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.

SourceResearch connectionFrom yearThrough year

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

At least 469 records · Page 26Linked to original sources

PubMed1991

Benjamin Felson lecture. Chronic interstitial lung disease of unknown cause: a new classification based on pathogenesis.

Chronic interstitial lung disease of unknown cause is usually classified on the basis of descriptive histology. In this lecture, a recently published series of 910 cases of chronic interstitial lung disease is used to show that these descriptive terms can be reorganized into a classification that is based on inflammatory and neoplastic processes. The proposed classification includes three major diagnostic categories, two of which are based on the chronic inflammatory response and a third that results from infiltration of the interstitial space by neoplastic cells of either a benign, borderline, or frankly malignant nature. An argument is presented that the steps involved in the development of the endstage of chronic interstitial lung disease are similar in all three groups. The advantage of this new classification is that it shifts the emphasis from descriptive terminology to pathogenesis, which provides a more critical basis for investigation of the causes of these diseases.

Humans↗

PubMed1990

DNA content of Hurthle cell nodules in autoimmune thyroiditis.

Hurthle cells are found in thyroid neoplasms and in reactive nodules in thyroiditis or goitrogenic processes. Cytometric studies have evaluated Hurthle cell neoplasms but not their reactive counterparts. DNA content of Hurthle cells in 22 cases of autoimmune thyroiditis was measured by flow cytometry and image content of Hurthle cells in 22 cases of autoimmune thyroiditis was measured by flow cytometry and image processing using nuclei extracted from paraffin-embedded tissue after microdissection of the Hurthle cell nodules. All 22 autoimmune thyroiditis Hurthle cell nodules were diploid, including 16 without associated neoplasms and six with associated malignant neoplasms (four papillary carcinomas, one follicular carcinoma and one follicular adenoma with papillary carcinoma). Concordance between flow cytometry and image processing was 100%. These findings indicate that the markedly atypical Hurthle cells in autoimmune thyroiditis are diploid by DNA quantitation. This suggests that atypia in Hurthle cells due to reactive or neoplastic processes may be differentiated by quantitative DNA analysis.

Adult↗

PubMed2004

Oligoclonal T-cell populations in an inflammatory pseudotumor of the pancreas possibly related to autoimmune pancreatitis: an immunohistochemical and molecular analysis.

Inflammatory pseudotumors (IPT), also known as inflammatory myofibroblastic tumors (IMT), are benign inflammatory processes that may have an infectious etiology and are very rare in the pancreatico-biliary region. Recent studies suggest a biological distinction between IPT and IMT, the latter being a true neoplastic process. We describe a case of pancreatic IPT, originally diagnosed as malignancy, which presumably recurred 4 months after the operation. Histologically, the tumor consisted of a smooth muscle actin and CD68-positive spindle cell population and a more abundant mononuclear inflammatory cell population, primarily composed of macrophages and T-lymphocytes. Inflammatory cells were the source of connective tissue growth factor and transforming growth factor-beta1 and tended to accumulate around nerves and blood vessels, as well as around residual pancreatic parenchymal elements, where an intense angiogenetic response was detected. Comparative genomic hybridization analysis of the tumor showed no chromosomal imbalances. Polymerase chain reaction-based analysis of T-cell receptor gamma gene rearrangement revealed an oligoclonal pattern. These findings suggest that the pathogenesis of aggressive cases of IPT could be related to the development of an intense and self-maintaining immune response, with the emergence of clonal populations of T-lymphocytes. The relation of the pancreatic IPT to autoimmune pancreatitis is emphasized.

Adenocarcinoma↗

PubMed1999

Disorganization of cortical structure and the brain tumors.

In the course of histopathological investigation of the temporal lobe sections, selected from 63 patients treated surgically for intractable epilepsy and finally presented with primary temporal tumors, we found 12 cases expressed both neoplastic process' and developmental disorders. The temporal mass lesions consisting of neuro-glial or pure glial tumors were associated with some developmental abnormalities such as cortical dysplasia, neuronal heterotopias and additional cortical neoplastic nodules. The possible "dual pathology" concerning these lesions are discussed in this paper.

