Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Neoplastic Processes”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 901 records · Page 50Linked to original sources
PubMed1981

Pathological changes associated with topical chemotherapy for superficial bladder cancer.

With use of previous observations in experimental animals as a basis for comparison the cytologic and histologic changes in human patients who underwent topical chemotherapy for superficial bladder cancer were documented. Despite the potential for inhibition of deoxyribonucleic acid replication these drugs apparently act in vivo as toxic substances, causing increased exfoliation with denudation of papillary and/or flat urothelium. Multinucleation was common but confined to superficial cells. Atypical cells, such as those observed after systemic chemotherapy with cyclophosphamide, rarely were present and could be distinguished readily from neoplastic elements. Although topical chemotherapy may suppress tumor growth and progression it apparently does not eradicate the neoplastic process.

Administration, Topical↗
PubMed1980

Nodal involvement as a prognostic indicator in patients with prostatic carcinoma.

Between 1969 and 1976, 92 patients with proved prostatic carcinoma in stages T0 and T4 underwent pelvic lymphadenectomy. Median followup has been 43 months. All patients had normal serum acid phosphatase levels and no clinical evidence of metastases as determined by physical examination, bone scans and metastatic bone surveys. Pelvic lymph node metastases were noted in 32 cases. Radical prostatectomy was done in 34 cases and 45 patients received radiotherapy, 11 of whom had 125iodine seeds implanted. Progression of the neoplastic process, almost exclusively in the form of bony metastases, occurred in 18 of the 32 patients who had positive pelvic nodes and in 6 of the 60 patients with negative nodes (p less than 0.001). Patients with poorly differentiated carcinoma were more likely to have progression of the disease than those with moderately differentiated carcinoma (p less than 0.01) and no patient with a well differentiated carcinoma had disease progression.

Aged↗
PubMed1977

Mesothelial hyperplasia in hernia sacs.

Mesothelial hyperplasia is a benign condition, which simulates a neoplastic process. Since it may occur in hernia sacs this entity must be recognized by the urologist to prevent over-treatment.

Child, Preschool↗
PubMed1975

Lipoplastic lymphadenopathy simulating malignant lymphoma and pelvic lipomatosis: Report of a case and review of the literature.

The second known cases of pelvic lipoplastic lymphadenopathy is presented. Roentgenographic studies including lymphangiography were instrumental in the diagnostic evaluation but a histopathologic diagnosis was essential to exclude a neoplastic process. The etiology and natural history of this disease are indeterminant but seemed to pursue a benign 17-year course in our patient. A retroperitoneal lymph node dissection is not indicated unless encroachment on adjacent pelvic viscera causes mechanical obstruction.

Diagnosis, Differential↗
PubMed2005

Blood eosinophilia: a new paradigm in disease classification, diagnosis, and treatment.

Acquired blood eosinophilia is considered either a primary or a secondary phenomenon. Causes of secondary (ie, reactive) eosinophilia include tissue-invasive parasitosis, allergic or inflammatory conditions, and malignancies in which eosinophils are not considered part of the neoplastic process. Primary eosinophilia is classified operationally into 2 categories: clonal and idiopathic. Clonal eosinophilia stipulates the presence of either cytogenetic evidence or bone marrow histological evidence of an otherwise classified hematologic malignancy such as acute leukemia or a chronic myeloid disorder. Idiopathic eosinophilia is a diagnosis of exclusion (ie, not secondary or clonal). Hypereosinophilic syndrome is a subcategory of idiopathic eosinophilia; diagnosis requires documentation of both sustained eosinophilia (absolute eosinophil count > or = 1500 cells/microL for at least 6 months) and target organ damage (eg, involvement of the heart, lung, skin, or nerve tissue). Genetic mutations involving the platelet-derived growth factor receptor genes (PDGFR-alpha and PDGFR-beta) have been pathogenetically linked to clonal eosinophilia, and their presence predicts treatment response to imatinib. Accordingly, cytogenetic and/or molecular investigations for the presence of an imatinib-sensitive molecular target should accompany current evaluation for primary eosinophilia. In the absence of such a drug target, specific treatment is dictated by the underlying hematologic malignancy in cases of clonal eosinophilia; however, the initial treatment of choice for symptomatic patients with hypereosinophilic syndrome is prednisone and/or interferon alfa.

Benzamides↗
PubMed1993

Rhinoscleroma: a growing concern in the United States? Mayo Clinic experience.

Rhinoscleroma is a chronic, progressive, granulomatous infection of the upper airways caused by the bacterium Klebsiella rhinoscleromatis. Although most cases occur in developing countries, recent immigration patterns have led to an increasing number of patients with rhinoscleroma in the United States. Rhinoscleroma may mimic various inflammatory and neoplastic processes, including leprosy, paracoccidioidomycosis, sarcoidosis, basal cell carcinoma, and Wegener's granulomatosis. Current therapy consists of a combination of surgical débridement and prolonged antimicrobial therapy. Rhinoscleroma should be added to the list of opportunistic infections that can occur in patients with human immunodeficiency virus.

