[Changes in the histologic picture during the evolution of a skin disease regarded at first as tumorous mycosis fungoides].
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Results for “tumor evolution”
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Evolution towards hormone independence of the MXT mouse mammary tumor is associated with a gradual change in its estrogen receptor molecular polymorphism.
Using a method based on [3H]tamoxifenaziridine ([3H]TAZ) labeling, sequential immunoadsorption with anti-ER monoclonal antibodies, sodium dodecyl sulfate-polyacrylamide gel electrophoresis(SDS-PAGE) and fluorography, we observed a striking change inthe estrogen receptor (ER) electrophoresis pattern of the transplantable MXT mouse mammary tumor. Early, ER "rich" tumors (approximately 100 fmol/mg prot) displayed classical cytosolic 67 and 50 KDa bands. These bands disappeared in favor of a "cytosolic" 35 KDa band during progression towards undifferentiated ER "poor" tumors (approximately 25 fmol/mg prot). Although we can not rule out that this 35 KDa peptide results from in vivo ER proteolysis, it seems unique in view of the following: 1. It is immunoadsorbed not only by an anti-ER monoclonal antibody (H-222) directed to the hormone-binding domain, but also by an anti-ER monoclonal antibody (H-226) which interacts with an epitope in the A/B region close to the DNA-binding domain and is mainly exposed under activation conditions. 2. It does not bind [3H]estradiol([3H]E2) and a tentative to restore its [3H]E2 binding capacity with calmodulin and ATP was unsuccessful. The observation of similar approximately 35 KDa ERs in the nuclear fraction of early tumor transplants and in control uterus suggests that this peptide is already in an activated form. Structural alterations of ER and/or associated "anchorage" nuclear proteins may beat the origin of its cytosolic localization. Moreover, the fact that the addition of calmodulin and ATP to late MXT transplants cytosols fails to increase their [3H]E2 binding capacity indicates that the low ER content of these tumors does not result from a deficiency in the phosphorylation status of the receptor.
Animals↗
[Giant primitive neuroendocrine cutaneous carcinoma of the leg].
INTRODUCTION: Primitive cutaneous neuroendocrine carcinoma or Merkel cell carcinoma is a tumor characterized by rapid evolution. The size at the time of diagnosis is a mean of 2 to 3 centimeters. We report a case of a particular clinical and anatomopathological presentation. OBSERVATION: A 76 year-old woman had a voluminous tumoral plaque on the left leg with multiple ulcero-necrotic lesions involving the bone structure without palpable, inguinal lymphadenopathy. The histological and immunocytochemistry examination led to the diagnosis of cutaneous neuroendocrine carcinoma. The normality of the chest, abdominal and pelvis investigations confirmed the primitive cutaneous origin. The patient died a few months later without lymph involvement. DISCUSSION: To the best of our knowledge, such a presentation of primitive cutaneous neuroendocrine carcinoma has never been reported. The absence of lymphadenopathy despite the tumor volume and extensive skin involvement suggest the hypothesis of a non lymphophilic form of primitive cutaneous neuroendocrine carcinoma. This case report shows that lymphophily depends neither on the tumoral size nor to the degree of differentiation of tumoral cell proliferation, but on biological factors that require specification.
Aged↗
Immunologic study of carcinoma of the digestive tract. Effects of the tumor stage. I. Cellular immunity in the preoperative period.
We studied the behavior of the cellular immune system in two types of carcinoma of frequent clinical occurrence: large bowel and gastric cancers. We contrasted both types of neoplasia with respect to the behavior of cellular immunity in the preoperative period, according to the evolutive stage of the tumor. Two hundred and nine subjects were studied: 86 with gastric adenocarcinoma, 63 with adenocarcinoma of colon-rectum and 60 healthy controls. Total lymphocytes were quantitated, as were B and T cell subpopulations, and T cell function by measuring the response to PHA. Summarizing the results, a clear depression in cellular immunity was observed in stage III of gastric cancer. In large bowel cancer the repression of cellular immunity is of lesser magnitude than in gastric cancer.
Adenocarcinoma↗
The E3/19K protein of adenovirus type 2 binds to the domains of histocompatibility antigens required for CTL recognition.
The E3/19K protein of human adenovirus type 2 binds to HLA class I antigens and blocks their terminal glycosylation and cell surface expression. The nature of this interaction is non-covalent and involves neither disulfide bridges between the two molecules nor their carbohydrates. The murine H-2 Kd antigen associates with the E3/19K protein in a similar fashion to human HLA antigens whereas the allelic product H-2 Kk does not. Hybrid genes between the Kd and Kk alleles were constructed and their products were expressed in embryonic kidney cells together with the E3/19K protein. This allowed us to identify the alpha 1 and alpha 2 domains as the essential structures of the histocompatibility antigens for binding the viral protein. Interestingly, these domains are also crucial for T cell recognition. The implications for the evolution of adenoviruses and their ability to cause persistent infections are discussed.
