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At least 685 records · Page 38Linked to original sources
PubMed1982

Endolymphatic stromal myosis. Surgical and hormonal treatment of extensive abdominal recurrence 20 years after hysterectomy.

This report describes the clinicopathologic features of a 49-year-old woman who was reoperated on for bulky abdominal metastases 20 years after hysterectomy for endometrial stromal myosis (ESM). The levels of estrogen (ER) and progesterone (PR) receptors measured in the resected tumorous tissue amounted to 48.3 and 71.4 femtomoles (fmol)/mg cytosol protein, respectively. After medroxyprogesterone acetate (Depo-Provera; Upjohn) treatment of 16 months duration, the unresected pelvic tumor mass compressing the bladder and the left ureter had decreased in volume and hydroureteronephrosis had regressed. The efficacy of the therapy was monitored by computed tomography. Two years and nine months after surgery, the evolution of the tumor seems well-controlled by continuous progestin therapy and the patient is living without symptoms.

Abdominal Neoplasms↗
PubMed1997

[Gynecomastia and Leydig cell tumor].

INTRODUCTION: Leydig cell tumors may generate estrogen production and gynecomastia. CASE PRESENTED: A 32-year man asked for medical advice due to gynecomastia. He had raised estrogen levels and diminished testosterone/estradiol index. A testicular echogram showed a nodular image in the right testis. Orchidectomy was performed and the diagnosis of a Leydig cell tumor was confirmed. The gynecomastia diminished, and estradiol remained lightly elevated, with little response to HCG. DISCUSSION: The more frequent hormonal manifestations of these tumors are high plasmatic and urinary estrogen levels, low serum testosterone, low testosterone/estradiol index, and FSH or LH low levels as well. The low response to HCG, the absence of metastasis and the good clinical evolution suggested the tumor was benign. Testicular echography is useful in the diagnosis of these tumors.

Adult↗
PubMed2006

Stochastic cancer progression driven by non-clonal chromosome aberrations.

Cancer research has previously focused on the identification of specific genes and pathways responsible for cancer initiation and progression based on the prevailing viewpoint that cancer is caused by a stepwise accumulation of genetic aberrations. This viewpoint, however, is not consistent with the clinical finding that tumors display high levels of genetic heterogeneity and distinctive karyotypes. We show that chromosomal instability primarily generates stochastic karyotypic changes leading to the random progression of cancer. This was accomplished by tracing karyotypic patterns of individual cells that contained either defective genes responsible for genome integrity or were challenged by onco-proteins or carcinogens that destabilized the genome. Analysis included the tracing of patterns of karyotypic evolution during different stages of cellular immortalization. This study revealed that non-clonal chromosomal aberrations (NCCAs) (both aneuploidy and structural aberrations) and not recurrent clonal chromosomal aberrations (CCAs) are directly linked to genomic instability and karyotypic evolution. Discovery of "transitional CCAs" during in vitro immortalization clearly demonstrates that karyotypic evolution in solid tumors is not a continuous process. NCCAs and their dynamic interplay with CCAs create infinite genomic combinations leading to clonal diversity necessary for cancer cell evolution. The karyotypic chaos observed within the cell crisis stage prior to establishment of the immortalization further supports the ultimate importance of genetic aberrations at the karyotypic or genome level. Therefore, genomic instability generated NCCAs are a key driving force in cancer progression. The dynamic relationship between NCCAs and CCAs provides a mechanism underlying chromosomal based cancer evolution and could have broad clinical applications.

Animals↗
PubMed2002

[Current findings on gastrointestinal stromal tumors: seven observations of malignant tumors].

PURPOSE: Gastrointestinal stromal tumors (GIST) are rare neoplasms, 1-3% of malignant gastrointestinal tumors. They are immature proliferations of spindled and/or epithelioid cells, developed in the muscular layer of the digestive tract, showing uncompleted or partial muscular, nervous or mixed differentiation. Immunohistologic knowledge about these tumors has recently progressed because of the discovery of specific markers (coexpression vimentin-CD117, oncogenes): GIST can now be distinguished from the other mesenchymal tumors. METHODS: Retrospective study of seven patients with GIST who received the same treatment. RESULTS: For our seven patients the mean age was 49 years with a male predominance (sex-ratio 4/3). The tumoral localisations are principally the small bowel (four cases), the rectum (two cases) and the stomach (one case). The treatment consisted of a first surgery, adapted to the tumoral localisation and extension, associated to chemotherapy in case of metastasis or local recurrence. The study of the histological grading for the seven patients showed tumors with poor prognoses. Six patients developed recurrence in a 2-year period; for the survey we are too close for a proper view. CONCLUSIONS: A review of the literature on stromal tumors finds older patients (59 years) with an equal sex ratio. Against the results of our series, the most frequent location is the stomach (50%). But the main problem is the better understanding of the particular evolution of these tumors. The bad short-date prognosis imposes carrying out larger studies, in order to confirm the principal hypothesis of histogenesis and to improve the survey by an optimal treatment.