Adult↗
PubMed1992

Dermatologic manifestations of human immunodeficiency virus infection.

Human immunodeficiency virus (HIV) infection and the acquired immunodeficiency syndrome (AIDS) have become major health problems in the United States, and patients with manifestations of these diseases are seen by physicians in all areas of medicine. Cutaneous manifestations develop in as many as 92% of HIV-positive persons. Familiarity with these manifestations facilitates early diagnosis and enhances the care of HIV-infected patients. The spectrum of mucocutaneous disorders in these patients includes an acute exanthem, multiple infections, neoplastic processes, and miscellaneous disorders. Herein we review the most common and the most specific dermatologic manifestations associated with HIV infection, which often are atypical, more severe, or less responsive to treatment than the corresponding diseases encountered in non-HIV-infected persons.

AIDS-Related Opportunistic Infections↗
PubMed2003

Complications of liver transplantation: imaging and intervention.

The radiologist can play a key role in diagnosis and management of many of the infectious, inflammatory, and neoplastic processes that affect patients after liver transplantation. Familiarity and skill with the full range of diagnostic and interventional tools are essential for radiologists dealing with transplant patients, even outside the medical centers where the transplantation takes place.

Diagnosis, Differential↗
PubMedDate not supplied

Nonthyroid causes of extraocular muscle disease.

Extraocular muscle involvement in orbital disease is most frequently seen as a feature of thyroid orbitopathy (Graves' disease). However, a wide range of other conditions may alter the size, shape, and function of these muscles, with characteristic clinical manifestations or abnormalities visible on orbital imaging. The differential diagnosis of muscle disease can be narrowed by careful analysis of clinical features and ancillary tests. Imaging facilitates recognition in many cases, but in some instances, accurate diagnosis requires biopsy. This review highlights the differential diagnoses for diseases of extraocular muscles based on the clinical and investigative records of 103 patients at our institution combined with data from the world literature. We found that the most common nonthyroid causes of muscle disease were inflammatory, vascular, and neoplastic processes (in decreasing order of frequency). Emphasis is placed on investigations that provide a logical approach to, and appropriate management of, disease of the extraocular muscles.

Amyloidosis↗
PubMed1982

T-lymphocyte subsets in follicular lymphomas compared with those in non-neoplastic lymph nodes and tonsils.

Using monoclonal antibodies on frozen sections, the authors define the anatomic localization of T-lymphocyte subsets in follicular lymphomas as well as in nonneoplastic lymph nodes and tonsils. The percentage of Leu-1+ T cells in the follicles of follicular lymphomas (20 per cent) was virtually identical to that seen in the follicles of nonneoplastic lymph nodes or tonsils (22 per cent). There were 50 per cent T cells in the interfollicular regions of follicular lymphomas and 75 per cent in the paracortical regions of the nonneoplastic specimens. In neoplastic follicles the number of Leu-3a+ cells was 67 per cent of the number of Leu-1+ cells, whereas, virtually the entire T-cell population in the nonneoplastic follicles expressed the Leu-3a antigen. These T cells of helper phenotype may facilitate the neoplastic process or an immune response against it or may be bystanders to the B-cell proliferation. Hum Pathol 13:618-625, 1982

Antibodies, Monoclonal↗
PubMed1982

Adenoid cystic carcinoma: a comparative pathologic study of tumors in salivary gland, breast, lung, and cervix.

Histologic, histochemical, and ultrastructural features of eight adenoid cystic carcinomas arising at diverse sites were compared in order to determine diagnostic values and to investigate histogenetic mechanisms. These tumors originated in the salivary glands, breast, uterine cervix, and tracheobronchial tree. By light microscopy each tumor was seen to have morphologic features of adenoid cystic carcinoma, yet only five of the eight cases showed differential staining for the two mucin types, stromal and epithelial, which are reportedly present in these tumors. In contrast, every case showed a set of fine structural features which, in aggregate, are specific for adenoid cystic carcinoma. These features include pseudocysts, intercellular spaces, basal lamina, and true glandular lumens. The most prominent feature is the pseudocyst, which mimics a glandular lumen by light microscopy but is actually a rounded extracellular space containing basal lamina. Ultrastructurally, the variation in composition of the extracellular compartments, including pseudocysts and true lumens, appears to explain the lack of uniformity in the histochemical staining. The tumors also contained cytoplasmic microfilaments in parallel bundles, consistent with myofilaments. The presence of these filaments combined with basal lamina suggests myoepithelial differentiation, yet it is not known whether these tumors truly originate from myoepithelium or show differentiation toward myoepithelium as a part of the neoplastic process. Regardless of their histogenesis, this study shows that true adenoid cystic carcinomas do arise in different organs. Knowledge of the specific ultrastructural features of adenoid cystic carcinomas can be useful in classifying these tumors in some cases.