Adenovirus Early Proteins↗
p16(INK4a) gene inactivation by deletions, mutations, and hypermethylation is associated with transformed and aggressive variants of non-Hodgkin's lymphomas.
The molecular mechanisms underlying the pathogenesis of aggressive lymphomas and the histological transformation of indolent variants are not well known. To determine the role of p16(INK4a) gene alterations in the pathogenesis of non-Hodgkin's lymphomas (NHLs) and the histological progression of indolent variants, we have analyzed the expression, deletions, and mutations of this gene in a series of 112 NHLs. Hypermethylation of the gene was also examined in a subset of tumors with lack of protein expression but without mutations or deletions of the gene. p16(INK4a) gene alterations were detected in 3 out of 64 (5%) indolent lymphomas but in 16 out of 48 (33%) primary or transformed aggressive variants. In the low-grade tumors, p16(INK4a) alterations were detected in 1 (4%) chronic lymphocytic leukemia (hemizygous missense mutation), 1 (6%) follicular lymphoma (homozygous deletion), and 1 (5%) typical mantle cell lymphoma (homozygous deletion). The two later cases followed an aggressive clinical evolution. In the aggressive tumors, p16(INK4a) gene alterations were observed in 2 (29%) Richter's syndromes (2 homozygous deletions), 3 (33%) transformed follicular lymphomas (1 homozygous deletion and 2 nonsense mutations), 3 (43%) blastoid mantle cell lymphomas (2 homozygous and 1 hemizygous deletions), 5 (28%) de novo large-cell lymphomas (1 homozygous deletion and 4 hypermethylations), 2 lymphoblastic lymphomas (2 homozygous deletions), and 1 of 2 anaplastic large cell lymphomas (hypermethylation). Protein expression was lost in all tumors with p16(INK4a) alterations except in the typical chronic lymphocytic leukemia (CLL) with hemizygous point mutation. Sequential samples of the indolent and transformed phase of three cases showed the presence of p16(INK4a) deletions in the Richter's syndrome but not in the CLL component of two cases, whereas in a follicular lymphoma the deletion was present in both the follicular tumor and in the diffuse large-cell lymphoma. In conclusion, these findings indicate that p16(INK4a) gene alterations are a relatively infrequent phenomenon in NHLs. However, deletions, mutations, and hypermethylation of the gene with loss of protein expression are associated with aggressive tumors and they may also participate in the histological progression of indolent lymphomas.
Cell Transformation, Neoplastic↗
[Adrenal hemangioma of atypical presentation. Bibliographical Review].
OBJECTIVE: To report a case of adrenal hemangioma presenting as spontaneous massive retroperitoneal hemorrhage that required surgical treatment without preoperative hormonal study. METHODS/RESULTS: Due to the intense pain and hemodynamic instability, the patient described herein was immediately submitted to laparatomy, adrenalectomy and drainage. The literature is reviewed with special reference to the clinical and radiological findings that could permit making a correct preoperative diagnosis. To our knowledge, a similar form of presentation has not been reported in the literature. The patient is asymptomatic 8 months postoperatively. CONCLUSIONS: Adrenal hemangioma is a rare tumor that usually presents as an incidental finding or with chronic pain in the abdominal flank. Although it is rarely malignant and some authors advocate conservative management based on the radiological findings, the difficulty lies in the similar evolution of other adrenal tumors that can produce similar findings. We therefore advocate surgical excision of adrenal incidentalomas due to their indeterminate histological and clinical behaviour.
Adrenal Gland Neoplasms↗
Pregnancy-dependent to ovarian-independent progression in mammary tumors delineated in primary culture: changes in signal transduction, growth factor regulation, and matrix interaction.