Brain Neoplasms↗

PubMed1991

Evidence that toxic injury is not always associated with induction of chemical carcinogenesis.

Long-term rodent bioassays with chemicals administered at maximum tolerated doses identify noncarcinogens as well as carcinogens. Thirty-one chemicals recently evaluated for carcinogenic potential by the National Toxicology Program provide unique data on the relationships between mutagenicity, toxicity, and carcinogenicity. Twenty-two substances were classified as carcinogens, and nine showed no evidence of carcinogenicity. Although cellular proliferation does play an intrinsic role in neoplastic processes, the responses associated with chronic toxicity in these studies were not always sufficient to induce neoplasia. Regardless of their mutagenic potential, 19 carcinogens induced toxic effects at sites that did not show neoplastic changes; similar toxic lesions were also seen among the mutagenic and nonmutagenic noncarcinogens. Although many nonmutagens induced neoplasia at sites that showed toxic effects, some of the same chemicals also exhibited toxicity at other sites that showed no neoplastic effect. These results suggest that for some chemicals, properties other than mutagenicity or toxicity may be responsible for their carcinogenic potential.

Animals↗

PubMed2005

Linking KSHV to human cancer.

Kaposi's sarcoma-associated herpesvirus (KSHV), also known as human herpesvirus 8 (HHV-8), has been linked to several malignancies in humans. KSHV is the etiologic agent associated with the development of Kaposi's sarcoma (KS), primary effusion lymphoma (PEL), and multicentric Castleman's disease (MCD). KSHV is a double-stranded DNA virus that has been classified as a gammaherpesvirus. Here, we review the association of KSHV with human cancer, viral genes that may potentially be involved in the neoplastic process, and current therapies used to treat KS, PEL, and MCD.

Animals↗

PubMed1997

Barrier between the supraglottis and the glottis: myth or reality?

Controversial opinions on the existence of a "barrier" between the supraglottic and glottic regions of the larynx are reported. Even if the two areas have different embryological derivations, there is no anatomic evidence of a "barrier" that could prevent supraglottic cancer from extending downward to the glottis. Numerous adequate pathologic studies, including whole organ sections, confirm that for advanced cancers, anatomic compartments delimiting the spread of the neoplastic process from the supraglottis to the glottis do not exist. Therefore, supraglottic laryngectomy should be performed not on the basis of embryological considerations, but on the basis of the actual extension of the neoplastic lesion.

Glottis↗

PubMed1985

[Value of nuclear magnetic resonance tomography in lung tumors].

A total of 93 patients with pulmonary diseases were examined by means of magnetic resonance tomography. Of these, 39 had a bronchial neoplasm of varying histological structure and varying hilar and mediastinal extension. Compared with other imaging methods, magnetic resonance tomography offers advantages in the imaging of a malignant process and accurate definition of its spatial extension. MR and CT seem to be essentially of equal value in respect of the diagnostic problem of deciding whether lymph node metastases are present in the mediastinum and in the hilus. On the other hand, CT is presently still superior to MR with regard to verifying small-scale processes which are in the process of undergoing endobronchial growth, since CT provides better spatial resolution. Hence, in our opinion the special value of magnetic resonance tomography is the exact definition of the extension of an already identified neoplastic process. This method can supply accurate pointers towards the operability of a bronchial neoplasm. In this regard it is an ideal complement to mediastinoscopy. However, MR will not be an important tool--even in the foreseeable future--for effecting early diagnosis of a neoplasm. The value of diagnostic information supplied by this method may improve by the future use of breath triggering, and additional diagnostic advantages are envisaged by the use of contrast media and the future possibility of producing thinner layers. That is why the catalogue of indications prepared at this time should be seen as a kind of momentary snapshot which may have to be supplemented or extended after the prevailing technical and equipment parameters have undergone further optimisation.

Adenocarcinoma↗

PubMed1987

Melatonin: perspectives in laboratory medicine and clinical research.

