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PubMed1989

Phenobarbital lacks promoting activity for neurogenic tumors in F344 rats transplacentally exposed to ethylnitrosourea.

A chronic rodent study in F344 rats was conducted to investigate the promoting ability of phenobarbital (PB) on neurogenic tumors initiated by transplacental administration of ethylnitrosourea (ENU). Pregnant F344 rats were given a single intravenous dose of 3.5 mg ENU/kg or vehicle on the twentieth day of gestation. A total of 192 male offspring were divided into four groups: ENU-PB, ENU-control, PB-control, and control-control. Rats in ENU-PB and PB-control groups received 0.05% PB in their drinking water from four to 78 weeks of age. Nervous system tumors were induced only in animals exposed to ENU. The difference in the incidence of neuroectodermal tumors in rats that were ENU initiated only (13/37; 35%) compared to the incidence in rats that were initiated and given PB (13/57; 23%) was not statistically significant (p greater than 0.05). ENU-control and ENU-PB treatment groups exhibited no differences in tumor multiplicity or tumor latency. These results demonstrate that PB lacks promoting activity for neurogenic tumors in F344 male rats transplacentally exposed to ENU.

Animals↗
PubMed1990

src expression in small-cell lung carcinoma and other neuroendocrine malignancies.

The proto-oncogene c-src codes for two tyrosine kinases, pp60c-src and pp60c-srcN. The latter protein appears to be exclusively expressed in neurons and neuronally differentiated tumors. In cell lines derived from neuroblastoma and small-cell lung carcinoma, src expression correlates positively with neuroendocrine differentiation. However, pp60c-srcN is expressed only in highly differentiated neuroblastomas. Although c-src expression in neuroendocrine tumors probably reflects and is the result of the differentiation stage at which the tumors have been arrested, high c-src expression and kinase activities in non-neuroectodermal tumors, e.g., colon carcinoma, breast carcinoma, might instead be a part of the malignant phenotype and contribute to the development of these tumors.

Carcinoma, Small Cell↗
PubMed1992

Expression of neuronal and glial markers in so-called oligodendroglial tumors induced by transplacental administration of ethyl-nitrosourea in the rat.

A series of 18 tumors with histological features of oligodendrogliomas, induced in the rat by means of transplacental ethyl-nitrosourea administration were studied for immunohistochemical demonstration of neuronal (synaptophysin and neurofilament protein) and glial (gliofibrillar acidic protein and vimentin) markers. Most of the tumors showed cells with strong positivity to synaptophysin and to a lesser degree, to neurofilament protein, suggesting the neuronal character of these neoplasms. In 10 tumors, cells with strong positivity to vimentin were found, and in three cases, tumoral cells expressed gliofibrillar acidic protein. The observation that ENU-induced oligodendroglial tumors express neuronal and, to a minor degree, glial markers, suggests their interpretation as primitive neuroectodermal tumors with clear neuronal differentiation.

Animals↗
PubMed1995

Frequent deletions of material from chromosome arm 1p in oligodendroglial tumors revealed by double-target fluorescence in situ hybridization and microsatellite analysis.

We undertook a cytogenetic analysis of 29 human brain tumors using double-target fluorescence in situ hybridization (FISH) and focusing on chromosome arm 1p. One or more tumor suppressor genes in this arm have been suggested to be important in a variety of neuroectodermal tumors. The series included 9 oligodendrogliomas, 4 mixed gliomas, 10 astrocytomas, 4 glioblastomas, and 2 central neurocytomas. We hybridized pericentromeric (1q12) and subtelomeric (1p36) DNA probes to cell nuclei prepared from paraffin-embedded tissues and observed a strikingly high incidence of deletion of at least part of 1p in oligodendrogliomas (100%) and mixed gliomas (75%). The results of the FISH analyses were confirmed by demonstration of loss of heterozygosity for a microsatellite polymorphism in 10 of the 29 tumors. As well as supporting the feasibility of FISH for detecting allelic deletions in chromosomes from paraffin-embedded tumor samples, the alteration of 1p reported here will contribute to an understanding of the molecular genetic events in oligodendroglial tumor development.

Brain Neoplasms↗
PubMed1993

Surgery, hyperfractionated craniospinal irradiation, and adjuvant chemotherapy in the management of supratentorial embryonal neuroepithelial neoplasms in children.

