[Study of a rare tumor of the tongue; basal cell epithelioma with cylindroma-like evolution].
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Carcinoma, Adenoid Cystic↗
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Results for “tumor evolution”
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[Contribution to the knowledge of tumors of the mesentery. (A case of fibroblastic sarcoma of pseudocystic evolution fistulized into the small intestine)].
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Fibrosarcoma↗
[Evolution and complications in a case of chylothorax caused by a tumor (lacking radiologic manifestation)].
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Adenocarcinoma↗
Evolution of cell-mediated immunity in mice bearing an antigenic tumor. Influence of tumor growth and surgical removal.
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Animals↗
Surgical treatment of malignant secondary tumors of the humerus: report of 45 cases.
Data from a series of 45 internal fixations for malignant secondary tumors of the humerus are analyzed. The tumors occurred late in the evolution of the cancer, and represented 24% of appendicular bone metastases for which operations were performed. Statistics of the patients, fractures, treatment, and results are presented and conclusions drawn. Prognosis should be related to the types of primary tumor. Blind nailing or pinning is recommended, and indications for preventive osteosynthesis are discussed.
Adult↗
Analytic modeling of breast elastography.
The elastic moduli of tumors change during their pathological evolution. Elastographic imaging has potential for detecting and characterizing cancers by mapping the stiffness distribution in tissues. In this paper a micromechanics-based analytical method was developed to detect the location, size, and elastic modulus of a tumor mass embedded in a symmetric two-dimensional breast tissue. A closed-form solution for the strain elastograms (forward problem) was derived. A computational algorithm for the inverse problem was developed for the detection, localization, and characterization of a heterogeneous mass embedded in a breast tissue. Numerical examples were presented to evaluate the proposed method's performance. The detectability of a tumor mass was estimated with respect to lesion location, size, and modulus contrast ratio. It was shown that the micromechanics theory provides a powerful tool for the diagnosis of breast cancer.
Absorptiometry, Photon↗
Stromal cell heterogeneity in fibroblast growth factor-mediated stromal-epithelial cell cross-talk in premalignant prostate tumors.
Homeostasis of normal prostate and two-compartment nonmalignant prostate tumors is dependent on two-way communication between epithelial and stromal compartments. Independence of epithelial cells on controlling instructions from stroma is a hallmark of extremely malignant epithelial cell tumors. To better understand the evolution of stromal independence during malignant progression, we performed a clonal analysis of stromal cells derived from a well-defined model of two-way stromal-epithelial cell communication that loses response to stroma during prostate tumor progression. Directionally specific signaling from stroma to epithelium contributes to homeostasis between the two compartments. Stromal cells were characterized in respect to expression and activity of isotypes of the fibroblast growth factor (FGF) family of ligands and receptors in addition to morphology and cytoskeletal markers. One stromal subtype (DTS1) exhibited a fibroblast-like morphology and did not display smooth muscle cell (SMC) alpha-actin. The other (DTS2) exhibited SMC alpha-actin and an SMC-like morphology in vitro. Both subtypes expressed FGF7 and equally low levels of FGFR2IIIc mRNA, whereas fibroblast growth factor receptor (FGFR) 1 predominated in DTS1 cells. DTS1 cells also expressed FGF10 and no detectable FGFR3, whereas the absence of FGF10 and presence of FGFR3 distinguished DTS2 cells. Epithelial cell-derived FGF9 bound to FGFR and stimulated growth of specifically FGFR3-positive DTS2 cells, not the FGFR3-negative DTS1 cells. These results demonstrate stromal cell heterogeneity in signal reception of FGF from epithelium. This correlated with potential heterogeneity in the response back to epithelial cells. Epithelium-dependent control of a stromal cell phenotype within a tumor may be a determinant of whether tumors remain in nonmalignant homeostasis or progress to malignancy.
Adenocarcinoma↗
[Current concepts in classification of lymphoid tissue tumors].
An analysis of the data of foreign literature and of the author's personal experiences allows a conclusion to be made concerning the evolution of views on lymphoid tissue tumors. The author proposes a classification of lymphomas, the algorithm of diagnosis of the lymphomas, describes certain clinical characteristics of different types of lymphomas.
Humans↗
Curable and non-curable malignancies: lessons from paediatric cancer.