A model for the evolution of hormone-independent tumors from a pregnancy-dependent precursor is exemplified by the TPDMT-4[pregnancy-dependent (PD)] and T4OI96 [ovarian-independent (OI)] in vivo tumor lines developed in DDD mice. In vivo, the OI tumor grows rapidly in virgin mice and is more anaplastic than the PD tumor which, in virgin mice, grows as a hyperplastic alveolar gland from which tumors arise only during pregnancy. The regulation of the proliferation of these two tumors was compared in primary culture using a three-dimensional, serum-free, collagen gel cell culture system. In medium containing insulin, the growth of cell organoids from PD tumors was stimulated by the same factors that stimulate the growth of normal mammary epithelial cells from virgin or pregnant mice. These factors include progesterone and prolactin (but not estrogen), epidermal growth factor, basic fibroblast growth factor, linoleic acid, cyclic AMP, prostaglandin E2, phosphatidic acid, and lithium. Most of these tumors (about 80%) could not grow in medium with only insulin present; of those that did, growth was slow and was stimulated further by the above agents. PD tumor cells formed stellate colonies in the collagen matrix similar to those of normal cells. These findings show that the growth regulation of PD tumor cells is, in all aspects examined, similar to that of normal cells. In addition, the capacity for growth in the presence of only insulin (more autonomous growth) is not necessarily accompanied by deletions in responses to growth factors or hormones, or in lipid response pathways. In contrast, organoids from OI tumors needed only insulin for growth. The growth of some of these tumors was stimulated further by only basic fibroblast growth factor and phosphatidic acid. Cyclic AMP and agents that elevate intracellular cyclic AMP inhibited growth, the opposite of the response seen in normal or PD cells. OI organoids grew as cell masses rather than as stellate structures. These data show that while PD tumors are remarkably similar to normal cells in the regulation of their proliferation, OI tumors have incurred multiple defects in growth-regulatory pathways possibly including the production of autocrine growth factor(s). In addition, the ability of OI tumor cells to adhere to the collagen gel matrix and undergo normal morphogenesis is reduced. These results may highlight specific events required for the progression from ovarian dependency to ovarian independency related to the hormonal regulation of growth.
Animals↗
The reserve-capacity hypothesis: evolutionary origins and modern implications of the trade-off between tumor-suppression and tissue-repair.
Antagonistic pleiotropy, the evolutionary theory of senescence, posits that age related somatic decline is the inevitable late-life by-product of adaptations that increase fitness in early life. That concept, coupled with recent findings in oncology and gerontology, provides the foundation for an integrative theory of vertebrate senescence that reconciles aspects of the 'accumulated damage' 'metabolic rate', and 'oxidative stress' models. We hypothesize that (1) in vertebrates, a telomeric fail-safe inhibits tumor formation by limiting cellular proliferation. (2) The same system results in the progressive degradation of tissue function with age. (3) These patterns are manifestations of an evolved antagonistic pleiotropy in which extrinsic causes of mortality favor a species-optimal balance between tumor suppression and tissue repair. (4) With that trade-off as a fundamental constraint, selection adjusts telomere lengths--longer telomeres increasing the capacity for repair, shorter telomeres increasing tumor resistance. (5) In environments where extrinsically induced mortality is frequent, selection against senescence is comparatively weak as few individuals live long enough to suffer a substantial phenotypic decline. The weaker the selection against senescence, the further the optimal balance point moves toward shorter telomeres and increased tumor suppression. The stronger the selection against senescence, the farther the optimal balance point moves toward longer telomeres, increasing the capacity for tissue repair, slowing senescence and elevating tumor risks. (6) In iteroparous organisms selection tends to co-ordinate rates of senescence between tissues, such that no one organ generally limits life-span. A subsidiary hypothesis argues that senescent decline is the combined effect of (1) uncompensated cellular attrition and (2) increasing histological entropy. Entropy increases due to a loss of the intra-tissue positional information that normally regulates cell fate and function. Informational loss is subject to positive feedback, producing the ever-accelerating pattern of senescence characteristic of iteroparous vertebrates. Though telomere erosion begins early in development, the onset of senescence should, on average, be deferred to the species-typical age of first reproduction, the balance point at which selection on this trade-off should allow exhaustion of replicative capacity to overtake some cell lines. We observe that captive-rodent breeding protocols, designed to increase reproductive output, simultaneously exert strong selection against reproductive senescence and virtually eliminate selection that would otherwise favor tumor suppression. This appears to have greatly elongated the telomeres of laboratory mice. With their telomeric failsafe effectively disabled, these animals are unreliable models of normal senescence and tumor formation. Safety tests employing these animals likely overestimate cancer risks and underestimate tissue damage and consequent accelerated senescence.
Aging↗
Surgical experience with skull base approaches for foramen magnum meningioma.