We are presently at a point in human pineal research where we have recognized through melatonin assay the presence of pineal dysfunction in a variety of disease categories. Melatonin may now be quickly and accurately quantified in a range of body fluids, and our well-developed knowledge of the basic biochemistry and neuroanatomical connections of the pineal enables us to see at least how abnormalities in melatonin secretion occur, if not why. The reported increases in melatonin secretion in early malignancy with a reduction in secretion during the neoplastic process is interesting, as is the great decline in the elevated melatonin level of oncological patients following institution of chemotherapy. The correlations between estrogen receptor status of breast cancer and melatonin level, and between neoplastic status of the prostate and melatonin secretion, points to interesting differential diagnostic utilities of melatonin analysis in these conditions. Furthermore, an etiological involvement of melatonin in neoplasia is suggested by experiments which have demonstrated the capacity of melatonin to induce mitotic arrest, and to increase the affinity of mammary carcinoma estrogen receptors for their substrate. These are important observations among many others of direct relevance to research and treatment in oncology, and warrant much further investigation. Melatonin assay may also prove useful in the prognostic monitoring of patients treated for melatonin-secreting pineal tumors, and in such cases may form a logical part of follow-up investigation in the screening for metastatic complication. In psychiatry research, melatonin analysis has functioned as a tool by which alterations in pineal function within specific psychiatric diagnoses have been demonstrated and assessed. Its uses in the assessment of the effects of antidepressant drugs on central beta-receptor function, as a tool in the investigation of light-induced alterations in pineal function in manic-depressive individuals, and as a tool in the investigation of the putative pineal-adrenocortical functional interaction have produced the fundamental building blocks of modern research into the pineal and psychiatry. The experimental clinical utility of melatonin assay is not localized to oncology and psychiatry, and significant alterations in melatonin secretion have been reported in several other disease categories. Indeed, the demonstration of markedly elevated melatonin secretion in patients with spina bifida occulta might suggest that assay of melatonin in amniotic fluid could be useful as an experimental adjunct in the prenatal diagnosis of this condition.(ABSTRACT TRUNCATED AT 400 WORDS)

Brain Neoplasms↗

PubMed1993

Chromosome abnormalities in oral squamous cell carcinomas.

Strong evidence in favour of the somatic mutation theory of cancer, which states that genomic rearrangements are early and essential events in tumour development, has during the past two decades been obtained from both cytogenetic and molecular genetic studies of neoplastic cells. More than 14,000 neoplasms with acquired clonal chromosome aberrations have been reported; the majority have, however, been haematological malignancies, whereas still little is known about the karyology of the quantitatively more important carcinomas. For oral squamous cell carcinomas (SCC), which constitute a substantial subset of human malignancies, only 63 short-term cultured tumours with karyotypic aberrations have been described. Simple numerical changes, mostly -Y, +Y, or +7, have been detected as the sole anomalies in 19 tumours, but these aberrations are probably not causally related to the neoplastic process. The remaining 44 SCC have had structural changes of varying complexity, often together with numerical aberrations. An assessment of the karyotypic imbalances resulting from these aberrations reveals that chromosomes 9, 13, 18 and Y are recurrently lost, and that deletions frequently involve chromosome arms 3p, 7q, 8p, 11q, 17p and the short arms of all acrocentric chromosomes. The chromosomal breakpoints in structural rearrangements frequently involve the centromeric regions of chromosomes 1, 3, 8, 14 and 15 as well as bands 1p22, 11q13 and 19p13. At least one of these bands has been rearranged in 70% of SCC with structural aberrations and they probably contain loci of importance in oral squamous cell carcinogenesis. A comparison of data obtained from oral and other types of SCC--laryngeal, oesophageal, lung, cervical, and anal canal--indicates that some of the events in the multistep process of SCC development involve the same genetic pathways irrespective of site of origin.

Carcinoma, Squamous Cell↗

PubMed1990

Cytogenetics in the investigation of haematological disorders.

