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Results for “tumor evolution”

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PubMed1990

Studies on inflammatory response induced by Ehrlich tumor in mice peritoneal cavity.

In the present study we investigated the inflammatory response induced by the inoculation of Ehrlich tumor cells (EAT) into the peritoneal cavity of mice. It was found that after inoculation of 10(3) EAT cells, the number of peritoneal leukocytes remained unchanged till the sixth day. Subsequently, the number of cells increased as a consequence of tumor growth. EAT cells did not induce influx of PMN leukocytes till six days after tumor implantation, but a significant influx was observed on the tenth day. Inoculation of the tumor cells did not induce production of H2O2 by peritoneal cells at any time examined and induced low levels of macrophage spreading only until the third day after tumor implantation but not later on. The levels of thromboxane in the peritoneal cavity were not affected by the presence of the tumor, whereas prostaglandin E2 levels were significantly increased at all times examined. The biological significance of these results on the evolution and escape of the tumor from host defense mechanisms is under investigation.

Animals↗

PubMed2004

Neuroradiology of multiple sclerosis in children.

Neuroimaging features of multiple sclerosis in children can differ from the usual adult pattern. Frequently, lesions can be more larger and pseudo-tumoral with a variable evolution. The most critical differential diagnosis in childhood is with acute disseminated encephalomyelitis that is a relatively frequent acquired inflammatory disease of the white matter with a polymorphous appearance. Some differences between multiple sclerosis and acute disseminated encephalomyelitis in children such as distribution of white matter lesions and frequency of gray matter involvement should be pointed out. Neveretheless only follow-up examination can make the definitive diagnosis in the majority of the cases.

Brain↗

PubMed1997

The genetic basis of head and neck carcinoma.

Research over the past few years has pointed to a genetic basis for numerous cancers. Efforts in this regard are ongoing in squamous carcinoma of the head and neck. Today surgeons and residents in training need to stay up to date on molecular biology and the genetic sequences that are necessary to form a malignancy. In addition, these changes offer diagnosticians and therapists novel ways both to diagnose and treat malignancies. An evolution in molecular genetics, tumor virology, and tumor biology has led to our understanding of how malignancies arise. There are two pathways of cancer production: the activation of an oncogene or the mutation of a tumor suppressor gene. This review discusses the interaction of these genetic changes in the development of squamous carcinoma of the head and neck, their relationship to tobacco and alcohol use, as well as methods to detect the presence of malignancy and novel techniques that may be used to treat malignancies in the future.

Alcohol Drinking↗

PubMed1984

Changing times in surgical management of bronchopulmonary carcinoid tumor.

The bronchopulmonary carcinoid tumor occurs at all levels from trachea to lung periphery. It should be managed by conservatism in airway or lung resection. The long-term survival is excellent: 82% at 10 years in this series of 111 resected patients. The atypical carcinoid tumor (10% of this series) has a more ominous prognosis and requires special surgical attention. Six conceptual changes in the evolution of management of the tumor are presented (the "changing times").

Adolescent↗

PubMed1979

Computed tomography in evolution of testicular cancer during intensive chemotherapy.

The evolution of malignant testicular tumor to mature teratoma has been studied in 4 patients. Computed tomography has been helpful in early diagnosis of this biologic phenomenon in these patients receiving intensive chemotherapy for disseminated non-seminomatous testicular cancer. Although the potential significance of this conversion in terms of survival is not known its early recognition by computed tomography has been useful in selecting and monitoring the therapy of these patients.

Adolescent↗

PubMed2002

Isolated cardiac recurrence of acute lymphoblastic leukemia characterized by t(11;19) two years after unrelated allogeneic bone marrow transplantation.

A 33-year-old male presented with acute lymphoblastic leukemia (ALL) characterized by translocation (11;19)(q23;p13.3). He received an allogeneic bone marrow transplant from a matched unrelated donor. Two years later his disease relapsed with an isolated intracardiac mass, presenting as right heart failure. He had no evidence of concomitant relapse in the bone marrow. Tumor cytogenetics revealed clonal evolution with the karyotype 46,XY,t(3;16)(q23;p13),t(11;19)(q23;p13.3), the chromosome 16 breakpoint involving the band where the genes for multidrug resistance-associated protein and CREB binding protein are known to reside. To our knowledge, this is the first report of an isolated extramedullary relapse of ALL in the heart.

Adult↗

PubMed2003

[Osseous lithiasis: an unusual condition].

