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At least 577 records · Page 32Linked to original sources
PubMed2002

Early development of cancer chemoprevention clinical trials: studies of dietary calcium as a chemopreventive agent for human subjects.

Early cancer chemoprevention clinical trials in human subjects had to be carried out with large numbers of subjects studied for long durations, measuring cancer as an end point. However new findings on abnormal epithelial cell growth and development during the multistage evolution of colonic tumors made it possible to carry out chemoprevention clinical trials in several stages, with fewer subjects studied for shorter durations, thus enabling investigators to analyze increasing numbers of chemopreventive agents and nutritional regimens in clinical trials. Supplemental dietary calcium was the first candidate chemopreventive agent studied in this multistage approach in human subjects, as a putative agent for colon cancer prevention. Early- and late-stage intermediate biomarker studies in humans have strongly suggested utility for supplemental dietary calcium to inhibit the development of benign and subsequent malignant colonic neoplasms. Preclinical experimental studies have further demonstrated the ability of increased dietary calcium to inhibit the evolution of colonic tumors when they were induced by targeted mutations, dietary factors, and particularly when given over a long duration of lifespan.

Anticarcinogenic Agents↗
PubMed1999

[Usefulness of P53 oncoprotein in urinary wash cytology: experience in patients with superficial bladder carcinoma].

OBJECTIVES: 1) To determine p53 expression in urinary wash cytology by immunohistochemistry in patients with superficial transitional cell carcinoma of the bladder and controls; 2) to correlate p53 in urinary wash cytology and anatomopathological characteristics of the bladder tumors analyzed; 3) to determine the utility of p53 expression in urinary wash cytology as a prognostic factor; and 4) to identify a subgroup of patients with superficial tumors of worse prognosis in order to improve control of the evolution of the tumor and treatment. METHODS: From 1993 to 1998, 141 cases were studied; 32 controls comprised group I and 109 (38 primary and 71 recurrence) patients with transitional cell carcinoma of the urinary bladder comprised group II. RESULTS: In group II, 29.5% were positive for p53 in urinary wash cytology, while no positive cases were found in group I. A total of 104 valid data were analyzed, which showed a higher percentage of p53-positive cases in grade III tumors (44.4%). Statistical analysis showed the percentage of p53-positive cases increased with tumor grade in a linear trend (p = 0.17). The recurrence rate in the p53-positive was 20% greater than in the p53-negative cases. Tumor progression was three times higher in the p53-positive than in the p53-negative patients. CONCLUSIONS: The application of biomolecular knowledge to cytology is a useful complement in follow-up of patients with superficial transitional cell carcinoma of the bladder and offers additional parameters to distinguish benign and malignant cells. Immunohistochemical determination of p53 in urinary wash cytology identifies patients with superficial tumors with a worse prognosis.

Adult↗
PubMedDate not supplied

[An unusual case of multiple endocrine neoplasia].

The patient A.M., woman, presented Multiple Endocrine Neoplasia, associating hyperparathyroidism, an adrenal tumor and pancreatic tumor; one can observe that the disease had features of Multiple Endocrine Neoplasia type-1 (pancreatic tumor), as well as Multiple Endocrine Neoplasia type-2 (MEN-2, pheochromocytoma), while the hyperparathyroidism is common for both two types of the syndrome. The development of the disease is extended over approximate forty years of life and finally led to death. The first symptoms appeared during pregnancy, at age 26, when the severe hyperparathyroidism determined bone mass acute loose, with decrease in height by affecting columnary vertebrae, severe bone pain due to bone resorption and soon after symptoms of renal stone disease. The patient suffered two surgical interventions for renal lithiasis. The biliary symptoms required also the surgical removal of the gall bladder, putting the diagnosis of active metabolic stone disease. At age 56, was established the diagnosis of carcinoma of the adrenal cortex, which was solved with surgical therapy. At age 66, digestive symptoms suggested the presence of a carcinoid tumor. Abdominal ultrasonography revealed a well-lined pancreatic tumor of 2-3 centimeters in diameter, probably adenoma. The malignant evolution of this tumor was rapid, leading to death in less than two years. The constant refuse of other investigations, by the patient, made us incapable to determine the type of secretion of the pancreatic tumor; we rather suspected a VIPoma, because of the watery diarrhea and severe weight loss. The most difficult to treat was anyway the hyperparathyroidism and its complications.

Adult↗
PubMed1990

Cytogenetic and molecular approaches of polyploidization in colorectal adenocarcinomas.