The surgical treatment of patients with foramen magnum meningioma remains challenging. This study evaluated the outcome of this tumor according to the evolution of surgical approaches during the last 29 years. A retrospective analysis of medical records, operative notes, and neuroimages of 492 meningioma cases from 1972 to 2001 identified seven cases of foramen magnum meningioma (1.4%). All patients showed various neurological symptoms corresponding with foramen magnum syndrome. The tumor locations were anterior in five cases and posterior in two. Surgical removal was performed through a transoral approach in one patient, the suboccipital approach in three, and the transcondylar approach in two. Total removal was achieved in all patients, except for one who refused any surgical treatment. The major complications were tetraparesis and lower cranial nerve paresis for tumors in anterior locations, and minor complications for posterior locations. One patient died of atelectasis and pneumonia after a long hospitalization. The transcondylar approach is recommended for anterior locations, and the standard suboccipital approach for posterior locations.
Adult↗
Immunohistochemical expression of tyrosine kinase (Trk) receptor proteins in mature neuronal cell tumors of the central nervous system.
The interactions of neurotrophins with the Trk family of tyrosine kinase receptors result in growth and maturational changes in neuronal cells. Although the histogenesis of brain tumors composed of mature neuronal cells is still not completely understood, neurotrophins and Trk receptors may be involved in the evolution, maturation, and persistence of these tumors. The clinical and anatomic pathological features of 8 primary neuronal cell tumors (ganglioglioma: 3 cases, cerebral neurocytoma: 3 cases, intraventricular neurocytoma: 2 cases) occurring in the central nervous system (CNS) have been examined. In addition to routine histological examinations, immunohistochemistry was used to evaluate the expression of neurotrophin receptors (TrkA, TrkB) and of neuronal differentiation markers such as neuron-specific enolase, neurofilament, synaptophysin, and chromogranin A. While neither TrkA nor TrkB expression was demonstrated in 2 intraventricular neurocytomas, the remaining 6 tumors did show positive immunohistochemical staining for TrkA and/or TrkB proteins; for TrkA protein, ganglionic cells showed membraneous or cytoplasmic staining, while small non-ganglionic neuronal cells with scant cytoplasm occasionally showed positive cytoplasmic immunoreactivity. For TrkB protein, small non-ganglionic neuronal cells showed a more intense immunoreaction than ganglionic cells. Gangliogliomas with high TrkA and TrkB expression showed higher levels of neuronal differentiation, as demonstrated by the neuron-specific enolase and neurofilament immunoreactivity. The existence of neurotrophin receptors in the tumor cells thus suggests that neurotrophic influence are involved in the evolution and subsequent cellular maturation in neuronal cell tumors of the CNS.
Adult↗
[The future of children cured of cancer: later morbidity].
The 476 children treated for solid malignant tumor from 1947 to 1968 at the Institut Gustave-Roussy, and living NED at 5 years, were reviewed after 5 to 36 years of follow-up (median 17 years). Two children were affected in the sibship in 9 families. Thirty patients died after 7 to 32 years, 15 from late evolution of their primary tumor, 7 from second cancer, and 8 from other causes. Late sequellae (3 lethal), mainly neurologic, orthopedic, endocrine, and others were observed in 271 patients, and not known in 48. A second tumor (19 malignant, 46 benign) occurred from 7 to 26 years after treatment, more than half in the previously irradiated area. These patients have presently 164 known children; two died in infancy, two have malformations. None has had tumor up until now. The long-term cure of cancer remains true in 95% of cases in our span of follow-up, with sequellae compatible with a useful life in most cases.
Adolescent↗
Specific histologic and cytogenetic evidence for in vivo malignant transformation of murine host cells by three human prostate cancer cell lines.
The chromosomal constitutions of three murine cell lines that developed in vitro from tumors that grew in nude mice after orthotopic and ectopic injections of three human prostate tumor cell lines were examined by histopathology, conventional G-banding, and with fluorescence in situ hybridization techniques. All three murine cell lines showed unique marker chromosomes involving mouse chromosome 12, with a common break point. Histopathologic evidence from a murine prostate gland into which SP 3031 cells had been injected indicated dysplastic glandular epithelium and carcinomatous areas. These observations further indicate that: (a) human prostate tumors are capable of transforming host organ cells, (b) host cells have specific chromosomal alterations that may be associated with transformation, and (c) the process of host cell transformation can be demonstrated in histological sections. Although cancer cell heterogeneity and drug-resistant phenotypes are caused by additional genetic alterations and clonal evolution of the original tumor, transformation of the host's distant organ cells may also contribute because most therapies are directed only to the original cancer cells.
Animals↗
NTRK-positive collision tumor of the gastrointestinal tract: a rare entity case report.