Bone lithiasis is an uncommon disease unfrequent reported in the literature. Its origin is supported on urothelium and conjuctive tissue bone metaplasia. High suspicious index is needed to establish its diagnosis; where radiological signs and extracorporeal lithotripsy resistence drive to these uncommon entity. Definitive diagnosis is based on histological exam. We report a 49-year-old patient with left obstructive uropathy due to a high ureteral lumbar lithiasis who precised ureterolithectomy and partial ureterectomy after extracorporeal litotripsy failure. Histological exam confirmed bone lithiasis and squamous metaplasia. Epidemiologic, diagnostic and therapeutic aspects are briefly reviewed in literature. Bone calculus treatment includes lithectomy and urothelium resection to avoid posterior recurrence. Possible association to tumoral transformation suggests close evolutive follow-up.

Humans↗

PubMed2002

Sequencing surgery, radiotherapy and chemotherapy: insights from a mathematical analysis.

We present results from a mathematical analysis that is aimed at finding the best way to sequence the three traditional cancer treatments: surgery (S), chemotherapy (C), and radiotherapy (R). The mathematical model tracks the temporal evolution of the primary tumor and its associated metastases, and incorporates the primary tumor's effect on the dormancy and growth of the metastases. We show that the SCR schedule (i.e., surgery followed by chemotherapy followed by radiotherapy) achieves a higher cure probability than SRC if the primary tumor is sufficiently large or if the metastatic population is sufficiently large relative to the primary tumor. We also show that a novel schedule, SRCR, which splits the radiotherapy regimen into two disjoint portions, is optimal among all schedules, provided that the patient's dormant metastatic tumors do not become vascularized within about 40 days after surgery.

Breast Neoplasms↗

PubMed2001

The evolution of diverse biological responses to DNA damage: insights from yeast and p53.

The cellular response to ionizing radiation provides a conceptual framework for understanding how a yeast checkpoint system, designed to make binary decisions between arrest and cycling, evolved in a way as to allow reversible arrest, senescence or apoptosis in mammals. We propose that the diversity of responses to ionizing radiation in mammalian cells is possible because of the addition of a new regulatory control module involving the tumour-suppressor gene p53. We review the complex mechanisms controlling p53 activity and discuss how the p53 regulatory module enables cells to grow, arrest or die by integrating DNA damage checkpoint signals with the response to normal mitogenic signalling and the aberrant signalling engendered by oncogene activation.

DNA Damage↗

PubMed2004

Clinical characteristics and factors predicting evolution of asymptomatic IgM monoclonal gammopathies and IgM-related disorders.

We evaluated the prognostic features of 384 asymptomatic IgM-monoclonal gammopathies (aIgM-MGs) and 74 IgM-related disorders (IgM-RDs), two clinically distinct groups as proposed by the Second International Workshop on Waldenström's Macroglobulinemia (WM). The cumulative probability of evolution to lymphoid malignancy at 5 and 10 years was 8% (95% CI, 5-13%) and 29% (95% CI, 21-38%), respectively, in aIgM-MGs; it was 9% (95% CI, 4-20%) and 16% (95% CI, 7-31%), respectively, in IgM-RDs (P=0.26). At a median follow-up of 45 months (12-233), 45 aIgM-MGs (11.7%) evolved to symptomatic WM (n=41), non-Hodgkin's lymphoma (NHL) (n=2), IgM multiple myeloma (n=1), and primary amyloidosis (n=1). At a median follow-up of 60 months (13-195), seven IgM-RDs (9.5%) evolved to symptomatic WM (n=6), and B-chronic lymphocytic leukaemia (n=1). At univariate analysis, in aIgM-MGs bone marrow lymphoplasmacytic infiltration, high erythrocyte sedimentation rate (ESR), haemoglobin level, IgM size, and lymphocytosis significantly correlated with evolution probability. At multivariate analysis, the latter two parameters strongly correlated with prognosis, haemoglobin being associated with a trend for a higher progression risk. In IgM-RDs IgM size, neutropenia, lymphocytosis, detectable Bence Jones proteinuria, and high ESR were associated with evolution probability. In conclusion, asymptomatic IgM-MGs and IgM-RDs are distinct clinical entities with similar probability of transformation to lymphoid malignancy.

Adult↗

PubMed1995

Cloning, expression and chromosomal localization of the rat pancreatitis-associated protein III gene.

