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PubMedDate not supplied

[Congenital melanotic tumors].

Congenital melanotic tumors are among the very rare tumors of early childhood. Their histogenesis and biological significance are still controversial today. The ideas of an odontogenic origin and of a neuroectodermal pathogenesis of these tumors range among the most frequently advocated hypotheses. Until about 1970 this type of tumor was almost always referred to as benign. Meanwhile there has been a change in the assessment of the character of congenital melanotic tumors. Above all, this is due to the fact that malignant cases have been repeatedly reported since 1970. Apart from an extensive review of the literature, 2 own cases are described which were treated surgically. The histological evaluation of the tumor material supports the assumption that these tumors are of odontogenic origin.

Female↗

PubMed1990

[Melanotic paraneurons].

Histogenetic scheme of three germ layers causes difficulties in explanation of some tumorous structures derived from different classes. A conception of paraneurons concedes (besides "central" neuroectodermal paraneurons) a possibility of their local origin. The idea anticipates a broader phylogenetic ability of divergent differentiation of single extraneural cells. Paraneuronal theory used in oncology can explain local origin of some presumable combination variants of tumours, e.g. carcinoid type paraneuromas with melanin pigmentation. Substantial frequency of such tumours eliminates possibility of random coincidence and argues for ranging "peripheral melanin system" among paraneurons.

Chromaffin System↗

PubMed1999

Mediastinal tumors of peripheral nervous system origin.

A wide spectrum of benign and malignant tumors of peripheral nervous system origin can arise in the mediastinum. These neoplasms are more frequent in the posterior mediastinum and can develop from peripheral nerves, sympathetic and parasympathetic ganglia, and neural tube embryonic remnants. The clinicopathologic features of mediastinal schwannomas, melanotic schwannomas, neurofibromas, ganglioneuromas, granular cell tumors, malignant tumors of peripheral nerve sheath origin, malignant melanocytic tumors of peripheral nerve sheath origin, neuroblastomas, ganglioneuroblastomas, and pigmented neuroectodermal tumors of infancy are reviewed.

Adult↗

PubMedDate not supplied

Melanotic differentiation in dysembryoplastic neuroepithelial tumor.

Dysembryoplastic neuroepithelial tumor (DNT) is an uncommon intracranial tumor which is usually encountered in patients with medically intractable complex partial seizures of temporal lobe origin. Melanotic differentiation in a DNT has not been reported previously. Herewith we report a case of DNT with unique melanotic differentiation in a 23-year-old female who presented with medically intractable epilepsy. She underwent craniotomy and tumor decompression with a good outcome. We present the histopathological features of DNT with melanotic differentiation and discuss its prognostic significance.

Adult↗

PubMed2001

Microphthalmia transcription factor and melanoma cell adhesion molecule expression distinguish desmoplastic/spindle cell melanoma from morphologic mimics.

Desmoplastic/spindle cell melanoma is a rare variant of melanoma. A number of factors complicate the diagnosis of desmoplastic/spindle cell melanoma, including the variable absence of a lentiginous component, its spindle cell morphology, and its many morphologic mimics, including scars, malignant peripheral nerve sheath tumor, neurofibroma, atypical fibroxanthoma, and spindled carcinoma. The immunohistochemical confirmation of desmoplastic/spindle cell melanoma may also be difficult, because the majority of tumors are negative for specific melanocytic markers such as HMB-45 and Melan-A, despite their usual expression of S-100 protein. Two new and potentially promising melanocytic markers, microphthalmia transcription factor (MiTF) and melanoma cell adhesion molecule (Mel-CAM), have been shown to be sensitive markers of epithelioid melanoma, but have not been tested in desmoplastic/spindle cell melanoma or in other rare melanocytic neuroectodermal tumors such as clear cell sarcoma. We immunostained 79 tumors (20 desmoplastic/spindle cell melanomas, 10 scars, 10 neurofibromas, 12 malignant peripheral nerve sheath tumors, 10 atypical fibroxanthomas, 10 clear cell sarcomas, 3 melanotic schwannomas, and 4 cellular blue nevi) for MiTF and Mel-CAM. MiTF expression was seen in 11 of 20 desmoplastic/spindle cell melanomas, 0 of 10 scars, 2 of 10 neurofibromas, 0 of 12 malignant peripheral nerve sheath tumors, 1 of 10 atypical fibroxanthomas, 7 of 10 clear cell sarcomas, 3 of 3 melanotic schwannomas, and 3 of 4 cellular blue nevi. Mel-CAM expression was present in 14 of 17 desmoplastic/spindle cell melanomas, 0 of 10 scars, 4 of 10 neurofibromas, 3 of 11 malignant peripheral nerve sheath tumors, 0 of 10 atypical fibroxanthomas, 9 of 10 clear cell sarcomas, 3 of 3 melanotic schwannomas, and 0 of 4 cellular blue nevi. MiTF and Mel-CAM were coexpressed in 6 of 17 desmoplastic/spindle cell melanomas and in no other tumor. Regarding desmoplastic/spindle cell melanoma, scar, neurofibroma, malignant peripheral nerve sheath tumor, and atypical fibroxanthoma, the sensitivity and specificity of MiTF for desmoplastic/spindle cell melanoma were 55% and 91%, respectively. For this same group of tumors, Mel-CAM had a sensitivity of 82% and a specificity of 83%. We conclude that the sensitivity and specificity of MiTF for desmoplastic melanoma equals or exceeds that of such markers as HMB-45 or Melan-A, and that MiTF should be part of the initial immunohistochemical panel for the work-up of such cases. Mel-CAM, while very sensitive, is relatively nonspecific, because it is also expressed in a variety of mesenchymal tumors and carcinomas. Mel-CAM is best reserved for cases morphologically suspected to be desmoplastic/ spindle cell melanoma, in which S-100 is positive and MiTF and other melanocytic markers are negative. These markers may also be helpful in certain other differential diagnoses, such as distinguishing clear cell sarcomas from epithelioid malignant peripheral nerve sheath tumors.