Supratentorial embryonal neuroepithelial tumors are undifferentiated neoplasms. We have used this term in preference to the controversial classification primitive neuroectodermal tumors (PNET). These lesions in children are malignant neoplasms which are usually fatal within 2 years of diagnosis in spite of therapy with surgery, radiotherapy, and chemotherapy. We have adopted an aggressive approach to the treatment of these tumors with surgical resection, hyperfractionated craniospinal irradiation of 30.6-43.9 Gy followed by a tumor boost to a total dose of 50-63.7 Gy, and adjuvant chemotherapy with cyclophosphamide, vincristine, and cis-platinum. We have treated five children, aged 4-18 years, with this approach. In contrast to the results reported in the literature, four children are alive without evidence of tumor from 4.3 to 8.0 years following diagnosis. One has suffered a tumor relapse at 2.3 years following diagnosis but remains alive. The basis of our therapeutic strategy for childhood supratentorial embryonal neuroepithelial tumors and the implications of our clinical results are discussed.

Adolescent↗
PubMed1988

Chest wall resection and reconstruction for malignant conditions in childhood.

This report evaluates the efficacy of extensive chest wall resection and prosthetic reconstruction in 15 children with chest wall malignancies. There were nine boys and six girls, with a mean age of 9.6 years. Eleven patients had primary chest wall tumors including Ewing's sarcoma (ES), six; rhabdomyosarcoma (RH), two; chondrosarcoma (CS), one; Askin's malignant neuroectodermal tumor, one; and mesenchymal sarcoma, one. Four children had metastases to chest wall and lung from Wilms' tumor (WT), two; osteogenic sarcoma (OS), one; and neuroblastoma (NB), one. Chest wall resection of two to six ribs and reconstruction with Marlex mesh (seven), lattisimus flap (two), prolene mesh (one), and more recently, a Gortex patch (five), was performed. Eight of the patients required concomitant en-bloc pulmonary resection (wedge, five; lobectomy, two; pneumonectomy, one) and two required resection of diaphragm. Fourteen received adjunctive therapy (chemotherapy, 14; irradiation, eight [preoperative, five; postoperative, three]. Six patients had second-look resections after chemotherapy. There was no operative mortality. Early pulmonary function was normal; however, pulmonary restrictive disease and scoliosis occurred with growth. One ES patient developed a radiation-induced second malignant tumor at age 10 and one ES child died at age 6 (no evidence of disease) of meningitis. Average survival length for ES patients was 77 months (range, 18 to 132 months.) Currently, eight patients are alive and five are free of disease. Extensive chest wall resection and reconstruction is useful in the treatment of primary chest wall tumors, but is palliative in metastatic cases. The Gortex patch is the current prosthetic of choice.

Adolescent↗
PubMed1998

A new pineoblastoma cell line, PER-480, with der(10)t(10;17), der(16)t(1;16), and enhanced MYC expression in the absence of gene amplification.

Pineoblastoma is a rare, but highly malignant tumor of the central nervous system (CNS) in children and is classified as a central primitive neuroectodermal tumor (PNET). Despite notable recent advances in understanding the molecular genetic basis of malignancies, the pathogenesis of PNETs remains enigmatic. There is scant information on the cytogenetics of PNETs arising in the pineal gland and the only three reported cases did not show any common aberrations. Here we report the establishment and characterization of a new pineoblastoma cell line, PER-480. The biopsy material and the cell line were characterized using light and electron microscopy and immunohistochemical analyses. The cell line was examined for expression of cell surface markers using a panel of monoclonal antibodies and by cytogenetic analysis. MYC family genes were studied at the DNA, RNA, and protein level. Cell line PER-480 showed neuronal differentiation and the karyotype demonstrated two abnormalities, a der(10)t(10;17) and a der(16)t(1;16). An intriguing finding is that all three pineoblastoma cell lines established in our laboratory, PER-452, PER-453, and PER-480, showed enhanced expression but not amplification of a member of the MYC family of proto-oncogenes. Cell line PER-480 reported here will be useful for the further investigation of the molecular genetic basis of central PNETs.

Brain Neoplasms↗
PubMed2004

Double immunolabeling of central nervous system atypical teratoid/rhabdoid tumors.

