent of the patients were subclinically affected; some of these patients could only be detected by pathological nerve conduction studies. A distal hereditary motor neuropathy type V phenotype characterized by predominant hand muscle involvement was found in 31.1%, whereas 14.5% showed typical Silver syndrome with amyotrophy of the small hand muscles and spasticity of the lower extremities. Moreover, the phenotype present in 20% was compatible with Charcot-Marie-Tooth disease. In 10%, the clinical diagnosis of pure or complicated hereditary spastic paraparesis was made. Electrophysiological studies showed an axonal neuropathy but also chronodispersion of compound motor action potentials and conduction blocks. Sensory nerve conduction studies were rarely pathological. Our study indicates that the dominant N88S mutation in the Berardinelli-Seip congenital lipodystrophy gene 2 leads to a broad spectrum of motor neuron disorders.

Action Potentials↗

PubMed1994

Histopathological analysis of metastatic melanoma deposits in patients receiving adoptive immunotherapy with tumor-infiltrating lymphocytes.

Tumor-infiltrating lymphocytes (TIL) from a wide range of human and murine tumors can be expanded in vitro using interleukin-2 (IL-2). These TIL are cytolytic T lymphocytes with in vivo and in vitro antitumor activity in mice and in humans. TIL from human melanoma can recognize autologous tumor in an MHC-restricted fashion, localize in vivo after 111In labeling, and mediate regression of large metastatic deposits. Although studied extensively in vitro, less is known in vivo about TIL activity associated with tumor regression. This study was undertaken, in association with a study of TIL localization, to investigate mechanisms of TIL action by evaluating histopathological changes that occur at the tumor site during TIL administration. A total of 106 pre- and post-treatment pathological specimens from 25 patients enrolled in phase II TIL treatment and 111In-TIL imaging protocols were examined blindly by a single pathologist. Histological subtype, lymphocytic infiltration, melanin content, vascularity, and necrosis were documented for each tumor specimen. Average baseline and post-treatment parameters were compared. Any significant changes were evaluated for correlation with clinical response and 111In-TIL localization to tumor. Melanin content and vascularity of the tumor did not change as a result of therapy or correlate with either response or TIL localization. However, both increased lymphocytic infiltration and tumor necrosis were present after TIL administration (P = 0.044 and 0.032 respectively). Furthermore, increases in lymphocytic infiltration correlated with tumor imaging using 111In-TIL, and with the percentage of 111In-labeled injectate present per gram of tumor specimen (P = 0.036 and 0.0041 respectively). This suggests that TIL either account for the increased lymphocytes directly, or localize to tumor and recruit endogenous lymphocytes. We were unable to demonstrate any pretreatment histopathological predictors of response or variables that significantly correlated with subsequent clinical response, although peak and average values of necrosis were higher in responding patients compared to non-responding patients.

Cohort Studies↗

PubMed1993

Inverse regulation of alpha- and beta-adrenoceptors during trinitrobenzenesulfonic acid (TNB)-induced inflammation in guinea-pig small intestine.

The hypothesis has been raised that intestinal motor disturbances induced by inflammation of the digestive tract may reflect alterations in intestinal cell-membrane receptors. This question has been addressed herein for adrenoceptors by performing [3H]prazosin, [3H]rauwolscine and [3H]DHA binding studies on guinea-pig jejunal smooth-muscle membrane preparations from both healthy controls and 3, 6, and 10 days after TNB-induced intestinal inflammation. Each of the adrenoceptor subtype-selective radioligands used bound selectively to a single saturable class of sites, with no significant (p < 0.05) variation of dissociation constant (KD) values along the inflammatory process. In contrast maximal binding capacities (Bmax) for the different radioligands varied moderately but significantly (p < 0.05 and p < 0.01) according to the time after TNB injection. The alpha-adrenoceptors were significantly upregulated, respectively from (mean +/- SE in fmoles/mg of proteins) 27 +/- 3.8 (controls) to 91 +/- 3.1 (day 10) for the alpha 1-subtype, and from 26 +/- 2.7 (controls) to 102 +/- 5.9 (day 10) for the alpha 2-subtype. In contrast beta-adrenoceptors were down-regulated from 384 +/- 34.6 (controls) to 158 +/- 17.2 (day 10). These findings highlighted an apparently inverse pathological regulation of intestinal alpha- and beta- adrenoceptor densities. They suggest that changes in intestinal adrenoceptors, probably resulting from functional denervation of the inflamed bowel tissue, may contribute to the altered intestinal motility observed in inflammatory bowel diseases.

Animals↗

PubMed1986

An analysis of possible prognostic features of long term and short term survivors of metastatic breast cancer.

Factors influencing the extremes of survival in disseminated breast cancer were analysed. From a pool of 1066 patients with distant metastatic breast cancer, the 41 patients who had survived 5 yr or more from first distant recurrence were matched with the 41 patients with the shortest survival times. Both groups were compared with the pool and, where relevant, with each other. There were no differences with respect to presentation clinical stage, histological subtype, adjuvant therapy or the likelihood of menopause during the disease-free interval. There were significant differences in age, menopausal status, primary treatment, grade, pathological node involvement, time to recurrence, situation and number of sites of metastatic involvement, and response to treatment. The interpretation of these relationships as causal or casual is uncertain; however, given the magnitude of the survival differences, we expected the associated differences to be much greater than we found.