Antigens, CD↗

PubMed1984

[Soft tissue clear cell sarcoma. Morphology, differential diagnosis and tumor classification].

Clear cell sarcomas of tendons and aponeuroses were first described by Enzinger in 1965 and are characterized by the occurrence in young adults, frequent location in the distal lower extremity and slow, but often relentless clinical course. The histologic features of 5 own cases are presented, the cellular arrangement in nest-, cluster- or "ball"-like formations and a prominent nucleolus are emphasized as most reliable diagnostic patterns. Some aspects of differential diagnosis are discussed, especially those concerning its histologic distinction from fibrosarcomas, malignant melanomas, malignant Schwannomas and synovial sarcomas. The electron microscopic examination of one case revealed findings which may be considered as typical for tumors developed from neural crest derived cells: envelopment of many tumor cells by basal lamina-like structures, specialized cellular contacts, interdigitations of cellular processes and "wrapping around"-phenomena (so-called mesocollagen formation). Some neurosecretory granules (not described till now in clear cell sarcomas) and fibrous long spacing collagen further support the suggestion that clear cell sarcomas pertain to the group of tumors with relationship to neuroectodermal cells and tissues. We feel that, because of their typical histologic picture and their particular clinical behavior, they should not be regarded as malignant (soft tissue) melanomas or malignant (melanotic) Schwannomas but retained as a defined clinico-pathological entity.

Adult↗

PubMed1989

Melanotic paraganglioma of the orbit: a case report.

A paraganglioma of the orbit in a 21-year-old woman is presented, containing oculo-cutaneous melanin in many tumor cells, occasionally adjacent to neurosecretory granules, and in macrophages. This tumor expands the list of neuroectodermal tumors with potential melaninization.

Adult↗

PubMed2006

Primary intramedullary primitive neuroectodermal tumor (PNET)--case report and review of the literature.

Spinal primitive neuroectodermal tumors (PNET) are very rare tumors, and intramedullary localization is even less common. Indeed, amongst the 23 cases of the spinal PNET described in the literature, only eight cases had an intramedullary localization. Following the WHO 2000 classification, PNETs have been considered embryonal tumors composed of undifferentiated neuroepithelial cells with a capacity of differentiation into different cellular lines, such as astrocytic, ependymal, melanotic and muscular. They have been considered to arise from a neoplastic transformation of primitive neuroepithelial cells, thereby making their presence possible in any part of the central nervous system. The optimal treatment for these malignant tumors is not yet clear, although, over the years, radiotherapy has been considered the best treatment for spinal PNETs. The described case is that of a 38-year-old man with a primary intra-extramedullary PNET, treated by laminectomy, open biopsy and chemotherapy. The patient, 18 months after the onset of his symptomatology, died without cerebral tumor involvement.

Adolescent↗

PubMed1980

Melanotic mucin-producing neuroepithelial neoplasm of mesencephalon with consideration of similar tumours in different locations.

A six month old boy had a mesencephalic melanotic neoplasm of the neuro-epithelial derivatives which produced mucin. Location in the mesencephalon and production of the mucin have not been described previously for this kind of intracranial tumour. The various cellular elements within the growth are in accord with diverse differentiations of the neuroepithelium of the neural tube, the neuroectodermal part of the neural crest, or both. Derivatives of the neural tube and crest can be melanotic, and some neuroepithelial derivatives (ependyma, oligodendrocyte, and choroidal epithelium) produce mucin. Hence, melanotic neuroepithelial neoplasms with mucinous product can occur. The present tumour is similar to lesions variously designated as melanotic medulloblastoma, retinal anlage tumour, and progonoma. Diverse differentiation of the neuroepithelium of the neural tube, or of the neuroectodermal part of the neural crest, or both would create these variously named tumours. The frequency of melanotic neuroepithelial neoplasms in infancy, and the presence of papillae strongly suggest congental derivation.