Adult↗
PubMed2001

Systematic esophageal endoscopy screening in patients previously treated for head and neck squamous-cell carcinoma.

BACKGROUND: An attempt was made to improve metachronous oesophageal cancer prognosis through bi-annual systematic esophageal endoscopy screening in patients treated for head and neck cancer. PATIENTS AND METHODS: Bi-annual esophageal endoscopy, without a staining procedure, was performed in 1560 patients from 1987 to 1997. The distribution of previous head and neck cancer was oral cavity (20%), oropharynx (30%), hypopharynx (34%), and larynx (16%). All patients had initial panendoscopic inspection before HNSCC treatment. Esophageal tumors were considered to be second synchronous primaries when discovered within the first six months of initial tumor diagnosis. RESULTS: Fifty metachronous esophageal asymptomatic cancers (42 T1 and 7 in situ carcinomas) were diagnosed by endoscopy. The median time between the HNC and the esophageal carcinoma was 43 months (7-137 months). Metachronous esophageal carcinoma was discovered in 2.6% of patients with oral cavity tumor, 5.7% of patients with oropharynx tumor, 2.3% of patients with hypopharynx tumor, and 1.7% of patients with larynx tumor. Causes of death were: 41.1% related to esophageal tumor with tumor progression, metastatic evolution, or treatment toxicity; 28.9% related to non malignant causes; 26.6% related to a cancer that was not of esophageal origin. CONCLUSIONS: Over a 10-year period, systematic bi-annual esophageal endoscopy uncovered metachronous esophageal tumors in 3.2% of 1560 patients originally treated for head and neck carcinoma, developing in a median time of 47 months. Patients with initial oropharyngeal tumors had a significantly higher risk of metachronous esophageal SCC, compared to the other tumor sites (P < 0.02 with Fisher exact test). Given the elevated death rate not related to the esophageal cancer and the median survival of 16 months, any potential benefit from this time-consuming procedure is debatable.

Adult↗
PubMed2006

Hypermethylation and expression regulation of secreted frizzled-related protein genes in colorectal tumor.

AIM: To investigate the functions of promoter hyper-methylation of secreted frizzled-related proteins (sFRPs) genes in colorectal tumorigenesis and progression. METHODS: The promoter hypermethylation and expression of sFRP genes in 72 sporadic colorectal carcinomas, 33 adenomas, 18 aberrant crypt foci (ACF) and colorectal cancer cell lines RKO, HCT116 and SW480 were detected by methylation-specific PCR and reverse transcription PCR, respectively. RESULTS: None of the normal colorectal mucosa tissues showed methylated bands of any of four sFRP genes. sFRP1, 2, 4 and 5 were frequently methylated in colorectal carcinoma, adenoma and ACF (sFRP1 > 85%, sFRP2 > 75%, sFRP5 > 50%), and the differences between three colorectal tissues were not significant (P > 0.05). Methylation in colorectal tumors was more frequent than in normal mucosa and adjacent normal mucosa. The mRNA of sFRP1-5 genes was expressed in all normal colorectal mucosa samples. Expression of sFRP1, 2, 4 and 5 and sFRP1, 2 and 5 was downregulated in carcinoma and adenoma, respectively. The downregulation of sFRP2, 4 and 5 was more frequent in carcinoma than in adenoma. Expression of sFRP3 which promoter has no CpG island was downregulated in only a few of colorectal tumor samples (7/105). The downregulation of sFRP1, 2, 4 and 5 expression was significantly associated with promoter hypermethylation in colorectal tumor. After cells were treated by DAC/TSA combination, the silenced sFRP mRNA expression could be effectively re-expressed in colorectal cancer cell lines. CONCLUSION: Hypermethylation of sFRP genes is a common early event in the evolution of colorectal tumor, occurring frequently in ACF, which is regarded as the earliest lesion of multistage colorectal carcinogenesis. It appears to functionally silence sFRP genes expression. Methylation of sFRP1, 2 and 5 genes might serve as indicators for colorectal tumor.

Adaptor Proteins, Signal Transducing↗
PubMed1987

Complete or partial homozygosity of chromosome 13 in primary retinoblastoma.