The central nervous system atypical teratoid/rhabdoid tumor (ATRT) is a highly malignant tumor with a heterogeneous immunohistochemical profile and with some morphologic similarity to central nervous system primitive neuroectodermal tumors (PNET). Although several studies have investigated double immunolabeling in PNET, we are aware of no studies of double labeling of ATRT. A total of 10 ATRT from surgical and consultation materials at the Children's Hospital of Philadelphia were selected and stained for a variety of antigens using indirect immunofluorescence to detect single and double labeling. Most tumor cells showed only single labeling; rare cells showed double labeling as follows: 70% of tumors coexpressed (VIM) and glial fibrillary acidic protein (GFAP), 30% smooth muscle actin and GFAP, 20% epithelial membrane antigen (EMA) and VIM, 20% EMA/GFAP, and 20% EMA/SMA. These results are discussed in view of current debates over the histogenesis of CNS PNET and ATRT, and in reference to the classification of rhabdoid tumors as an entity or phenotype.

Actins↗
PubMed2000

Suppression of the Ewing's sarcoma phenotype by FLI1/ERF repressor hybrids.

Fusion of the 5' half of the Ewing's sarcoma (ES) gene EWS with the DNA-binding domain of several transcription factors has been detected in many human tumors. The t(11;22)(q24;q12) chromosomal translocation is specifically linked to ES and primitive neuroectodermal tumors and results, in the majority of cases, in the fusion of the amino terminus of the EWS gene to the carboxyl-terminal DNA-binding domain of the FLI1 gene. The chimeric protein has been shown to be oncogenic, a potent transcriptional activator, and necessary for the maintenance of the Ewing's phenotype, making it an attractive target for gene therapy. In this study, we demonstrate that the ES transformed phenotype can be suppressed by chimeric transcriptional repressors containing the DNA-binding domain of FLI1 and the regulatory and repressor domain of ERF, a transcription suppressor and member of the ets gene family. The hybrid repressor is expressed at levels comparable with EWS/FLI1, does not affect EWS/FLI1 expression, and exhibits similar DNA-binding specificity but suppresses transcriptional activity. The FLI1/ERF repressor, like the wild-type ERF, is regulated by mitogen-activated protein kinase-dependent subcellular localization. Our data suggest that transformation by EWS/FLI1 may partially be due to activation of specific EWS/FLI1-regulated genes involved in cell proliferation.

Amino Acid Sequence↗
PubMed2006

Caveolin-1 (CAV1) is a target of EWS/FLI-1 and a key determinant of the oncogenic phenotype and tumorigenicity of Ewing's sarcoma cells.

Tumors of the Ewing's sarcoma family (ESFT), such as Ewing's sarcoma (EWS) and primitive neuroectodermal tumors (PNET), are highly aggressive malignancies predominantly affecting children and young adults. ESFT express chimeric transcription factors encoded by hybrid genes fusing the EWS gene with several ETS genes, most commonly FLI-1. EWS/FLI-1 proteins are responsible for the malignant phenotype of ESFT, but only few of their transcriptional targets are known. Using antisense and short hairpin RNA-mediated gene expression knockdown, array analyses, chromatin immunoprecipitation methods, and reexpression studies, we show that caveolin-1 (CAV1) is a new direct target of EWS/FLI-1 that is overexpressed in ESFT cell lines and tumor specimens and is necessary for ESFT tumorigenesis. CAV1 knockdown led to up-regulation of Snail and the concomitant loss of E-cadherin expression. Consistently, loss of CAV1 expression inhibited the anchorage-independent growth of EWS cells and markedly reduced the growth of EWS cell-derived tumors in nude mice xenografts, indicating that CAV1 promotes the malignant phenotype in EWS carcinogenesis. Reexpression of CAV1 or E-cadherin in CAV1 knockdown EWS cells rescued the oncogenic phenotype of the original EWS cells, showing that the CAV1/Snail/E-cadherin pathway plays a central role in the expression of the oncogenic transformation functions of EWS/FLI-1. Overall, these data identify CAV1 as a key determinant of the tumorigenicity of ESFT and imply that targeting CAV1 may allow the development of new molecular therapeutic strategies for ESFT patients.

Animals↗
PubMed2006

Ewing's sarcoma in the spinal nerve root: a case report and review of the literature.