The tremendous progress achieved in understanding the molecular basis of cancer, was unfortunately not followed by a mutual improvement in the morbidity and mortality of adult cancer. In contrast, the success rate achieved in paediatric oncology has increased significantly during the past 30 years, and more than two-thirds of the children with cancer can now be cured. p53 has been shown to have a central role on apoptosis in various cells. As apoptosis is a final common pathway for much of our anti cancer therapy, resistance to apoptosis due to a normal activity of p53 is an important mechanism of tumor resistance and treatment failure. Contrary to the findings in most adult tumors, where about 50% of the tumors lack p53 activity, the rate of p53 mutations in childhood cancer is surprisingly low. This may be the key to the much better prognosis of children with cancer. In most adult tumors, multiple genetic events, between five and seven, are usually involved. The oncogenes involved in such tumors usually represent those located upstream of the nuclear transcription factors. In most paediatric tumors, in contrast, the initiating event is the activation of nuclear transcription factors secondary to chromosomal translocations. It can be speculated that multiple events activating various components of the signal transduction machinery are needed for tumorigenesis, and hence the evolution and progression of such tumors is slow. Moreover, if the malignant cell has to accumulate multiple mutations, the chances of crippling the apoptotic mechanism are higher. Genomic instability evidenced by microsatellite variation has been found in colon, pancreas, breast, liver and ovarian adult tumors, and not in paediatric tumors. As multiple somatic mutations are needed for the initiation and progression of the common adult malignancies, inherent genomic instability can dispose to accumulation of multiple mutations. All these molecular interactions are discussed with relevance to the difference between non-curable, mostly adult tumors, and curable, mostly paediatric tumors.
Antineoplastic Agents↗
Molecular mechanisms of parathyroid hyperplasia and neoplasia.
In the past decade we have witnessed an explosion in our knowledge of the molecular bases of hyperparathyroidism. In spite of the generally benign phenotype of parathyroid tumors, several of the well-recognized mechanisms in tumor biology are applicable to parathyroid tumorigenesis. The concept of evolution of nonneoplastic endocrine hyperplasia into a true tumor is as operative for the parathyroid tissue as for any other neoplasia. The molecular mechanisms underlying parathyroid tumor development, either on the ground of tissue hyperplasia or as neoplasia "ab initio', are starting to be recognized. Oncogenes as well as tumor-suppressor genes and trophic factors appear to play a role in the process of parathyroid tissue growth. The unique opportunity of evaluating at least four distinct organs greatly contributed to the knowledge of the genetic basis of parathyroid tumor development, a field relatively undeveloped in comparison to that of other cancers.
Calcium↗
[Chordoma of the mobile spine. Report of 9 cases. Review of the literature].
The authors reported 9 cases of chordomas of the mobile spine: 6 lumbars and 3 cervicals. There are 5 men and 4 women. Mean age at diagnosis is 60 years old. Mean delay between the first clinical manifestations and the diagnosis is 22 months. Clinical findings are not specific. Roentgenologic findings show 2 typicals aspects: a lytic lesion on the lateral side of the vertebrae frequently involving more than one cervical vertebrae, a mixed lesion (lytic and sclerotic) or only sclerotic was detected only at the lumbar spine. Magnetic resonance imaging and computed tomography are the most useful investigations to determine the local extension of the tumor. Certitude of the diagnosis is always microscopic. Evolution is difficult to precise in this kind of embryological tumor. Radical surgery at the earliest time is the best guarantee of a better prognosis which still remain severe.
Adult↗
Intratumoral patterns of clonal evolution in meningiomas as defined by multicolor interphase fluorescence in situ hybridization (FISH): is there a relationship between histopathologically benign and atypical/anaplastic lesions?