Adult↗
PubMed1984

Demonstration of secretory component, IgA, and IgM by the peroxidase-antiperoxidase technique in inverted papillomas of the nasal cavities.

Fifteen inverted papillomas were examined by the peroxidase-antiperoxidase method for their ability to synthesize secretory component (SC) and to take up IgA and IgM. In each case, SC and IgA could be localized to the apical cytoplasm of some tumor cells. In addition, secretory component, IgA, and IgM were observed as the main constituents of hyaline globules lying in the intracytoplasmic lumina of one columnar cell variant of inverted papilloma, suggesting an intact transepithelial transport mechanism of polymeric immunoglobulins. Goblet cells, found only in the transitional cell variant of inverted papilloma, did not react with anti-SC, anti-IgA, or anti-IgM. Since SC can be utilized as a marker to differentiate columnar cells from goblet cells, transitional cell papillomas may originate from undifferentiated reserve cells, which retain their capacity to differentiate into both columnar cells and goblet cells. In contrast, in columnar cell papillomas only differentiated columnar cells are integrated into the neoplastic process.

Humans↗
PubMed1986

Intramitochondrial lamellar bodies in acute myeloblastic leukemia.

Intramitochondrial lamellar bodies were observed in three cases of acute myeloblastic leukemia. Two of the patients had M1 leukemia and the remaining patient M4 leukemia, by the FAB classification. In all three cases neoplastic cells contained dilated mitochondria that varied in size and shape and contained decreased numbers of cristae. Some mitochondria contained lamellar structures that resembled myelin figures and, occasionally, primary granules; these structures were more conspicuous in the central portion of the mitochondria. Regardless of the proliferating cell type (lymphoblasts, myeloblasts, or monoblasts), there are common ultrastructural changes that represent abnormal metabolic function, such as disorders of intramitochondrial protein synthesis. The exact meaning of these findings is not known; adequate interpretation will require further investigation of the biology of these neoplastic processes.

Adult↗
PubMed1986

Pseudoangiomatous hyperplasia of mammary stroma.

Grossly circumscribed, nonhemorrhagic breast masses consisting of mammary stromal proliferations that simulated vascular lesions were studied in nine women. Histologically, a striking pattern, which appeared to consist of complex inter-anastomosing channels lined by slender spindle cells, was present in the mammary parenchyma. The importance of this benign lesion, referred to as pseudoangiomatous hyperplasia of mammary stroma, is its distinction from angiosarcoma. The patients ranged in age from 22 to 52 years; all were premenopausal. Each presented with a palpable unilateral mass, measuring up to 7 cm in diameter. The patients were treated by excisional biopsy and remained well for up to 2.5 years after excision. One patient had two local recurrences within one year of the original excision, and a second patient had a local recurrence at 14 months. No patient had another concurrent or metachronous malignant tumor of the breast or other organ, and no abnormal hormonal status was found. Complete local excision appears to be adequate treatment. It remains to be determined whether this is a neoplastic process. However, there is no evidence that it is a precursor of angiosarcoma, and ultrastructural observations demonstrate that the spaces found in the lesion are not true vascular channels. Rather, they appear to arise by a process that involves disruption and separation of stromal collagen fibers. Since small foci of this change are common in hyperplastic breast tissue from premenopausal women, it is likely that the development of a discrete tumor with this pattern represents an exaggerated form of stromal hyperplasia.

Adult↗
PubMed1987

Expression of carcinoembryonic antigen, T-antigen, and oncogene products as markers of neoplastic and preneoplastic colonic mucosa.

Several crypt abnormalities have been demonstrated in the mucosa of neoplastic and preneoplastic lesions of the large intestine. In addition, certain tumor markers are expressed in large intestinal carcinoma but not in normal mucosa. To determine whether any correlation exists between tumor marker expression and crypt abnormalities and at what stage markers are expressed, we studied specimens of large intestinal mucosa from 13 patients with preneoplastic conditions (adenomatous polyp, familial polyposis, Crohn's disease, and ulcerative colitis). The tumor markers examined include carcinoembryonic antigen (CEA), the ras gene products p21 and p21ser (mutated form), and beta-D-galactosyl-(1----3)-alpha-N-acetyl-D-galactosamine (gal--gal NAc, also known as T-antigen). Results were compared to those of five cases of adenocarcinoma of colon and three control cases of colonic mucosa obtained at immediate autopsy. All four markers were expressed in three of the five cases of adenocarcinoma, but none were expressed in the control cases. Variable expression of each marker was demonstrated in the dilated, distorted crypts of preneoplastic lesions. CEA and gal--gal NAc appeared to be expressed most frequently, suggesting that these are common markers or are expressed at an earlier stage in the neoplastic process than p21 or p21ser. Demonstration of such markers in preneoplastic conditions may be of use in determining the malignant potential and in monitoring these lesions.