Ewing's sarcoma (ES) is a highly malignant tumor composed of uniform small round cells. Recently, a single biologic entity, Ewing's sarcoma family of tumors (ESFT) has been accepted. The entity includes ES, extraskeletal Ewing's sarcoma (EES) and primitive neuroectodermal tumor (PNET). ESFT cells have immunoreactivity for CD99, an antigen determined by the MIC2 gene. Most ESFT has the (11;22) (q24;q12) translocation. The translocation results in the fusion of the EWS gene with the transcription factor gene FLI1 which has been considered a hallmark of ESFT. We present an extremely unusual case with ESFT in a spinal nerve root mimicking a neurogenic dumbbell tumor. A male aged 20 years noticed pain in his right buttock. Magnetic resonance imaging (MRI) revealed a mass in the right L5/S intervertebral foramen and the lesions in the sacrum. Surgery was performed with a presumptive diagnosis of a nerve sheath tumor. At surgery, the tumor was located in the right L5 nerve root sleeve. The sacral lesions were observed closely. At one month after surgery, radiologically multiple lesions were detected in the pelvic bones. Microscopically the lesions from the root and ilium were composed of small round cells immunoreactive for CD99. Reverse transcription-polymerase chain reaction detected transcripts resulting from the fusion of the EWS gene with FLI1 genes in the iliac lesion. Immunoreactivity for CD99 and detection of the EWS-FLI1 hybrid transcripts are important for the correct diagnosis of ESFT arising in an unusual location.

Adult↗
PubMed1997

Complications associated with intraventricular chemotherapy in patients with leptomeningeal metastases.

The authors studied complications associated with intraventricular chemotherapy in patients with leptomeningeal metastases (LM). One hundred twenty consecutive patients with LM (71 females and 49 males) ranging in age from 10 to 72 years (median 42 years) were treated with involved-field radiotherapy and intraventricular chemotherapy using an Ommaya reservoir and intraventricular catheter system. The diagnosis of LM was determined by a combination of clinical presentation (114 patients); cerebrospinal fluid cytological studies (100); or neuroradiographic studies (42). Systemic tumor histological findings included breast (34 patients); non-Hodgkin's lymphoma (22); melanoma (16); primitive neuroectodermal tumors including medulloblastoma (10); glial neoplasms, leukemia, small cell lung, nonsmall cell lung, and colon (six each); prostate and kidney (three each); and gastric cancers (two). Sixteen patients, all with non-Hodgkin's lymphoma, also had acquired immune deficiency syndrome. Patients received one to four (median two) chemotherapeutic drugs and underwent a total of 1110 cycles of intraventricular chemotherapy (median 10). Intraventricular chemotherapy administration and diagnostic Ommaya reservoir punctures totaled 4400, with a median of 46 per patient. Complications included aseptic/chemical meningitis (52 patients); myelosuppression due to intraventricular chemotherapy (21); catheter-related infections (nine); unidirectional catheter obstruction (six); intraventricular catheter malpositioning (two); Ommaya reservoir exposure (two); leukoencephalopathy (two); and chemotherapy-related myelopathy (one). There were no treatment-related deaths; however, seven patients (6%) required additional surgery for either catheter repositioning (two) or reservoir removal (five). Seven patients with catheter-related infections were treated successfully with intraventricular and systemic antibiotic drugs, thereby preserving the Ommaya system. The authors conclude that Ommaya reservoirs are convenient and pharmacologically rational systems for administering intraventricular chemotherapy. Overall, serious complications requiring surgery are infrequent (6%) and most often secondary to catheter infections, Ommaya reservoir exposure, or initial catheter malpositioning. In the majority of instances, catheter infections may be managed medically, as may the most common complications of intraventricular chemotherapy including aseptic meningitis (43% of patients) and myelosuppression (18%).

Adolescent↗
PubMedDate not supplied

Rhabdoid glioblastoma.

Rhabdoid phenotypic change has been described in a number of different neoplasms from diverse organ sites. These tumors share common light and electron-microscopic features, display a polyphenotypic immunohistochemical profile and often show cytogenetic abnormalities of chromosome 22. In the central nervous system (CNS), most rhabdoid tumors occur in the posterior fossa of very young children and are associated with a primitive neuroectodermal tumor (PNET) component and are designated atypical teratoid/rhabdoid tumors. Infrequently, other rhabdoid tumors of the CNS have been described, including rhabdoid meningiomas and malignant rhabdoid tumors of uncertain histogenesis. Several examples of conventional gliomas displaying significant areas with rhabdoid morphology were also presented in an abstract by Kepes and Moral [1991], although never published in final manuscript form. We now detail the case of an 18-year-old male with an aggressive, supratentorial CNS rhabdoid tumor that was associated with an epithelioid glioblastoma and apparently arose from areas of low-grade glioma. The rhabdoid tumor component was present in the original tumor but became more predominant with each of 3 successive resections. No areas of PNET were identified. Electron microscopy and immunohistochemistry showed features classic for rhabdoid tumors and cytogenetic studies demonstrated multiple tumor clones with monosomy 22. This case documents progressive rhabdoid transformation of a glioma, expands the spectrum of CNS tumor types that can display a rhabdoid phenotype and highlights the diagnostic and therapeutic challenges with this type of tumor.