PAP III belongs to the family of pancreatitis-associated proteins, recently characterized as pancreatic secretory proteins structurally related to C-type lectins, and whose expression is induced during the acute phase of pancreatitis. In this paper, we describe the cloning, characterization and chromosomal localization of the rat PAP III gene. The gene was isolated from a genomic library using a PCR-based method and characterized over 2.5 kb of gene sequence and 1.7 kb of 5'-flanking sequence. The 5' end of the coding sequence was determined by primer extension of the PAP III transcript. The PAP III coding sequence spanned over six exons. We found striking similarities between PAP III and PAP I and II genes, in genomic organization as well as in promoter sequences. Moreover, the rat PAP III gene was mapped to chromosome 4 using mouse-rat hybrid cells, a localization which coincides with that of the PAP I and II genes. The three genes could therefore derive from the same ancestral gene by duplication. Expression of the PAP III gene was compared with that of PAPs I and II. Expression levels were similar in pancreas, where PAP III mRNA concentration increased within 6 h following induction of pancreatitis, reached maximal levels (> 200 times control values) at 24-48 h, and decreased thereafter. In the intestinal tract, where PAP II is not expressed, the pattern of PAP III expression was comparable with that of PAP I; fasting induced a decrease in its mRNA concentration by more than 80%, which could be reversed within 6 h upon feeding. PAP III is therefore a new member of the PAP gene family, more closely related to the PAP I gene.

Acute Disease↗

PubMed2003

The linear process of somatic evolution.

Cancer is the consequence of an unwanted evolutionary process. Cells receive mutations that alter their phenotype. Especially dangerous are those mutations that increase the net reproductive rate of cells, thereby leading to neoplasia and later to cancer. The standard models of evolutionary dynamics consider well mixed populations of individuals in symmetric positions. Here we introduce a spatially explicit, asymmetric stochastic process that captures the essential architecture of evolutionary dynamics operating within tissues of multicellular organisms. The "linear process" has the property of cancelling out selective differences among cells yet retaining the protective function of apoptosis. This design can slow down the rate of somatic evolution dramatically and therefore delay the onset of cancer.

Animals↗

PubMed2004

The evolutionarily conserved Kaposi's sarcoma-associated herpesvirus ORF57 protein interacts with REF protein and acts as an RNA export factor.

ORF57 (MTA) one of the earliest Kaposi's sarcoma-associated herpesvirus (KSHV) regulatory proteins to be expressed is essential for virus lytic replication. A counterpart is present in every herpesvirus sequenced, indicating the importance of this signature viral protein and those examined act post-transcriptionally, affecting RNA splicing and transport. In KSHV-infected cells, ORF57 protein was present in a complex with REF (Aly) and TAP (NXF1), factors involved in cellular mRNA export. The ORF57 N-terminal region interacts with REF, whereas both N- and C-terminal domains of REF interact with ORF57. The ORF57-REF interaction was direct, whereas TAP appeared to be recruited via REF. In somatic cells, ectopically expressed ORF57 protein was shown to function as a CRM1-independent nuclear mRNA export factor, promoting export of mRNAs that are poor substrates for splicing. The gamma-herpesvirus ORF57 protein, and its alpha-1 herpesvirus ICP27 counterpart both export RNA through pathways involving REF and TAP proteins, although divergence of these herpesvirus subfamilies occurred some 180-210 million years ago. The TAP-mediated cellular mRNA export pathway is CRM1-independent. However, human immunodeficiency virus type 1 Rev protein-mediated RNA export, which is CRM1-dependent, was considerably inhibited by ORF57, suggesting that Rev and ORF57 compete for a common export component. These data strengthen arguments that TAP and CRM1 pathways converge in accessing similar components of the nuclear pore complex. We propose that ORF57-mediated RNA export may use different export factors to accommodate the KSHV-infected host cell environments, for example, in B-cells or endothelial cells and during the different phases of lytic virus replication.

Active Transport, Cell Nucleus↗

PubMed1991

Replication.

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Biological Evolution↗

PubMed1998

PTEN (MMAC1) mutations are frequent in primary glioblastomas (de novo) but not in secondary glioblastomas.

Loss of heterozygosity (LOH) on chromosome 10 is the most frequent genetic alteration associated with the evolution of malignant astrocytic tumors and it may involve several loci. The tumor suppressor gene PTEN (MMAC1) on chromosome 10q23 is mutated in approximately 30% of glioblastomas (WHO Grade IV). In this study, we assessed the frequency of PTEN mutations in primary glioblastomas, which developed clinically de novo, and in secondary glioblastomas, which evolved from low-grade (WHO Grade II) or anaplastic astrocytomas (WHO Grade III). Nine of 28 (32%) primary glioblastomas contained a PTEN mutation and an additional case showed a homozygous PTEN deletion. This indicates that after overexpression/amplification of the EGF receptor, loss of PTEN function is the most common alteration in primary glioblastomas. In this series, 5 of 28 (18%) primary glioblastomas showed both a PTEN mutation and EGFR amplification. In contrast, only 1 of 25 (4%) secondary glioblastomas contained a PTEN mutation, and none of them showed a homozygous PTEN deletion. The secondary glioblastoma with a PTEN mutation developed from an anaplastic astrocytoma that already carried the mutation. The observation that secondary glioblastomas have a p53 mutation as a genetic hallmark but rarely contain a PTEN mutation supports the concept that primary and secondary glioblastomas develop differently on a genetic level.