Meningiomas are cytogenetically heterogeneous tumors in which chromosome gains and losses frequently occur. Based on the intertumoral cytogenetic heterogeneity of meningiomas, hypothetical models of clonal evolution have been proposed in these tumors which have never been confirmed at the intratumoral cell level. The aim of this study was to establish the intratumoral patterns of clonal evolution associated with chromosomal instability in individual patients as a way to establish tumor progression pathways in meningiomas and their relationship with tumor histopathology and behavior. A total of 125 meningioma patients were analyzed at diagnosis. In all cases, multicolor interphase fluorescence in situ hybridization (iFISH) studies were performed on fresh tumor samples for the detection of quantitative abnormalities for 11 different chromosomes. In addition, overall tumor cell DNA content was measured in parallel by flow cytometry. iFISH studies were also performed in parallel on tissue sections in a subset of 30 patients. FISH studies showed that 56 (45%) of the 125 cases analyzed had a single tumor cell clone, all these cases corresponding to histologically benign grade I tumors. In the remaining cases (55%) more than one tumor cell clone was identified: two in 45 cases (36%), three in 19 (15%), and four or more clones in five cases (4%). Overall, flow cytometric analysis of cell DNA contents showed the presence of DNA aneuploidy in 44 of these cases (35%), 30% corresponding to DNA hyperdiploid and 5% to hypodiploid cases; from the DNA aneuploid cases, 35 (28%) showed two clones and 9 (7%) had three or more clones. A high degree of correlation (r >/= 0.89; P < 0.001) was found between FISH and flow cytometry as regards the overall quantitative DNA changes detected with both techniques, the former being more sensitive. Among the cases with chromosome abnormalities, the earliest tumor cell clone observed was frequently characterized by the loss of one or more chromosomes (64% of all meningiomas); loss of either a single chromosome 22 or, less frequently, of a sex chromosome (X or Y) and del (1p) was commonly found as the single initial cytogenetic aberration (30%, 5%, and 5% of the cases, respectively). Interestingly, an isolated loss of chromosome 22 was only found as the initial abnormality in one out of 14 atypical/anaplastic meningiomas, while the same cytogenetic pattern was present in the ancestral tumor cell clone of 32% of the benign tumors. Cytogenetic patterns based on chromosome gains were found in the ancestral tumor cell clone in 4% of the patients, 2% corresponding to tetraploid tumors. Overall, cytogenetic evolution of the earliest tumor cell clones was frequently associated with tetraploidization (31%). Our results show that meningiomas are genetically heterogeneous tumors that display different patterns of numerical chromosome changes, with the presence of more than one tumor cell clone detected in almost half of the cases including all atypical/anaplastic cases. Interestingly, the pathways of intratumoral clonal evolution observed in the benign tumors were different from those observed in atypical/anaplastic meningiomas, suggesting that the latter tumors might not always represent a more advanced stage of histologically benign meningiomas.
Adolescent↗
The molecular biology of esophageal and gastric cancer and their precursors: oncogenes, tumor suppressor genes, and growth factors.
The evolution of sequential histological changes from normal cells through invasive cancer affords the cancer biologist the opportunity to identify separate molecular steps involved in cancer progression. As one studies the development of human carcinoma, it becomes apparent that multiple genetic alterations affecting both cellular proto-oncogenes and tumor suppressor genes are involved during the development and progression of both esophageal and gastric cancers. The different histological forms of both esophageal and gastric carcinomas as well as their differing etiologies result in the possibility that a spectrum of genetic changes is involved in different tumor types. p53 abnormalities occur frequently in tumors arising in both organs, and in both sites p53 abnormalities can be observed in precancerous lesions as well as in overt cancer. Subsequent abnormalities affecting other genes (eg, epithelial growth factor receptors [EGFRs]) potentially enhance the growth potential of tumors. This review focuses on abnormalities of oncogenes, tumor suppressor genes, and growth factors commonly found in cancers of the esophagus and stomach.
Carcinoma, Squamous Cell↗
Evolution of outcomes in cranial base surgery.
Cranial base surgery is a young field of head and neck and neuro-oncology. It deals with solid tumors at the skull base which were not previously treated with surgery. The development of new cranial base approaches incorporating intracranial exposure and new reconstructive techniques now enable an "en bloc" resection of most of these difficult tumors. In order to analyze the evolution of cranial base surgery and its contribution to the treatment of carcinomas and sarcomas, we reviewed the results reported in the literature over the past 40 years. We have designated three periods of time that reflect the advances and impact of skull base surgery and have summarized the outcomes of the major contributors in each era. The pioneers of the first period (1960s-1970s) achieved 3- and 5-year survivals of 52 and 49% while attempting resection of tumors without intracranial or pytergopalatine extension. In the second period (1970s-1980s), improved surgical techniques allowed resection of more extensive tumors, including intracranial invasion, and 3-year survivals rose to 57-59% with limited reports of 5-year survivals in the range of 49%. The third period of cranial base surgery (1980s-1990s) brought further refinement of techniques, introduced the concept of a coordinated multispecialty approach, and resulted in increased 5-year survivals to 56-70%.