Adolescent↗
PubMed2002

[Incidence of pediatric brain tumors in Hungary between 1989 and 1999].

INTRODUCTION: The incidence of primary brain tumors in childhood has increased all over the world in the last decades, so it is the second most frequent tumor after leukaemias. AIMS OF THE STUDY: The aim of this study was to examine the incidence and relative frequency of central nervous system tumors diagnosed under 15 years of age in Hungary. METHODS: The data obtained from the Hungarian Pediatric Oncology Group and the National Neurosurgical Institute between 1989 and 1998, and the reports of the head pediatricians of the counties were used. RESULTS: There were 685 reported cases between 1989 and 1998. The prevalence of cerebral tumors has increased during the last decade in Hungary like that in several developed countries. The increase of the incidence of primary central nervous system tumors in the last ten years was 4.2% per year. In 1998 the incidence of central nervous system tumors was 42.9 cases per million children. The most frequent histological categories were: astrocytoma (30%), medulloblastoma/primitive neuroectodermal tumors (21%), ependymoma (9%) and other tumors (40%). CONCLUSION: The results suggest an increase in the incidence of primary brain tumors in Hungary, similar to those reported in several countries.

Adolescent↗
PubMed2004

[Experience and discussion on treatment of high-grade soft tissue sarcomas of crura in youth].

OBJECTIVE: To summarize the experience and investigate better method on treatment of high-grade soft tissue sarcomas of crura in youth. METHODS: Six young cases suffered from high-grade soft tissue sarcomas of crura were treated by interpolatory chemotherapy using vindesine 4mg or vincristine 2 mg combined with cisplatin 40 - 60 mg and 4'-Epidoxorubicin (4'-epi-ADM) 50 - 80 mg. There were 3 males and 3 females, and their ages rang from 12 to 23. The primary tumor locations were: calf in 4, thigh in 1, popliteal fossa in 1. The pathological type of these 6 cases were: 1 small round cell tumor from soft tissue, one rabdomyosarcoma, one alveoliar soft part sarcoma, one synovial sarcoma, one primitive neuroectodermal tumor and one without classification. All cases received interpolatory chemotherapy twice. Before their receiving interpolatory chemotherapy they had no tumor metastases. The maximum diameters of tumors rang from 4 - 15 cm. One patient's tumor disappeared after interpolatory chemotherapy and she received no further therapy. The other 5 cases received operations and one of them received additional pre-operational radiotherapy using Co(60) and pre-operational systemic chemotherapy using ifosfamide and dacarbazine. RESULTS: The tumors dwindled in size of 1 - 8 cm after interpolatory chemotherapy. All cases saved their crura and had normal functions. After interpolatory chemotherapy, all patients suffered from edema and ache of crura. One patient suffered from lymphatitis. All these patients were followed up for 6 - 20 months. All of them were alive and had pigmentations on their crura. A lung metastasis was found in 1 patient by CT 2 months after surgery, then he was in hospital and treated by chemotherapy. CONCLUSIONS: For treatment of high-grade soft tissue sarcomas of crura which are difficult to resect in youth, interpolatory chemotherapy is a good choice.

Adolescent↗
PubMed1988

Characterization of a human endocrine tissue and tumor-associated Ewing's sarcoma antigen.