Chronic and acute, myeloid and lymphatic haematological neoplasms are characterized by acquired genetic rearrangements that, in the majority of cases, can be detected as clonal chromosomal abnormalities. The aberrations are either primary, meaning that they contribute to the establishment of the neoplasm, or secondary, in which case they are acquired during the clonal evolution and malignization of the neoplastic cells. The abnormalities are non-randomly distributed; the aberration pattern differs from disease to disease and sometimes is so characteristic that individual rearrangements may be virtually pathognomonic for particular neoplasms. The cytogenetic characterization of haematological malignancies is of two-fold importance. First, the recurrent aberrations provide us with an insight into the pathogenetic mechanisms that are operative. They pinpoint those areas of the human genome that carry genes or regulatory sequences whose function is disturbed in leukaemias and lymphomas. Using DNA recombinant techniques in addition to chromosome-level investigations of these cancer-associated rearrangements, the molecular pathology of leukaemias and lymphomas is now gradually being unravelled. Second, even before the long-term goal of a more fundamental understanding of the neoplastic process is reached, the cytogenetic aberrations have a direct clinical importance. The finding of an acquired, clonal chromosome abnormality in haematopoietic cells (-Y in old men is an exception) means that the patient has a neoplastic disease. Often, but by no means always, the type of aberration is also informative as to which type of neoplasm is present. During therapy, remission and relapse can be monitored by cytogenetic analyses. Finally, the karyotypic pattern influences prognosis and may thus be taken into account when the choice of therapy is made.

Chromosome Aberrations↗

PubMed1978

[Ultrastructure and secretory cycle of the islands of Langerhans cells in pancreatic cancer].

By electron microscopy, the islets of Langerhans of 5 patients with cancer of the pancreas were studied. The most obvious ultrastructural changes were found in the insulin-producing B-cells. Their cytoplasm contained a reduced number of secretory granules. Many B-cells were seen at different stages of the secretory cycle, part of them being destructed. On studying secretory process, the formation and maturation of B-granules was demonstrated in the cistern of ergastoplasm without the Golgi complex being involved. The data obtained suggest the functional tensity of the insular tissue at the neoplastic process in the exocrine part of the pancreas.

Adenocarcinoma↗

PubMed1981

[Carcinosarcomas of the lung].

The authors analysed the literature on pulmonary carcinosarcomas and described two own observations of this rare pathology. The predominant occurrence of this tumor in men of 40-65 years, rapid development of the process, frequent asymptomatic course and late surgical help are noted. Clinico-anatomical manifestations of pulmonary carcinosarcomas are nonspecific. Their histological structure is variable and depends on the nature of tissue components involved in the neoplastic process. The authors emphasize a great diagnostic value of prophylactic fluorographic examinations of the population.

Aged↗

PubMed1999

Simultaneous alterations of retinoblastoma and p53 protein expression in astrocytic tumors.

The genetic alterations frequently involved in glial malignancies are in the tumor suppressor genes, Rb and p53. An altered Rb expression or p53 overexpression is thought to indicate defective tumor suppression and subsequently more aggressive tumors. Therefore, to assess the alterations in the conjoint expression of Rb and p53 proteins in formalin fixed paraffin embedded sections, 64 astrocytic tumors were studied (16 astrocytomas,7 gemistocytic astrocytomas, 19 anaplastic astrocytomas and 22 glioblastomas) using the avidin biotin immunoperoxidase technique. Fifty two cases (81.25%) were found to be positive for p53 protein. Seventeen of these showed aberrant heterogenous staining for pRb, of which 7 were glioblastomas. Only one case of astrocytoma showed aberrant expression of both p53 and Rb. Thus, of the 64 tumors, simultaneous aberrant expression of both p53 and Rb was seen in 21.9% of cases. This was more commonly observed among glioblastoma cases (7/22). No statistical difference was found between the survival rate of heterogenous pRb and p53 positivity in different grades of tumors. In glioblastomas, the survival rate appeared to be less in patients expressing heterogenous pRb, but this was not statistically significant. These results lead us to suspect that p53 and pRb pathways are inactivated, either through mutation or as part of the neoplastic process in astrocytic tumors.

Adolescent↗

PubMed1995

Identification of differentially expressed genes in T-lymphoid malignancies in an animal model system.

