Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Molecular Classification”

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 451 records · Page 25Linked to original sources
PubMed1999

[Molecular evolution and genotype classification of TT virus].

Based on sequences data, TTV have a partial Rep protein motifs found among Circoviridae and the conserved region of parvoviral nonstructural polypeptides (NS)-1 genes, however we could not perform phylogenetic analyses among TTV and other viruses because of few similar sequences. Putative ORF2 among G2 and G4 encoded 49 aa because of in-frame stop codon, although that of G1 encoded 202 aa. Just down-stream of the stop codon, another putative new ORF(ORF3) were found around 150 aa. A phylogenetic analysis, using the ORF1 sequences of 93 TTV obtained from various geographical areas, indicated that the virus could be classified into six different genotypes. Further studies using more than 350 isolates obtained from DDBJ showed at least nine genotypes.

Amino Acid Sequence↗
PubMed2000

Molecular phylogenetics and the classification of honey bee viruses.

We present the phylogenetic relationships of several picorna-like RNA viruses found in honey bees, with respect to 13 additional plant and animal positive-strand RNA viruses. Most of the honey bee viruses fall into an unnamed family of insect RNA viruses typified by the Drosophila C virus. Different bee viruses are broadly distributed within this group, suggesting either that the ability to infect honey bees has evolved multiple times, or that these viruses are generalistic in their abilities to infect insect hosts. At least one major change in gene order has occurred among the bee viruses, based on their phylogenetic affiliations. At the amino-acid level, the bee viruses differed by 15-28% at three conserved loci. Most differed by greater than 50% at the RNA level, indicating that sequence-based methods for bee virus identification must be tailored to at least three different virus clades independently.

Amino Acid Sequence↗
PubMed1997

A prospective study of minimal residual disease in childhood B-lineage acute lymphoblastic leukaemia: MRD level at the end of induction is a strong predictive factor of relapse.

We prospectively investigated minimal residual disease (MRD) in 51 children with B-lineage acute lymphoblastic leukaemia (ALL) treated according to the Fralle 93 protocol. PCR follow-up was performed in children in morphological and cytogenetic complete remission, provided an immunoglobulin (IgH) gene rearrangement could be detected using FR 3/J(H) amplimers. MRD was studied according to our previously described methodology, with a few modifications including the use of a consensus J(H) probe to control for PCR efficiency variations. Out of the initial 51 patients, 34 were assessable for MRD at the end of induction at the time of analysis. MRD levels were as follows: > 1/10(3) in 26%, 1/10(3) to 1/10(4) in 50% and < 1/10(4) or not detectable in 24%. With a median follow-up of 20 months there were five relapses, all of which occurred in the group of patients with MRD > 1/10(3). To date, none of the patients with MRD < or = 1/10(3) (good molecular responder) has relapsed. Classification according to molecular response at the end of induction did not correlate with the conventional risks groups: there were no statistically significant differences between good and bad molecular responders. Of particular interest is the absence of correlation between WBC at diagnosis and MRD level at the end of induction. We conclude that classification of patients into good and bad molecular responders using PCR seems to be a better prognostic indicator than conventional risk factors in childhood B-lineage ALL. Patients with MRD level > 1/10(3) have a particularly poor outcome and should always be considered for alternative therapeutic strategies in the future, whereas in good molecular responders belonging to poor or intermediate risk categories, treatment de-escalation might be contemplated.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed1997

Molecular neuropathology of astrocytic brain tumors.

Both surgical and molecular neuropathologists have recently achieved remarkable progress in the histogenetic classification and molecular characterization of human gliomas. Major histopathological achievements in the revised WHO classification include the introduction of immunohistochemical reagents for glial fibrillary acidic protein and for the proliferation-associated antigens, the definition of glioblastoma multiforme as an astrocytic neoplasm and the recognition of the pleomorphic xantho--astrocytomas as a novel clinico-pathological entity. In molecular neuropathology, alterations of oncogenes and tumor suppressor genes and their potential functions have been identified, microsatellite analyses have revealed novel loci for putative tumor suppressor genes and distinct molecular pathways for different tumor entities are beginning to emerge. Mutations in cell cycle regulatory genes are present in most glioblastomas and may account for their striking growth potential. Autocrine and paracrine growth factors and their respective protein tyrosine kinase receptors appear to contribute both to glial and endothelial cell proliferation. In our contribution, we would like to focus on astrocytic gliomas. Findings with potential diagnostic relevance include changes associated with malignant progression of low grade astrocytomas, patterns of genetic alterations which allow to further differentiate histopathological entities such as the glioblastoma multiforme into genetically distinct subsets and mechanisms of tumor angiogenesis in malignant gliomas. One of the major tasks ahead is to establish correlations and relationships between histopathological, molecular and clinical data. This will require a long-term collaboration between molecular neuropathologists, neurosurgeons and clinical neuro-oncologists.