Sixteen retinoblastomas were examined with chromosome 13 polymorphic probes to determine the frequency of homozygosity for the chromosome in the tumors. Each of the tumors had two cytogenetically normal appearing No. 13 chromosomes. Nontumorous cells from the same patients were heterozygous for the various polymorphic chromosome 13 probes used. At least partial homozygosity for a single chromosome 13 was observed in 75% of the tumors. These studies confirm and extend previous studies which suggest that homozygosity or hemizygosity at RBI occurs in the majority of retinoblastomas. We also demonstrate in an additional tumor that rapid clonal evolution from hemizygosity to homozygosity can occur in the tumor.

Cells, Cultured↗
PubMed1991

Chromosome 9 deletion mapping reveals interferon alpha and interferon beta-1 gene deletions in human glial tumors.

We have applied restriction fragment length polymorphism analysis to a 30-member panel of primary glioma DNAs, which had been previously examined for loss of genetic information (C. D. James, E. Carlbom, J. P. Dumanski, M. Hansen, M. Nordenskjold, V. P. Collins, and W. K. Cavenee, Cancer Res., 48:5546-5551, 1988), to determine the frequency and sublocalization of loss of genetic information from chromosome 9. We have also utilized scanning densitometry for dosage determination of the 9p-localized interferon alpha and interferon beta-1 genes among these same tumors. Our results reveal the following: (a) for those cases in which loss has occurred, the region of common loss lies on the short (p) arm of the chromosome; (b) loss of genetic information from the short arm of chromosome 9 occurs frequently in glial tumors of intermediate (anaplastic, grade III) and high (glioblastoma, grade IV) histological malignancy (10 of 20 cases) but not in tumors of low (grade II) histological malignancy (0 of 10 cases); (c) tumors with 9p deletions are hemi- or nullizygous for interferon beta-1 and the interferon alpha gene cluster; (d) cases of interferon nullizygosity occur exclusively among tumors of highest histological malignancy (glioblastoma). These data, especially the determination of a region of nullizygosity, suggest proximity to or residence within a gene(s) whose function(s) is (are) critical to the suppression of the malignant evolution of glial tumors.

Adolescent↗
PubMed1996

A follow-up study of determinants of second tumor and metastasis among subjects with cancer of the oral cavity, pharynx, and larynx.

We conducted a follow-up study of 380 incident cases of cancer of the oral cavity, pharynx, or larynx, who had been included in a previous case-control study. Information pertaining to potential risk factors, clinical characteristics, and evolution of the tumor (vital status, metastases, and second primary tumors) was obtained. From a multivariate proportional hazard model including terms for risk factors and clinical variables, the incidence of metachronous second primary tumors occurring in the head and neck was positively associated with employment as a farmer as opposed to white collar (hazard ratio [HR] = 3.3) and with tobacco smoking before first tumor diagnosis (HR = 4.3 for heavy versus never or very light smoker). The risk of second primary tumor decreased with increasing dietary "beta-carotene" intake (HR = 0.4 for high versus low intake in tertiles). Less differentiated first primary tumors were followed more frequently by second tumors as compared to grade 1 tumors. The incidence of metastases was not associated with etiological factors of the first tumor, but with stage.

Adult↗
PubMed2003

Genetic variability in MCF-7 sublines: evidence of rapid genomic and RNA expression profile modifications.

BACKGROUND: Both phenotypic and cytogenetic variability have been reported for clones of breast carcinoma cell lines but have not been comprehensively studied. Despite this, cell lines such as MCF-7 cells are extensively used as model systems. METHODS: In this work we documented, using CGH and RNA expression profiles, the genetic variability at the genomic and RNA expression levels of MCF-7 cells of different origins. Eight MCF-7 sublines collected from different sources were studied as well as 3 subclones isolated from one of the sublines by limit dilution. RESULTS: MCF-7 sublines showed important differences in copy number alteration (CNA) profiles. Overall numbers of events ranged from 28 to 41. Involved chromosomal regions varied greatly from a subline to another. A total of 62 chromosomal regions were affected by either gains or losses in the 11 sublines studied. We performed a phylogenetic analysis of CGH profiles using maximum parsimony in order to reconstruct the putative filiation of the 11 MCF-7 sublines. The phylogenetic tree obtained showed that the MCF-7 clade was characterized by a restricted set of 8 CNAs and that the most divergent subline occupied the position closest to the common ancestor. Expression profiles of 8 MCF-7 sublines were analyzed along with those of 19 unrelated breast cancer cell lines using home made cDNA arrays comprising 720 genes. Hierarchical clustering analysis of the expression data showed that 7/8 MCF-7 sublines were grouped forming a cluster while the remaining subline clustered with unrelated breast cancer cell lines. These data thus showed that MCF-7 sublines differed at both the genomic and phenotypic levels. CONCLUSIONS: The analysis of CGH profiles of the parent subline and its three subclones supported the heteroclonal nature of MCF-7 cells. This strongly suggested that the genetic plasticity of MCF-7 cells was related to their intrinsic capacity to generate clonal heterogeneity. We propose that MCF-7, and possibly the breast tumor it was derived from, evolved in a node like pattern, rather than according to a linear progression model. Due to their capacity to undergo rapid genetic changes MCF-7 cells could represent an interesting model for genetic evolution of breast tumors.