The molecular events characterizing lymphoid malignancy have been examined in an animal model system, specifically, the retroviral induction of leukemia and lymphoma in the domestic cat following infection with feline leukemia virus (FeLV). Genes differentially expressed in FeLV-induced lymphomas were isolated using a strategy of differential hybridization. Six genes were identified which demonstrate a higher level of expression in an FeLV-induced feline thymic tumor as compared with normal thymus. The differentially expressed genes encode the feline homologues of ribosomal proteins S3a, S4, S17, and L41, elongation factor-1 alpha, and cytochrome oxidase sub-unit I. Northern-blot analysis and quantification by phosphorimaging demonstrates that these genes are expressed at levels from 1.5- to 3.1-fold higher in J5-1 thymic tumor as compared with normal thymus. Expression of the selected ribosomal protein mRNA was further examined in a series of human and feline tissues, including normal tissues, malignant tumors and cell lines. Our data reveal that elevation of the selected ribosomal protein mRNA is associated with all FeLV-induced thymic lymphomas examined. The differentially expressed ribosomal protein mRNA accumulates in a balanced manner in thymic lymphomas. By contrast, the elevation in ribosomal protein mRNA levels is not associated uniformly with hematopoietic malignancy. T-lymphoid malignancy, solid tumors or actively proliferating cells. Rather, the elevation appears to be a uniform and distinctive feature of T-cell malignancy of this particular type. The elevated expression of these genes may be causally related to the neoplastic process.

Adult↗

PubMed2006

Akt-mediated phosphorylation and activation of estrogen receptor alpha is required for endometrial neoplastic transformation in Pten+/- mice.

PTEN is a tumor suppressor gene frequently mutated in human cancers. In vitro and in vivo studies have shown that PTEN can exert its tumor suppressive function through a variety of mechanisms, including regulation of cell death and cell proliferation. However, it is still unclear which of the many downstream pathways are critical in each different tissue, in vivo. Loss of PTEN is the earliest detectable genetic lesion in the estrogen-related type I (endometrioid) endometrial cancer. Pten(+/-) mice develop endometrial neoplastic lesions with full penetrance, thus providing a model system to dissect the genetic and biochemical events leading to the transition from normal to hyperplastic and neoplastic endometrial epithelium. Here, we show that loss of Pten in the mouse endometrium activates Akt and results in increased phosphorylation of estrogen receptor alpha (ERalpha) on Ser(167). ERalpha phosphorylation results, in turn, in the activation of this nuclear receptor both in vivo and in vitro, even in the absence of ligand, and in its increased ability to activate the transcription of several of its target genes. Strikingly, reduction of endometrial ERalpha levels and activity dramatically reduces the neoplastic effect of Pten loss in the endometrium, in contrast to complete estrogen depletion. Thus, we provide for the first time in vivo evidence supporting the hypothesis that loss of Pten and subsequent Akt activation result in the activation of ERalpha-dependent pathways that play a pivotal role in the neoplastic process.

Animals↗

PubMed1989

[Bioactivation of xenobiotics by cytochrome P-448 and its role in the process of carcinogenesis].

The paper presents the general data concerning cytochrome P-448, as well as its participation in the formation of oxygen radicals and active metabolic intermediates, originated during xenobiotics' oxidation. Also, induction of synthesis of cytochrome P-448 (aromatic hydrocarbons hydroxylase), along with the role this phenomenon plays in the initiation of neoplastic process, are discussed.

Acetaminophen↗

PubMed1992

The effect of ammonia on the respiratory nasal mucosa of mice. A histological and histochemical study.

The effects of prolonged exposure to ammonia vapour on the histological pattern and enzymatic activity of the respiratory nasal mucosa of 75 adult male mice were investigated and compared with a control group. In the exposed animals, the nasal epithelial cells showed patches of squamous metaplasia, dysplasia, and even malignant changes in the nose of 2 animals. As regards the histochemical changes, the apical border of epithelial cells showed increased succinic dehydrogenase activity denoting increased energy production. The acid phosphatase activity was also higher, and this seemed to be a constant feature in metaplastic and neoplastic transformation. The alkaline phosphatase activity was detected only in the basal parts of epithelial and goblet cells, which was attributed to an increased activity of basal cells to form a thicker basement membrane. The periodic acid Schiff's reaction was weak in the cilia due to their partial degeneration. Prolonged exposure to ammonia interfered with the normal physiological mucociliary action resulting in accumulation of particulate matter initiating or promoting a neoplastic process.

Acid Phosphatase↗