Adult↗

PubMed1983

Intermediate filaments in malignant melanomas. Identification and use as marker in surgical pathology.

Intermediate-sized filaments have been studied in human malignant melanomas and in normal melanocytes by immunofluorescence microscopy with antibodies directed against keratin, vimentin, desmin, neurofilament protein, and glial filament protein. Both human melanotic and amelanotic tumor cells and tumor metastases as well as normal melanocytes in human skin and in the rat eye contain exclusively intermediate filaments of the vimentin type. No reaction was seen with antibodies to keratin, desmin, neurofilaments, or glial filaments. These latter four antisera, however, gave strong reactions in epidermis and other epithelial tissues, muscle, or neural tissues, respectively. The results favor a mesenchymal character of melanocytes, although a neuroectodermal origin in an early developmental stage is possible. The finding that melanomas contain exclusively vimentin intermediate filaments may prove useful in differential diagnosis of melanomas from other tumor types.

Fluorescent Antibody Technique↗

PubMed1977

[Neuroectodermal tumors of the skin (a normative study)].

A group of bioptically examined neuroectodermal tumours of the skin and soft tissues consisting, in particular, of 170 Schwannomas and 350 tumours has been reevaluated in a retrospective study. The following common classification of these tumours has been recommended: I. Tumours of Schwann's cells: 1. neurilemmoma [A and B], 2. neurofibroma [with the following variants v. Recklinghausen's type, plexiform, pigmented, Paccinian, with Meissner-Wagner's bodies and meningiomatous], 3. amputation neuroma, 4. neurosarcoma, 5. others. II. Melanogenic tumours: A. pigmented naevi (junction, mixed, intradermal, epithelioid, clear cell, halo, neurocutaneous, fibrous, blue, proliferating blue, melanotic progonoma, others). -B. praecancerous melanosis. -C. malignant melanoblastoma (common type, from praecancerosis). III. Tumours of ganglion cells: 1. ganglioneuroma, 2. neuroblastoma, 3. paragangliomas (with granules, without granules, alveolar soft part sarcoma).

Ganglioneuroma↗

PubMed1989

Clear cell sarcoma. An immunohistochemical and ultrastructural study.

The histogenesis of clear cell sarcoma was investigated by immunohistochemical examination of five tumors (two melanotic and three amelanotic) and electron microscopic examination of two of these tumors (one melanotic and one amelanotic). Melanin production was observed histologically in two of the tumors. The cytoplasm of cells in both types of tumor contained various numbers of melanosomes. Melanoma-specific antibody (HMB-45), anti-S-100 protein, and anti-vimentin antibodies gave positive reactions in four tumors, while all tumors showed Leu-7 immunoreactivity. No cytokeratin or epithelial membrane antigen (EMA) was detected immunohistochemically in any tumor. The immunoreactivity of this type of tumor with HMB-45 antibody strongly suggests melanocytic differentiation rather than schwannian or synovial differentiation. The reaction of the cells of one tumor with only Leu-7 indicates the existence of undifferentiated clear cell sarcoma of neuroectodermal origin that does not show definite melanocytic differentiation.

Adult↗

PubMed1982

Pigmented olfactory neuroblastoma: a new example of melanotic neuroepithelial neoplasm.

The light and electron microscopic features of a pigmented olfactory neuroblastoma are described. The neuroblastic nature of the tumor was confirmed by the demonstration of axons, some of which originated from the neoplastic cells, and by the presence of dense-core vesicles in the perikarya and processes of the tumor cells. The tumor contained a large amount of pigment, most of which had the histochemical reactions of melanin, but some of which had that of lipofuscin. Electron microscopy failed to demonstrate the presence of melanosomes or premelanosomes: the pigment showed some of the features of neuromelanin, although the fine structural appearances were not typical. The pigment was interpreted in this case as presumably representing a modified catecholamine degradation product, perhaps related to lipofuscin. The presence of melanotic pigment in an example of olfactory neuroblastoma, unreported until now, augments the list of neurogenic neoplasms in which an association with melanin formation has been described. The significance of this association in tumors originating from the nervous system or its coverings needs further investigation, as the nature of pigment appears to be heterogeneous. These tumors may contain either melanosomal pigment or pigment identified as neuromelanin (or a related substance), seemingly regardless of the derivation of the pigment-bearing cells.

Adult↗

PubMed1989

Melanotic ganglioglioma of the pineal region.