Antigens, Neoplasm↗
PubMed1996

p53 and p21(WAF1/CIP1/SDI1) gene products in Barrett esophagus and adenocarcinoma of the esophagus and esophagogastric junction.

The WAF1 (CIP1/SDI1) gene encodes a cyclin-dependent kinase inhibitor which is induced by wild-type, but not mutated, p53 gene product. WAF1 immunohistochemistry has been suggested to clarify the phenotype of overexpressed p53 gene product. We evaluated both p53 and WAF1 gene products by immunohistochemistry in 98 esophagectomy specimens with Barrett esophagus and/or adenocarcinoma of the esophagus and esophagogastric junction. Diffuse positive p53 staining was found in 40 of 88 adenocarcinomas (45%) and in dysplastic Barrett epithelium in 20 of 65 cases (31%), but not in Barrett mucosa without dysplasia (n = 36, P = .0004). Eighty-eight percent of cancers exhibited WAF1 expression, but there was no association with p53 and WAF1 staining. WAF1 protein was also identified in Barrett epithelium and in esophageal squamous and gastric epithelium. In contrast to carcinomas, a unique pattern of mutually exclusive p53 and WAF1 expression was found in five cases of dysplastic Barrett epithelium; a missense mutation at codon 175 of p53 was identified in one. p53 staining of adenocarcinoma was associated with shorter patient survival but was not independent of stage; WAF1 status added no prognostic information. Our findings show that WAF1 immunohistochemistry complements p53 immunohistochemistry in some cases of Barrett dysplasia but not in adenocarcinomas. Positive p53 immunostaining can serve to confirm a neoplastic process in Barrett mucosa. Positive staining of adenocarcinomas may be an indication of advanced stage.

Adenocarcinoma↗
PubMed1995

Tumor-induced osteomalacia.

Tumor-induced (oncogenic) osteomalacia is a rare clinicopathologic entity in which the clinical signs and symptoms of osteomalacia and the specific laboratory abnormalities of hypophosphatemia, hyperphosphaturia, and low serum levels of 1,25(OH)2 vitamin D are associated with the finding of a neoplastic process in the patient. To date, less than 100 cases of oncogenic osteomalacia have been described. We report a new case of adult-onset hypophosphatemic osteomalacia leading to the discovery of an asymptomatic phosphaturic mesenchymal lung tumor. Complete resection of the pulmonary neoplasia was followed by rapid normalization of the laboratory findings and clinical remission. The clinical, laboratory, and histopathologic spectrum of tumor-induced osteomalacia is presented, and the postulated mechanism of this condition is discussed in light of the relevant literature. The presence of occult neoplasms should be considered in cases of unexplained adult osteomalacia, with the physician's efforts being rewarded by the dramatic cure that follows excision of the tumor.

Adult↗
PubMed1984

Protoneoplasia: the molecular biology of murine mammary hyperplasia.

The mouse mammary tumor virus has provided a window into the inner workings of the mammary epithelial cell at the earliest stages of neoplasia. Techniques of molecular biology permitted us to look through that window revealing a new biology which deserves consideration as a model for mammary tumorigenesis in all species. According to this model the neoplastic process originates in a single mammary epithelial cell as a result of a critical genetic alteration, such as integration of MuMTV (MuMHV) into a key site in the mouse genome (Fig. 4). The genetic alteration immortalizes the cell and provides it with selective growth advantages which result in a clonal proliferation. This original proliferation emerges as the protoneoplastic mammary hyperplasia. The protoneoplastic cells have limited growth potential and are not obligated to undergo malignant transformation but they represent a genetically evolving population highly susceptible to full blown malignancy after exposure to carcinogens. Protoneoplastic cells which undergo further genetic alterations that provide additional selective growth advantages proliferate and emerge as malignant tumors. The genetic alterations are sometimes reflected by changes in viral DNA but this is not essential and most mouse mammary tumors probably do not occur as the result of new host-virus interactions. No doubt the current work on the mouse "int" loci will help define the genes responsible for the induction and maintenance of the protoneoplastic state. Since such host genes have proven so ubiquitous, one must also predict that analogous genes will be found in human mammary protoneoplasias. Detection of such sequences may help distinguish protoneoplastic processes from nonneoplastic, low risk hyperplasias in the human breast. Finally, the gene or genes involved in the more lethal malignant transformation await elucidation. Based on past and current progress one can be sure that the mouse mammary tumor system will help point the way.

Animals↗