Brain Neoplasms↗
Clonal evolution demonstrated by flow cytometric DNA analysis of a human colonic carcinoma grown in nude mice.
A spontaneous change in DNA content of a human colonic carcinoma grown in nude mice was observed fortuitously. The tumor initially had a G1 cell DNA content of 1.3 times that of normal cells. Flow cytometric DNA analysis showed in transplant generation 56 the appearance of a new subpopulation which in three passages completely overgrew the original population. The DNA content of the new subpopulation was twice that of the original population. The observation supports the hypothesis of clonal evolution of tumor cell populations. The growth rates of the tumor before and after the change showed no significant difference (p greater than 0.05). Cell kinetic factors, therefore, offer no obvious explanation of how the overgrowth took place. It is not known whether the original population disappeared completely or survived as a small population below the detection limit. The heterogeneity created by clonal evolution of a tumor would be less pronounced if old subpopulations often become extinct as new ones emerge. Heterogeneity of human tumors is of clinical importance because the individual subpopulations may have different sensitivity patterns to antineoplastic drugs.
Animals↗
Tenascin-C aptamers are generated using tumor cells and purified protein.
Tenascin-C (TN-C) is an extracellular matrix protein that is overexpressed during tissue remodeling processes, including tumor growth. To identify an aptamer for testing as a tumor-selective ligand, SELEX (systematic evolution of ligands by exponential enrichment) procedures were performed using both TN-C and TN-C-expressing U251 glioblastoma cells. The different selection techniques yielded TN-C aptamers that are related in sequence. In addition, a crossover procedure that switched from tumor cell to purified protein selections was effective in isolating two high-affinity TN-C aptamers. When targeting tumor cells in vitro, the observed propensity of naive oligonucleotide pools to evolve TN-C aptamers may be due to the abundance of this protein. In vivo, TN-C abundance may also be well suited for aptamer accumulation in the tumor milieu. A size-minimized and nuclease-stabilized aptamer, TTA1, binds to the fibrinogen-like domain of TN-C with an equilibrium dissociation constant (K(d)) of 5 x 10(-9) m. At 13 kDa, this aptamer is intermediate in size between peptides and single chain antibody fragments, both of which are superior to antibodies for tumor targeting because of their smaller size. TTA1 defines a new class of ligands that are intended for targeted delivery of radioisotopes or chemical agents to diseased tissues.
Animals↗
[Presentation of 6 cases of cystadenocarcinoma of the pancreas].
Cystadenocarcinomas represent approximately 1% of the pancreatic tumors and are difficult to diagnose clinically and by pathology. Due to their rarity, published series are small. We present 6 cases of pancreatic cystadenocarcinoma collected over a period of 15 years at the Visceral Surgery Service of the Valencia University Hospital. The better evolution and prognosis of these tumors in comparison with pancreatic adenocarcinomas is noteworthy.
Adult↗
Genetic evolution in the metastatic progression of human pancreatic cancer studied by CGH.
Metastases are thought to be derived from emerging clones within primary tumors. Although the concept of the clonal evolution of cancer is well defined, the genetic grounds and significance of this process in human cancer progression are still poorly understood. To gain insight into the genetic basis and clonal evolution underlying the metastatic progression of human pancreatic cancer in vivo, we analyzed by comparative genomic hybridization (CGH) chromosomal imbalances in seven metastases originated in nude mice and their three corresponding orthotopically xenografted human pancreatic tumors. All metastases were found to be closely related to the corresponding orthotopic implant, adding many additional changes to the already altered copy number profile of the pancreatic tumors. Recurrent metastasis-specific alterations included gains at 16cen-q22 and 17q21-qter. CGH results from paired specimens strongly suggest that the majority of additional genetic alterations present in metastases are likely to be present in subclones in the primary tumor.
Animals↗