Animals↗
PubMed1993

Trypanosoma cruzi: correlation between karyotype variability and isoenzyme classification.

Forty-three Trypanosoma cruzi isolates from Chile and Colombia and three cloned stocks from Bolivia and Brazil were studied at the karyotype level by hybridization with four different parasite gene probes to chromosomes separated by pulsed-field gel electrophoresis. The results showed that classification of parasite isolates based on isoenzyme analysis at 12 or more genetic loci correlated with the classification obtained by molecular karyotype analysis. However, less correlation was found between molecular karyotypes and the zymodemes Z1, Z2Bra, Z2Bol, and Z3 based on analysis at only two genetic loci. All the four probes used in this study allowed differentiation between different T. cruzi stocks but the SAPA and the antigen 13 probes were most informative. Isolates which were unclassified at the isoenzyme level were also studied and in most cases similar hybridization patterns were observed as obtained with one or more isoenzyme-classified isolates. The results demonstrate the potential of using molecular karyotyping as a tool for classification. A few pulsed-field gel electrophoresis hybridization experiments provide the same information as obtained by isoenzyme analysis using a dozen or more enzymes. The clonal theory of T. cruzi propagation is supported by our results since the strong correlation between isoenzyme classification and molecular karyotype is difficult to explain with a sexual mode of replication. No minichromosomes were detected in any of the T. cruzi samples studied. Neither was any strong correlation found between the clinical manifestations of Chagas' disease and the molecular karyotypes of the T. cruzi isolates.

Animals↗
PubMedDate not supplied

[Classification of low-molecular-weight RNA of mammals].

On the basis of the published date, an attempt has been made to classify low-molecular-weight RNA of eukaryotes in terms of a comprehensive nomenclature. About species of low-molecular-weight RNA were isolated, which are marked by their sedimentation constants. The isolated fractions have been characterized.

Animals↗
PubMed1993

Myelodysplastic syndromes: from morphology to molecular biology. Part I. Classification, natural history and cell biology of myelodysplasia.

The myelodysplastic syndromes are a heterogeneous group of clonal hematopoietic disorders predominantly affecting the elderly. Patients frequently develop acute leukemia, but the majority suffer from the consequences of bone marrow failure. The underlying acquired genetic abnormality is the inadequate production of dysplastic and poorly functional cells resulting from defective differentiation and premature cell death of the abnormal hematopoietic clone. Although the pathogenesis is unknown, recent evidence suggests that a sequence of DNA lesions leads to alteration of the cellular function, emergence and consequent evolution of the premalignant clone.

Humans↗
PubMed2004

Gene expression based classification of gastric carcinoma.

The aim of the present work is to identify molecular markers that allow classification of gastric carcinoma with respect to important clinicopathological parameters. Gastric adenocarcinomas were subjected to cDNA microarray analysis with a 2.504 gene probe set. Using the Rosetta rough-set based learning system, good classifiers were generated for gene-expression based prediction of intestinal or diffuse growth pattern according to Laurén's classification and presence of lymph node metastases. To our knowledge, this is the first study on gastric carcinoma in which molecular classification has been achieved for more than one clinicopathological parameter based on microarray gene expression profiles.

Adenocarcinoma↗
PubMed2003

Molecular markers in myeloproliferative disorders: from classification to prognosis?