We present the cytogenetic analysis of 23 cases of polyploid colorectal adenocarcinomas. We took advantage of the high intratumoral heterogeneity of the karyotypes to identify clones, subclones, and cell-to-cell variations. This allowed us to reconstruct the chromosomal evolution of each tumor and to propose a schema of the chromosomal changes in relation to the endoreduplication process. All but one case were characterized by a relative deficiency of chromosomes 17p and 18. Other deficiencies affecting the late-replicating X, and to a lesser degree, 1p, 5q, 14, 15, 8p, 10, 21, and 4, and excesses affecting the early-replicating X, 8q, 13, 16, 17q, and 11 were frequently associated. This pattern of imbalances is very similar to that of the monosomic type previously described in near-diploid tumors. The pattern of the 23rd tumor corresponded to those of the trisomic type tumors. These data largely confirm the existence of two distinct processes of chromosomal evolution in colorectal adenocarcinomas, with a strong tendency to undergo endoreduplication for the monosomic type near-diploid tumors. To correlate cytogenetic and molecular data, allelic losses analyses were investigated for probes of chromosomes 17p and 18. In all 12 informative tumors, a loss of heterozygosity for probes of the short arm of chromosome 17 indicated the occurrence of a rearrangement of chromosome 17 before the endoreduplication. The same was true for allelic losses for probes of chromosome 18 found in 11 of 12 informative tumors. The correlation between cytogenetic and molecular data is thus excellent and indicates that losses of 17p and 18 are early events in the tumor process.

Adenocarcinoma↗
PubMed2004

Pretumor progression: clonal evolution of human stem cell populations.

Multistep carcinogenesis through sequential cycles of mutation and clonal succession is usually described as tumor progression, or the clonal evolution of tumor cell populations. However, many mutations found in cancers are also compatible with normal appearing phenotypes and therefore genetic progression may precede tumor progression. To better characterize such pretumor progression (mutations in the absence of visible phenotypic changes), a quantitative model was developed that postulates most oncogenic cancer mutations first accumulate in normal appearing colon crypt niche stem cells. Each crypt contains multiple stem cells, and random niche stem cell loss with replacement eventually leads to the loss of all stem cell lineages except one. This niche succession or crypt clonal evolution is similar to the clonal succession of tumor progression except it does not require selection or change visible phenotype. Mutations may sequentially accumulate during stem cell clonal evolution either through drift (passenger mutations) or selection. To determine the feasibility of pretumor progression, mutation rates sufficient to recreate the epidemiology of colorectal cancer were estimated. Pretumor progression may completely substitute for visible tumor progression because it is theoretically possible for all cancer mutations to first accumulate in normal appearing colon with normal replication fidelity. Elevated mutation rates or tumorigenesis may be unnecessary for early progression.

Adult↗
PubMed1995

Allelic loss in squamous cell carcinomas of the larynx: discordance between primary and metastatic tumors.

The mutational inactivation of suppressor genes, a process required for cancer progression, generates new genetic subclones within a tumor. The allelic losses that frequently unmask these mutations serve not only as markers of the chromosomal locations of these genes but also as clonal fingerprints of the shifting relationships between these genetically heterogeneous cell populations. The rise of the metastasis-competent subclone to dominance within the primary tumor should be reflected in the similarity of the genetic fingerprints of the primary tumor and its resultant metastases. We have tested this hypothesis by comparing the patterns of allelic loss of individual primary laryngeal squamous cell carcinomas and their resultant cervical lymph node metastases at 16 different genetically polymorphic loci on 15 chromosome arms. Although primary tumors and metastases both frequently lose heterozygosity on the same chromosome arms (3p, 9p, 9q, 13q, and 17p), five of the 12 metastases differed from their primary tumors at one or two of the loci examined. Discordance between the two tumor cell populations from the same patient is suggestive of either subclone heterogeneity within the primary tumor at the time of establishment of the metastasis or further clonal evolution of both tumors after metastasis.

Alleles↗
PubMed1989

[hCG and its subunits as tumor markers].

hCG is known to be produced by trophoblastic cells as well as by many normal tissues and malignancies. hCG is considered as a reliable marker for gonadal and extra gonadal choriocarcinomas; moreover it has been evidenced by immunohistochemical techniques in other malignancies. In this study, hCG and/or its alpha and beta subunits were detected in 73 males. Intact hCG was detected in 48 patients with gonadal tumors (n = 37) or extragonadal malignancies (n = 11), with or without free alpha or beta subunits. In the other 25 patients, native hCG was not detected but there were significant amounts of free beta subunit in 8 germ cells tumors and 17 extragonadal tumors. The production of free beta chains is correlated with a severe evolution in extragonadal tumors. hCG should be considered as a good marker for many tumors, but it is absolutely necessary to evaluate intact hCG as well as free beta chains.

Biomarkers, Tumor↗
PubMed1993

Multistep evolution of B-cell-derived tumors in humans and rodents.