Adult↗

PubMedDate not supplied

The practicability of FIGO 2000 staging for gestational trophoblastic neoplasia.

The FIGO 2000 gestational trophoblastic neoplasia (GTN) staging and classification has recommended three major changes in the management of GTN. The criteria for diagnosis of GTN following molar pregnancy were defined. The methods used for investigation of spread of the disease were recommended. A major change in the concept of FIGO staging in adding risk scoring to anatomical staging is novel but considered essential to best reflect the behavior of this disease which is different from other solid tumors. The history of evolution of this staging and classification system and practical points in applying this system were discussed. If this system would be used worldwide, it would be a big leap in the management of GTN where results can be compared among different centers and large multicenter trials would be possible.

Adult↗

PubMedDate not supplied

Evolution of treatment of high-risk metastatic gestational trophoblastic tumors: Ain Shams University experience.

The aim of the current study is to evaluate the different treatment modalities used in the management of high-risk metastatic gestational trophoblastic tumors (GTT) between June 1992 and December 2004 at the Gynecologic Oncology Unit, Ain Shams University. Out of 261 patients diagnosed and treated for GTT, 70 (26.8%) were high risk metastatic patients based on the National Institutes of Health clinical classification. The mean age was 29.39 +/- 9.38 years (16-55 years), with six patients (8.6%) being older than 39 years, and the mean duration of follow-up was 79.74 +/- 40.44 months (6-157 months). Forty patients (57.14%) were diagnosed after molar pregnancy, 22 (31.43%) after abortion, and 8 (11.43%) after term pregnancy. Forty-two patients (60%) were diagnosed within 4 months of the occurrence of the disease, and 28 (40%) were diagnosed after more than 4 months. Sixty-seven patients were treated using different regimens according to the protocol of treatment at that time. The MAC regimen was used initially but has been subsequently abandoned in favor of EMA-CO (etoposide, methotrexate, dactinomycin, cyclophosphamide, and vincristine [Oncovin]) regimen, which was later modified by omitting the CO arm to decrease its toxicity. If resistance developed, platinum-based therapy was given in the form of EMA-EP. Recently, our unit incorporated paclitaxel in the third-line treatment. Surgical intervention was used selectively. Fifty-seven (81.4%) patients could be cured; 43 by initial chemotherapy, with a mean of 7 +/- 0.46 courses (6-15), and 14 were salvaged by second- or third-line chemotherapy. Fourteen patients (20%) died during the study period; one was unrelated to GTT, while three died of acute respiratory distress syndrome before instituting proper therapy and two died of treatment complications. Using univariate and multivariate Cox regression analyses, the presence of brain and/or liver metastases was found to be the worst prognostic variable affecting the survival, followed by resistance to combination chemotherapy and then the type of antecedent pregnancy. The projected 5-year survival as estimated by Kaplan-Meier method was 78%.

Adolescent↗

PubMed2005

Absence of p16 and p27 gene rearrangements and mutations in de novo myelodysplastic syndromes.

Myelodysplastic syndromes (MDS) represent a group of clonal hematopoietic disorders characterized by dyshemopoiesis and frequent evolution to acute leukemia. Tumor suppressor gene inactivation may be involved in MDS pathogenesis. The two families of cyclin-dependent kinase inhibitors (CDKIs) (INK4 family of p15, p16, p18 and p19 and CIP/KIP family of p21, p27 and p57) that negatively regulate cell cycle progression are known tumor suppressor genes. To determine whether genetic alterations of p16 and p27 genes play an important role in MDS pathogenesis, we examined DNA from 51 patients classified as 17 refractory anemias (RA), four refractory anemias with ringed sideroblasts (RARS), 19 refractory anemias with an excess of blasts (RAEB), 5 refractory anemias with excess of blasts in transformation (RAEB-t) and 6 chronic myelomonocytic leukemias (CMML). Southern blot analysis detected no homozygous deletions of p16 and p27. Polymerase chain reaction-single-strand conformation polymorphism (PCR-SSCP) and sequencing did not reveal point mutations for both genes with the exception of two allelic polymorphisms, namely a C --> G transition at 447 bp of p16exon3 and a T --> A transition at 791 bp of p27exon1 genes. Our results suggest that mutations of p16 and p27 genes resulting in abnormal p16 and p27 proteins do not represent a mechanism of gene inactivation involved in the pathogenesis of MDS.

Base Sequence↗