The histogenesis of Ewing's sarcoma (ES), the second most frequent primary bone tumor in humans, remains controversial. A new cell line (SIM-1) was derived from a peripheral neuroectodermal tumor (PNET) and used for the production of a monoclonal antibody (HBA-71), which recognizes a novel cell surface antigen of ES- and PNET-derived cells and paraffin-embedded tumor sections. The HBA-71 antigen expression is restricted to PNET/ES and the antigen was not detected on cell lines or tissue sections of any other tumor tested, with the exception of ependymoma. Three proteins with molecular weights of 300,000, 185,000, and 90,000 were isolated from SIM-1 membrane extracts by HBA-71 affinity chromatography. Trypsin treatment of intact SIM-1 cells destroys the HBA-71 epitope and cleaves off two proteins with molecular weights of 210,000 and 95,000. HBA-71 antigen expression is not influenced by treatment of ES cell lines with differentiation inducers. Within normal tissues reactivity was observed with the adenohypophysis, ependymal cells, endocrine pancreas, Sertoli, and ovary granulosa cells. The reagent links ES with PNET and provides a highly valuable probe for (a) the immunohistological differential diagnosis of ES/PNET using fresh tissue or paraffin sections from other small round cell tumors, (b) the histogenetic studies of ES/PNET, and (c) the in vivo diagnostic and therapeutic procedures in patients with ES and PNET.

Adolescent↗
PubMed1987

Phase II trial of ifosfamide in children with malignant solid tumors.

Ifosfamide was given to 61 patients with malignant solid tumors diagnosed before the age of 21 years. In this phase II study, all patients received 1.6 g/m2/day X 5 iv over 15 minutes followed by mesna at a dose of 400 mg/m2 iv at 15 minutes and 4 and 6 hours after ifosfamide. Responses were observed in five of 15 patients with osteosarcoma, two of ten with neuroblastoma, two of six with Wilms' tumor, two of five with rhabdomyosarcoma, four of eight with other soft tissue sarcomas, one of one with retinoblastoma, one of two with germ cell tumors, one of one with B-cell lymphoma, and one of one with a primitive neuroectodermal tumor. Fifty-nine of 61 patients had received prior alkylating agent therapy which included cyclophosphamide, cisplatin, mechlorethamine, melphalan, or dacarbazine. Fourteen of 19 responses developed in patients whose tumors were resistant to treatment with cyclophosphamide. A patient with malignant Schwannoma who had received no prior chemotherapy developed a complete response which lasted 12 months. A patient with brain metastases of osteosarcoma has had complete response for greater than 2 years. Complete response was also observed in a patient with B-cell lymphoma. Toxicity consisted of mild to moderate nausea and vomiting, transient reversible myelosuppression, occasional elevation of serum BUN or creatinine, and transient neurotoxicity characterized by somnolence, confusion, weakness, tremor, hallucinations, or seizures. We conclude that ifosfamide is an important alkylating agent without apparent complete cross-resistance with cyclophosphamide, and as such should be further investigated for determination of its activity in patients with pediatric neoplasms and considered for incorporation into phase II-III trials for certain tumors.

Adolescent↗
PubMed1984

Surface topography and extent of invasiveness of SV40 virus-transformed hamster brain cells and transformed cell-produced tumors.

Scanning electron microscopy (SEM) was used to study the surface configuration of SV40 virus-transformed 1 day old Syrian hamster brain cells and transformed cell-produced tumors and the alterations in cell membrane configuration that become evident with the development of invasiveness. Cell cultures of dissociated cerebral cortex, brain-stem, cerebellar vermis and cerebellar hemisphere were transformed to a neoplastic state with SV40 virus. The transformed cells were then inoculated intracerebrally into hamsters to produce intracranial tumors, and cell cultures were obtained from these tumors. Invasiveness was determined by reinoculating the transformed or tumor cells intracerebrally into hamsters and examining histological sections of the resulting tumors. Cultures of the transformed and tumor cells were also critical point dried and studied with SEM. Tumors of cerebral cortex and brainstem derivation (Group I) had the histological appearance of astrocytomas and were invasive for adjacent normal brain. With SEM, they were flat, epithelioid, and surrounded by ruffles and microvilli. They grew only in monolayers and showed few of the rounded forms with blebs and/or microvilli typical of mitosis. Tumors of cerebellar vermis and cerebellar hemisphere derivation (Group II) had the histological appearance of primitive neuroectodermal tumors and were not invasive. With SEM, they were more rounded, fusiform or stellate, and lacked surface specializations at their borders. They exhibited multilayered growth and the rounded forms associated with mitosis. Tumor cells of both groups had more surface activity than transformed cells. These observations give some support to the concept that a decrease in contact inhibition of locomotion and an increase in density-dependent inhibition of locomotion and in mobilization are essential for the development of invasiveness in tumors.

Animals↗