Breast Neoplasms↗
PubMed2003

Risk stratification in hemangiomas of infancy.

Hemangiomas of infancy are very common tumors, but they are heterogeneous in their behavior. A small, but significant, subset causes medical complications or permanent disfigurement, but due to their heterogeneity, there is no appropriate "one size fits all" approach to management. In addition, the rapid evolution of this tumor over the first weeks-to-months of infancy renders even more difficult the task of predicting which infants will have medical complications or permanent disfigurement. This article outlines the clinical characteristics that help to stratify hemangiomas into those which are high risk, and likely to require either active treatment or closer scrutiny, and those which are low risk, and likely to behave in an innocuous manner. Five major factors are emphasized: the age of the child, the location of the hemangioma(s), the total number of hemangiomas present, the hemangioma subtype, and the presence and nature of dermal involvement.

Child, Preschool↗
PubMed1984

[CT volumetry of intrathoracic space-occupying processes].

Preoperative CT volumetry was performed in 39 patients with intrathoracic neoplasms. The results are compared to postoperative volume measures of the surgical preparation. The correlation of both measuring series was very high (p = .94). The estimated influence of systematic and stochastic errors was only 10 to 15%. The authors outline the consequences for clinical practice: by means of the better quantification in the T category of the TNM system, the surgeon is in a position to make a more precise preoperative planning. The reliable numeric in vivo determination of regression and growth velocity of tumors and/or metastases allows for the first time an exact quantification of control examinations during and after radiotherapy or chemotherapy. This will possibly lead to a more precise individual prognosis. In experimental radiotherapy a more detailed description of the evolution of experimental tumors in the living animal will be possible by this procedure.

Humans↗
PubMed1996

[Molecular biology of tobacco smoke associated neoplasia].

Adducts, formed by carcinogens of tobacco smoke with DNA, can be detected by means of molecular techniques and are used as marker of internal exposure. Carcinogen-DNA adducts produce specific mutations in tumor-suppressor genes (e.g. p53) and oncogenes (e.g. ras), which can be involved in tumor initiation or in later stages of tumor progression (e.g. evolution of an invasive phenotype). Benzo(a)-pyrene, an important carcinogen of tobacco smoke, induces GT transversions, as demonstrated in in vitro systems and animal models. Mutations in the p53- or ras-gene are more common in human tumors of the lung, head and neck, bladder and pancreas in smokers than in non-smokers. Molecular biology of cancer gains increasing significance in clinical practice since 1.) the presence of certain mutations confers an unfavorable prognosis to malignant disease (e.g. ras mutations in lung cancer), 2.) ras and p53 mutations often occur early during tumor development and can thus facilitate diagnosis of malignant disease, and 3.) minimal residual disease can be detected using molecular techniques. After resection of cancer of the head and neck, tumor recurred more frequently in patients with no evidence of residual disease as assessed by pathohistologic criteria than in patients with no evidence of residual disease as evaluated by p53 immunostaining.

Carcinogens↗
PubMed1978

Meningeal seeding from rhabdomyosarcoma of the head and neck with base of the skull invasion: recognition of the clinical evolution and suggestions for management.

Rhabdomyosarcomas of the head and neck may spread by diffuse local invasion, resulting in erosion of the base of the skull with possible extension to the leptomeninges, brain, and cranial nerves, as well as invasion of the ventricular system with possible intradural, extramedullary metastases anywhere along the neuraxis. Meningeal spread of tumor is difficult to eradicate, and nearly all patients reviewed died soon after meningeal disease was evident. Patients with erosion of the base of the skull or abnormal cranial nerve findings seem to have a risk of seeding the meninges with tumor. The clinical evolution of this pattern of metastatic spread is reviewed, diagnostic studies are recommended, and therapeutic considerations are discussed. Tentative treatment guidelines are also offered.

Ataxia↗
PubMedDate not supplied

Delineation and quantitation of brain lesions by fuzzy clustering in positron emission tomography.