Adult↗

PubMed2004

Correlation between computed tomographic findings, bronchioloalveolar carcinoma component, and biologic behavior of small-sized lung adenocarcinomas.

OBJECTIVE: Differentiation of bronchioloalveolar carcinoma from other subtypes of lung adenocarcinomas is important in the preoperative assessment of patients. We examined the biologic aggressiveness of small-sized adenocarcinomas according to the pathologically defined bronchioloalveolar carcinoma degree and its correlation with computed tomography findings. In addition, we attempted to predict which patients were suitable for a lesser resection. METHODS: Of 424 consecutive patients who underwent operation for primary lung cancer in the last 3 years, 114 with a histopathologically proven adenocarcinoma 3 cm or less in diameter underwent complete removal of the primary tumor. We examined the characteristics of patients classified into 3 groups based on the proportion of the bronchioloalveolar carcinoma component: 0% to 20% (n = 40), 21% to 50% (n = 38), and 51% to 100% (n = 36). We also investigated the correlation of the bronchioloalveolar carcinoma component with computed tomography findings such as ground-glass opacity (defined as a hazy increase on the lung window) and tumor shadow disappearance rate (defined as the ratio of the tumor area of the mediastinal window to that of the lung window). RESULTS: Male gender (P =.0001), advanced pathologic stage (P =.001), larger size of the tumor (P =.004), nodal involvement (P =.04), pleural invasion (P =.0003), lymphatic invasion (P =.002), and vascular invasion (P =.0002) were observed more often among patients with a smaller proportion of bronchioloalveolar carcinoma. A positive and significant correlation was found between the rate of bronchioloalveolar carcinoma component and ground-glass opacity (R(2) = 0.488, P <.0001) and tumor shadow disappearance rate (R(2) = 0.727, P <.0001). As an independent predictor of nodal status, tumor shadow disappearance rate (P =.015) and bronchioloalveolar carcinoma component (P =.015), as well as tumor size, were significantly valuable, although ground-glass opacity proportion (P =.086) was marginally informative. CONCLUSIONS: Small-sized adenocarcinomas with a greater ratio of bronchioloalveolar carcinoma component showed less aggressive behavior. Both tumor shadow disappearance rate and ground-glass opacity ratios, which are obtained preoperatively, were well associated with bronchioloalveolar carcinoma ratios, which are determined postoperatively. Furthermore, tumor shadow disappearance rate had a stronger impact as a predictor of bronchioloalveolar carcinoma component. Preoperative assessment of tumor shadow disappearance rate may be useful to identify patients requiring a less extensive pulmonary resection.

Adenocarcinoma↗

PubMed1996

Pathophysiology of Hodgkin's disease: functional and molecular aspects.

Hodgkin's disease (HD) is characterized by the presence of the typical, clonal malignant Hodgkin and Reed-Sternberg (H-RS) cells in a hyperplastic background of normal reactive lymphocytes, plasma cells, histiocytes, neutrophils, eosinophils and stromal cells. The neoplastic nature of HD is based on aggressive clinical progression, presence of the proliferating and atypical H-RS cells, aneuploidy and cellular clonality. Immunophenotypical studies have demonstrated frequent expression of lymphoid "activation markers' including CD15, CD25, CD30, CD40, CD54, CD70, CD71, CD80, CD86 and MHC class II and less frequent expression of T- or B-cell-associated antigens by the neoplastic H-RS cells. The clonality of H-RS cells is demonstrated by clonal EBV integration, clonal cytogenetic abnormalities including p53 mutations and clonal immunoglobulin rearrangements in some HD cases. There is involvement of diverse molecules with oncogenic potential, including presence of viruses (Epstein-Barr virus and human herpes virus-6) and/or oncogenes/tumour suppressor genes (bcl-2/bcl-x, p53/MDM-2, c-myc, c-fms, N-ras, lck). The histopathological presentation and characteristic clinical features of HD correlate with an unbalanced production of multiple cytokines and define HD as a tumour of cytokine-producing cells. The proportion of malignant H-RS cells to reactive cellular components and fibrosis is dependent on the production of particular cytokines and allows subtyping of HD cases. The combined use of immunohistochemical, biochemical and molecular techniques has thus allowed recognition that HD represents more than one clinico-pathological entity with different types of H-RS cells. The defined mechanism for the biological nature, origin and oncogenesis of H-RS cells remains not fully understood, but is susceptible to further analysis using modern technology.

Antigens, CD↗

PubMed2002

Hodgkin's disease primarily involving the oropharynx: case report and review of the literature.

We report a rare case of Hodgkin's disease primarily involving the oropharyngeal region. The patient presented with stage IIEA disease with a favorable response to treatment. Our literature search revealed that this disease affected rarely the lymphoid tissues of Waldeyer's ring. In this atypical location, tonsil and nasopharynx represent the most frequently involved sites. The involvement of the posterior wall of the oropharynx by Hodgkin's disease has been reported only once so far. When Waldeyer's ring is involved, the disease is usually localized, with occasional involvement of cervical lymph nodes. In this location, mixed cellularity is the most frequent histologic subtype and the Epstein-Barr virus is found in the majority of cases. This report is followed by a discussion on the clinical and pathological features, the implication of Epstein-Barrs virus and a literature review for Hodgkin's disease involving Waldeyer's ring.

Antineoplastic Combined Chemotherapy Protocols↗