A melanotic ganglioglioma was biopsied in the pineal region of a 12-month-old girl who preoperatively underwent a ventriculo-peritoneal shunt for hydrocephalus and postoperatively received radiotherapy. The tumor was subtotally excised when the girl was 7 years and 4 months of age. Histologically, it demonstrated mature neurons in disorganized clusters and in well-differentiated cerebrum-like tissue, rare binucleated neurons, glia similar to normal gray matter, and bands of fibrous tissue containing heavily pigmented cells. Ultrastructurally, melanosomes of stages I to IV were identified in the pigmented cells. An origin involving retinal differentiation of the primitive pineal gland was not supported; the tumor was negative for both retinal S-antigen (MAbA9-C6) and cellular retinal-binding protein (CRALBP). This report demonstrates the ability of a cerebral neoplasm to contain neurons, glia, and melanin-containing cells; all of which are neuroectodermally derived.

Brain Neoplasms↗

PubMed1988

Melanotic medulloblastoma. A case report with immunohistochemical and ultrastructural examination.

A melanotic medulloblastoma is reported with electron microscopic and immunohistochemical findings. The cerebellar tumor had seeded through the cerebrospinal fluid to cerebrum and spinal cord, spread through the dura, and metastasized to the lungs. It consisted of (i) anaplastic cells with slight neuronal differentiation, but without the fibrillary background of neuroblastomas, and (ii) epithelial islands pigments with melanin. The latter participated in the spread through the subarachnoid space, but did not extend beyond the dura. Electron microscopy revealed in the pigmented cells tight junctions and oculo-cutaneous melanin, including premelanosomes. The anaplastic cells had undistinguished organelles and only small junctions. On immunohistochemistry, the cytoplasm of the anaplastic cells was positive for neuron-specific enolase and neurofilament, and some of the nuclei were positive to S-100, confirming neuronal differentiation. The cells did not stain for glial fibrillary acidic protein, carcinoembryonic antigen, cytokeratin, alpha fetoprotein, vimentin, and epithelial membrane antigen. The melanotic cells were negative to all reagents tested, even to S-100 protein. The presence of oculo-cutaneous melanin and of neuronal elements indicate a neuroectodermal or neural crest origin.

Cerebellar Neoplasms↗

PubMed2002

Melanotic neuroectodermal tumour of infancy involving the orbit and maxilla: surgical management and follow-up strategy.

Melanotic neuroectodermal tumour (MNET) of infancy is a rare benign but locally aggressive tumour. We describe our surgical treatment of MNET of the orbital region. There was osteogenic relapse involving the bone of the orbit, 20 days after macroscopically complete excision of the primary tumour when the patient was 12 weeks old. This is only the second report of osteogenic relapse in MNET. The relapse was treated by excision of the involved orbital floor, preserving the orbital periosteum. The tumour has not recurred in 23 months of follow-up. Residual tumour islets may regress spontaneously after incomplete excision of MNET, but the relapse rate is between 15% and 45%. In our opinion, excising a safety margin of a few mm of apparently healthy bone reduces the risk of relapse. In contrast, the orbital contents should be preserved if they are macroscopically normal. Follow-up consisted of frequent physical examinations and CT scans.

Humans↗

PubMed2002

Molecular genetic analysis of the TP53, PTEN, CDKN2A, EGFR, CDK4 and MDM2 tumour-associated genes in supratentorial primitive neuroectodermal tumours and glioblastomas of childhood.

Supratentorial primitive neuroectodermal tumours (sPNETs) are malignant central nervous system tumours of childhood which are histologically characterized by poorly differentiated neuroepithelial cells with the capacity for divergent differentiation into glial, neuronal, myogenic or melanotic lines. The histological differential diagnosis between sPNET and glioblastoma multiforme (GBM) may be difficult, particularly as GBMs can sometimes demonstrate a poorly differentiated PNET-like phenotype. To identify molecular genetic markers that may distinguish sPNET and GBM, we investigated 12 cerebral sPNETs and six GBMs from paediatric patients for genetic alterations of the TP53, PTEN, CDKN2A, EGFR, CDK4 and MDM2 genes, as well as for allelic loss on chromosome arms 10q and 17p. Mutations of the TP53 tumour suppressor gene were found in one of 12 sPNETs (8%) and two of six GBMs (33%). None of the sPNETs but two of six GBMs (33%, including one GBM with a TP53 mutation) showed allelic losses on chromosome arm 17p. PTEN mutations were detected in one of 12 sPNET (8%) and one of six GBMs (17%). None of the sPNETs and GBMs carried a homozygous deletion involving the CDKN2A tumour suppressor gene. No amplification of the EGFR, CDK4 or MDM2 proto-oncogenes was detected. Taken together, our results indicate that paediatric GBMs differ from sPNETs by a higher incidence of allelic losses on 17p and TP53 mutations. In addition, the patterns of genetic alterations in sPNETs and paediatric GBMs appear to be distinct from those in cerebellar medulloblastomas and adult GBMs, respectively.

Adolescent↗