In this study, we investigate the application of the fuzzy clustering to the anatomical localization and quantitation of brain lesions in Positron Emission Tomography (PET) images. The method is based on the Fuzzy C-Means (FCM) algorithm. The algorithm segments the PET image data points into a given number of clusters. Each cluster is an homogeneous region of the brain (e.g. tumor). A feature vector is assigned to a cluster which has the highest membership degree. Having the label affected by the FCM algorithm to a cluster, one may easily compute the corresponding spatial localization, area and perimeter. Studies concerning the evolution of a tumor after different treatments in two patients are presented.

Algorithms↗
PubMed2004

Long term survival in a patient with recurrent malignant glioma treated with intratumoral infusion of an IL4-targeted toxin (NBI-3001).

Intratumoral infusion of a recombinant targeted toxin (NBI-3001) consisting of the receptor binding domain of human interleukin 4 (IL-4) and Pseudomonas aeruginosa exotoxin A is an investigational treatment for malignant brain tumors. This 27-year-old male patient presented with a recurrent malignant glioma WHO grade IV after surgery and adjuvant radiation and chemotherapy. The recurrence was treated with intratumoral infusion of NBI-3001 at a dose of 9 microg/ml in 66 ml of infusate. Treatment resulted in long-term survival for 3 years after toxin infusion with a durable tumor response. There were some permanent neurological side effects resulting from toxin infusion. The patient eventually died after a late local recurrence of the known brain tumor. Such clinical evolution of a malignant glioma after a single round of immunotoxin infusion is rather unusual. The late local recurrence may suggest that repeated courses rather than a single infusion of intratumoral toxin are possibly needed for successful long-term tumor control.

Adult↗
PubMed2001

Squamous carcinoma in a major salivary gland: a review of the diagnostic considerations.

CONTEXT: Squamous carcinoma in a major salivary gland has several possible sources: (1) high-grade mucoepidermoid carcinoma, (2) metastasis or direct invasion from a primary skin carcinoma, (3) metastasis from a distant primary carcinoma, or (4) a primary malignant neoplasm. The latter is conventionally regarded as a diagnosis of exclusion after a history of squamous carcinoma elsewhere has been obtained or there is a positive mucin stain. DESIGN: Eleven cases of squamous carcinoma in a major salivary gland are presented and the literature reviewed. RESULTS: Two cases, 1 metastatic from a histologically identical squamous carcinoma from the ipsilateral tonsil and 1 with in situ squamous carcinoma in a duct, demonstrated positive mucicarmine stains. Two cases were high-grade mucoepidermoid carcinomas, also with positive mucin stains. Five cases represented metastases from cutaneous squamous carcinomas. Only 2 cases were regarded as primary carcinomas. There were no histologic clues as to correct subclassification. Six patients died, 4 from their disease. Three of the 5 still alive had recurrence or metastasis. CONCLUSION: The occurrence of squamous carcinoma in a major salivary gland exhibits a histologic sameness that precludes accurate subclassification and assignation of origin. Also irrespective of tumor origin, the clinical approach to diagnosis and treatment is similar. Adjuvant therapy (eg, radical neck dissection, radiation, chemotherapy) is not uniformly applied. Most patients present with a sizable (>3-cm) mass for which total excision is attempted. The natural evolution of the tumor is aggressive, irrespective of clinical context. The traditional subclassification of squamous carcinoma in a major salivary gland may not be clinically relevant.

Aged↗
PubMed1998

Eyelid basal cell carcinoma with intracranial extension.

We describe a case of basal cell carcinoma (BCC) situated on the external upper margin of the right eyelid in a young man aged 28 years. The tumor was diagnosed as an "extended wart in a degenerative phase" and removed during reconstructive plastic surgery. No pathologic examination was performed. Seven years later, the operation was followed by a first recurrence. Pathologic examination was then performed, and the diagnosis was BCC. Therapy was with radiotherapy and chemotherapy. Subsequent recurrences were treated with radiotherapy and surgery (enucleation, exenteration of the orbit), but the evolution of the tumor was not halted. It ended 25 years after its first manifestation with the death of the patient of a hemorrhage of the upper airways during an operation, the aim of which was to reexamine the orbital cavity. The autopsy revealed intracranial extension of the tumor, and all the histological examinations confirmed the diagnosis. No histopathological feature was found that could differentiate a particularly aggressive nature of the tumor. Basal cell carcinoma is a tumor more frequently encountered in elderly patients. Its appearance in a young subject may cause grounds for suspicion, requiring initial radical surgical treatment and careful surveillance of the evolution of the lesion. This case documents the fatal consequences that may arise from the failure to recognize BCC in its first manifestation and highlights the ineffectiveness of repeated radiation and surgical therapy against continual recurrence.

Adult↗