At least three genetic changes are known to contribute to the genesis of Burkitt's lymphoma (BL): the Ig/myc translocation, the presence of Epstein-Barr virus (EBV) in the vast majority of the endemic and a minority of sporadic tumors, and a p53 mutation, present in approximately 60% of the BL-derived lines. Activation of c-myc by juxtaposition to Ig sequences is a universal common denominator in endemic and sporadic EBV positive and negative BLs. It acts by preventing the cell from leaving the cycling compartment and by facilitating immune escape. EBV probably acts by expanding the target cell population at risk and prolonging its life span. This, together with the malaria co-factor, would increase the risk of the translocation accident. The p53 mutation may be essential for the continued growth of the tumors where it occurs, since introduction of wild-type p53 leads to their apoptotic death.

Animals↗
PubMed2004

Origins and evolution of cell phenotypes in breast tumors.

This study presents a stochastic model that correlates genomic instability with tumor formation. The model describes the time- and space-variant volumetric concentrations of cancer cells of various phenotypes in a breast tumor. The cells of epithelial origin in the cancerous breast tissue are classified into four different phenotypes, normal epithelial cells and the grade 1, grade 2 and grade 3 cancer cell types with increasing potential for growth and invasion. Equations governing the time course of volumetric concentrations of cell phenotypes are derived by using the principle of conservation of mass. Cell migration into and from the stroma is taken into account. The transformations between cell phenotypes are due to genetic inheritance and chromosome aberrations. These transformations are assumed to be stochastic functions of the local cell concentration. The simulations of the model for planar geometry replicate the shapes of human breast tumors and capture the time history of tumor growth in animal models. Simulations point to transformation of tumor cell population from heterogeneous compositions to a single phenotype at advanced stages of invasive tumors. Systematic variations of model parameters in the computations indicate the important roles the migration capacity, proliferation rate, and phenotype transition probability play in tumor growth. The model developed provides realistic simulations for standard breast cancer therapies and can be used in the optimization studies of chemotherapy, radiotherapy, hormone therapy and emerging individualized therapies for cancer.

Animals↗
PubMed1999

Hemoperitoneum due to a ruptured gastric stromal tumor.

BACKGROUND/AIMS: Gastrointestinal stromal tumors form a group of uncommon neoplasms originated from pluripotential mesenchymal cells. Many patients are asymptomatic and the tumor is discovered during an abdominal operation. Massive intraperitoneal bleeding is an exceptional complication associated with high mortality rates. Our aim is to report a case of a gastric stromal tumor in an 83-year-old patient presenting with intraperitoneal hemorrhage and hypovolemic shock, successfully operated. METHODS: Emergency laparotomy showed a hemoperitoneum caused by rupture of a large exogastric tumor attached to the greater curvature. Total gastrectomy and esophagojejunostomy was performed. RESULTS: Histological examination revealed proliferation of spindle-shaped cells but immunocytochemistry failed to identify specific markers of smooth muscle and neural cells. Diagnosis of a gastric stromal tumor was made. Postoperative evolution was uncomplicated. CONCLUSION: Gastric stromal tumor is a relatively rare neoplasm of mesenchymal origin whose nature and prognosis is unclear.

Aged↗
PubMed2005

Influence of tumor location on the presentation and evolution of craniopharyngiomas.

OBJECT: This study was performed to optimize the management of craniopharyngiomas, particularly by identifying factors predicting weight changes to prevent obesity. METHODS: A series of 35 patients who had undergone surgery at a mean age of 7.4 +/- 3.7 years (standard deviation [SD]) and had been followed up until 14.9 +/- 5 years of age by the same endocrinologist were assigned to one of three groups according to their hypothalamic involvement: Group 1 (10 patients) had no involvement, Group 2 (eight patients) had compression without involvement, and Group 3 (17 patients) had severe involvement. Abnormal height and/or weight evolution indicated the craniopharyngioma in only 17% of the patients, although these elements were present at diagnosis in 85%. Before surgery, 85% of the patients lacked growth hormone, 24% lacked thyroid-stimulating hormone, 15% lacked adrenocorticotropin hormone, and 12% lacked antidiuretic hormone. All had complete hypothalamic-pituitary deficiencies after surgery. The body mass index (BMI) before surgery (mean SD 1.1 +/- 1.6) was positively correlated with BMI 1 year after surgery (mean SD 3.1 +/- 2), which correlated with the BMI at the last evaluation (mean SD 3.1 +/- 1.9; p < 0.0001 for both). Before surgery, patients in Group 3 had a greater BMI than did Group 1 (p < 0.02). The BMI of Group 1 patients did not change, but those of Groups 2 and 3 patients increased during the 1st year after surgery (p < 0.02 and p = 0.0003, respectively), with no further change. The changes occurred mainly during the first 3 months after surgery in Group 1, during the first 6 months in Group 2, and throughout the year in Group 3. CONCLUSIONS: The degree of hypothalamic involvement by the craniopharyngioma determines the presentation and predicts weight changes after surgery.

Body Height↗