The recent description of molecular markers in patients with myeloproliferative disorders (MPDs) has raised several questions: does the presence of multiple markers coincide in individual patients or can a patient acquire some markers selectively? Do the markers distinguish molecular categories of MPDs? Do these categories coincide with the clinically defined subgroups of MPDs: PV, ET and IMF? If not, which system of categorization is more useful to the patient and his physician, the molecular one or the clinical one, and why? The present review will summarize the current knowledge of molecular markers in MPDs and discuss today's answers to the above questions. Since our knowledge of the molecular basis of MPDs is rapidly expanding, it is my hope that this review will soon be outdated.

Antigens, Neoplasm↗
PubMed2004

Combined histopathological and molecular cytogenetic stratification of medulloblastoma patients.

This study examined the utility of stratifying children with medulloblastomas by a combination of refined histopathological classification and molecular cytogenetic evaluation. Detailed histopathological classification of tumors from a cohort of patients (n = 87) composed mainly of children entered into the International Society of Pediatric Oncology (SIOP)/United Kingdom Children's Cancer Study Group PNET3 trial (n = 65), included identification of the large cell/anaplastic phenotype. Fluorescence in situ hybridization was used to detect chromosome 17 abnormalities, losses of 9q22 and 10q24, and amplification of the MYCC and MYCN oncogenes. The large cell/anaplastic phenotype, which was present in 20% of medulloblastomas, emerged as an independent prognostic indicator. Loss of 17p13.3 (38% of medulloblastomas) was found across all of the histopathological variants, whereas MYCC/MYCN amplification (6%/8% of medulloblastomas) was significantly associated with the large cell/anaplastic phenotype. Both of these genetic abnormalities emerged as prognostic indicators. Loss of 9q22 was associated with the nodular/desmoplastic medulloblastoma variant, whereas loss of 10q24 was found in all of the variants. Together with metastatic tumor at presentation, the large cell/anaplastic phenotype, 17p13.3 loss, or high-frequency MYC amplification defined a high-risk group of children whose outcome was significantly (P = 0.0002) poorer than a low-risk group without these tumor characteristics. Combined evaluation of novel histopathological features and molecular cytogenetic abnormalities promises to allow stratification of patients with medulloblastoma, such that those likely to be cured will be spared the side effects of maximal therapy, which can be targeted at those with aggressive disease.

Cerebellar Neoplasms↗
PubMed2006

A consensus prognostic gene expression classifier for ER positive breast cancer.

BACKGROUND: A consensus prognostic gene expression classifier is still elusive in heterogeneous diseases such as breast cancer. RESULTS: Here we perform a combined analysis of three major breast cancer microarray data sets to hone in on a universally valid prognostic molecular classifier in estrogen receptor (ER) positive tumors. Using a recently developed robust measure of prognostic separation, we further validate the prognostic classifier in three external independent cohorts, confirming the validity of our molecular classifier in a total of 877 ER positive samples. Furthermore, we find that molecular classifiers may not outperform classical prognostic indices but that they can be used in hybrid molecular-pathological classification schemes to improve prognostic separation. CONCLUSION: The prognostic molecular classifier presented here is the first to be valid in over 877 ER positive breast cancer samples and across three different microarray platforms. Larger multi-institutional studies will be needed to fully determine the added prognostic value of molecular classifiers when combined with standard prognostic factors.

Breast Neoplasms↗
PubMed2003

[New trends in the diagnosis and treatment of malignant lymphoma].

The present status of the following aspects of diagnosis and treatment of malignant lymphoma are reviewed, and future directions are discussed. 1. Epidemiology 2. Pathological classification 3. Molecular analysis of oncogenesis and disease progression 4. Staging classification and response evaluation 5. State-of-the art therapy of major subtypes 1) Hodgkin's lymphoma 2) Aggressive non-Hodgkin's lymphoma 3) Indolent B-cell non-Hodgkin's lymphoma 4) Salvage therapy for relapsed cases 6. New agent development focusing on antibody therapy 1) Principles and history of antibody therapy 2) Clinical development of rituximab in the USA and Japan 3) Radioimmunotherapy Recently, the importance of evidence-based medicine has been widely recognized not only by physicians but also by patients themselves. To further improve the therapeutic results, it is extremely important to conduct well-designed clinical trial consecutively.

Antineoplastic Combined Chemotherapy Protocols↗