Neurotrophic receptor tyrosine kinase (NTRK) fusion-positive colorectal cancer (CRC) represents a rare molecular subset of CRC. We report an exceptional case of a collision tumor composed of two anatomically adjacent but histologically and genomically distinct primary colorectal carcinomas, each giving rise to a corresponding metastasis. Comprehensive histopathologic and molecular analyses demonstrated that one primary tumor and its matched metastasis consisted predominantly (> 90%) of a solid carcinoma harboring a TPR::NTRK fusion, high microsatellite instability (MSI-H), elevated tumor mutational burden (TMB), and loss of MLH1 and PMS2 expression by immunohistochemistry. In contrast, the second primary tumor and its corresponding metastasis exhibited conventional adenocarcinoma morphology with mucinous differentiation, lacked an NTRK fusion, and carried canonical driver mutations in KRAS, APC, SMAD4, and TP53. This case underscores the importance of integrated histopathologic and molecular evaluation in CRCs with heterogeneous morphology, as the identification of multiple, genomically distinct tumor components may have significant diagnostic, prognostic, and therapeutic implications.
NTRK gene fusion↗
[Thalamic tumors in children. A study of 38 cases (author's transl)].
The main clinical, evolutive and therapeutic features of thalamic tumors are reviewed in 38 children. Signs of increased intracranial pressure (76% of the cases) and of controlateral hemiparesis of varying degree (76% of the cases) were the main clinical symptoms. CT-scan is the best means of investigation. Therapeutic protocols that seem to obtain the best results consist of radiotherapy (between 45 and 55 grays) associated with shunting, when intracranial hypertension results from obstruction of an interventricular foramen by the tumor. Surgery is contra-indicated in most tumors in this area.
Adolescent↗
Telomere DNA content and allelic imbalance demonstrate field cancerization in histologically normal tissue adjacent to breast tumors.
Cancer arises from an accumulation of mutations that promote the selection of cells with progressively malignant phenotypes. Previous studies have shown that genomic instability, a hallmark of cancer cells, is a driving force in this process. In the present study, two markers of genomic instability, telomere DNA content and allelic imbalance, were examined in two independent cohorts of mammary carcinomas. Altered telomeres and unbalanced allelic loci were present in both tumors and surrounding histologically normal tissues at distances at least 1 cm from the visible tumor margins. Although the extent of these genetic changes decreases as a function of the distance from the visible tumor margin, unbalanced loci are conserved between the surrounding tissues and the tumors, implying cellular clonal evolution. Our results are in agreement with the concepts of "field cancerization" and "cancer field effect," concepts that were previously introduced to describe areas within tissues consisting of histologically normal, yet genetically aberrant, cells that represent fertile grounds for tumorigenesis. The finding that genomic instability occurs in fields of histologically normal tissues surrounding the tumor is of clinical importance, as it has implications for the definition of appropriate tumor margins and the assessment of recurrence risk factors in the context of breast-sparing surgery.
Adolescent↗
Ileal carcinoid tumor with liver metastases and cardiac involvement treated with intraarterial liposomal doxorubicin and valve replacement.
Unless carcinoid are in general slow-growing tumors, some cases could be frankly malignant. The commonest cause of death in patients suffering a carcinoid tumor is liver failure due to tumor progression. When tumors have a fast evolution a multidisciplinary approach must be perform. This case report is an example of this specific situation.
Antibiotics, Antineoplastic↗
Atypical carcinoid tumor of the larynx: an immunohistochemical, ultrastructural, and flow cytometric analysis.
The clinicopathologic features, including a detailed immunohistochemical, ultrastructural, and flow cytometric analysis, are described in three cases of atypical carcinoid tumor of the larynx. All patients had metastatic disease within cervical lymph nodes at presentation and eventually developed distant metastases. Special stains revealed focal intracytoplasmic mucin accumulation, and immunohistochemistry showed the tumors to be positive for CAM 5.2, CEA, chromogranin A, and calcitonin. In two cases, double-staining techniques revealed occasional cells that stained for both mucin and chromogranin A. The histochemical and immunohistochemical findings in these two cases were confirmed at the ultrastructural level, with most tumor cells containing many neurosecretory granules. Smaller numbers of cells contained mucin vacuoles and, in occasional cells, both mucin and neuroendocrine granules were identified. The three tumors exhibited positive staining with D07 (anti-p53), and flow cytometric analysis revealed DNA aneuploidy and polyploidy. The double-staining and ultrastructural features indicate that laryngeal atypical carcinoid qualifies for the designation of true amphicrine carcinoma. Further study is necessary to determine whether mutation of the p53 gene is important in the evolution of laryngeal neuroendocrine tumors and whether DNA aneuploidy or polyploidy identifies a subset of these tumors with a poor prognosis.
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