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PubMed2000

Pigmented (melanotic) neurofibroma: a clinicopathologic and immunohistochemical analysis of 19 lesions from 17 patients.

Neurofibromas with melanin-laden pigmented cells are rare, accounting for less than 1% of all neurofibromas accessioned to the Soft Tissue Registry of the Armed Forces Institute of Pathology between the years 1970 and 1996. This study analyzes the clinicopathologic features associated with 19 specimens removed from 17 patients. Eleven males and six females, ranging in age from 2 to 61 years (median, 28 years), participated in the study. Nine of 15 patients whose race was provided were black. Eight patients (47%) are known to have neurofibromatosis, and two others (12%) are strongly suspected of having this disorder; two patients have similarly affected family members. Eight patients were noted to have multiple skin tumors, and in each of two cases, two pigmented neurofibromas were available for review. Two patients had hypertrichosis and cutaneous hyperpigmentation resembling a hairy nevus, and one had a café au lait spot directly overlying a pigmented neurofibroma. Tumors ranged in size from 1.7 to 50 cm in greatest dimension and involved the buttock or leg (n = 6), head or neck (n = 8), trunk (n = 2), wrist or hand (n = 2), and an unspecified site (n = 1). The neurofibromas exhibited diffuse (n = 15), combined diffuse and plexiform (n = 2), combined diffuse and intraneural epithelioid (n = 1), and nonspecific (n = 1) growth patterns. The process involved the skin (n = 14), subcutis (n = 18), and/or skeletal muscle (n = 3). Wagner-Meissner-like bodies were identified in 11 tumors, and mitoses (average, less than one mitosis per 10 high-power fields) were present in three lesions. All examples contained scattered pigmented cells with dendritic, tadpole-shaped, spindled or epithelioid morphology. These cells were positive with Fontana-Masson (nine of nine) and Warthin-Starry (pH, 3.2; four of four) stains, and were depigmented with a melanin bleach method (two of two). An iron stain was negative. The tumors had immunoreactivity for S-100 protein (11 of 11), HMB-45 ( 10 of 11), Melan-A (four of four), tyrosinase (four of four), and CD34 (four of four). Although recurrences are documented, none of the tumors are known to have undergone malignant transformation. A pigmented neurofibroma can be confused with a pigmented dermatofibrosarcoma protuberans (Bednár tumor) because the melanin-laden cells of both processes are similar. However, the latter entity exhibits a more extensive storiform growth, has greater immunoreactivity for CD34, and lacks a diffuse proliferation of S-100 protein-positive Schwann cells.

Adolescent↗
PubMed2004

Is a plexiform neurofibroma pathognomonic of neurofibromatosis type I?

OBJECTIVES/HYPOTHESIS: Several prominent textbooks have claimed that a plexiform neurofibroma is pathognomonic for neurofibromatosis type I. This is not in agreement with the National Institutes of Health criteria, which require two signs to be present, one of which can be a plexiform neurofibroma. Is a plexiform neurofibroma pathognomonic for neurofibromatosis type I? STUDY DESIGN: Retrospective chart review. METHODS: Fifty-one patients with surgically resected plexiform neurofibromas between the years 1991 and 2001 were identified, and their charts reviewed. The presence and absence of any manifestation of neurofibromatosis type I as detailed in the National Institutes of Health criteria were recorded. The pathology database at the Hospital for Sick Children (HSC) was searched retrospectively. RESULTS: Five of the 51 patients had a single solitary plexiform neurofibroma. They were followed at the neurofibromatosis clinic at the HSC with regular detailed examinations and no other stigmata were found. CONCLUSION: Although plexiform neurofibromas are highly suggestive of neurofibromatosis type I, they are not pathognomonic as claimed.

Adolescent↗
PubMed2004

Plexiform neurofibromas express the transcription factor Gli1.

BACKGROUND: Plexiform neurofibromas occur commonly in individuals with neurofibromatosis type 1 (NF1) and consist of neurofibromatous change in multiple nerve fascicles. Previously, we had observed that both plexiform neurofibromas and normal cutaneous nerves expressed Hedgehogs (Hhs), which are intercellular signaling molecules and regulate growth and patterning during embryonic development, and their receptors. In the present study, we examined the expression of Gli1, a transcription factor which mediates Hh signaling to investigate the activation of Hh signaling in plexiform neurofibromas and normal cutaneous nerves. METHODS: An antihuman Gli1 antibody was used with a standard immunoperoxidase technique to determine Gli1 expression in 5 specimens of plexiform neurofibromas and 5 specimens of normal cutaneous nerves. RESULTS: Our results showed Gli1 expression in S-100-positive tumor cells within the involved nerve fascicles in plexiform neurofibromas but not in control normal skins. CONCLUSIONS: Our findings indicate that the Hh signaling pathway is activated in plexiform neurofibromas.

Biomarkers, Tumor↗
PubMed1994

Semiquantitative aspects of mast cells in normal skin and in neurofibromas of neurofibromatosis types 1 and 5.

Mast cells are supported to influence the growth of neurofibromas, because some of their mediators may also act as growth factors. Accordingly, mast cell stabilizers are claimed to reduce proliferation and itching of neurofibromas. Therefore, we quantified the mast cells of 19 neurofibromas and compared them with normal skin. We saw a statistically significant increase in mast cells in neurofibromas versus normal skin. However, there is no correlation between the age of neurofibromatosis (NF) patients and mast cell density. In our study the density of mast cells in neurofibromas is also independent of NF type; age of neurofibroma and chronic ultraviolet exposure in contrast to normal skin. Different tumors of the same patient had similar mast cell counts.

Adolescent↗
PubMed2004

Immunohistochemical staining for calretinin is useful for differentiating schwannomas from neurofibromas.

We studied 25 cases of schwannoma and 42 cases of neurofibroma immunohistochemically with antibodies to calretinin and S-100 protein to explore the potential usefulness of calretinin in differentiating schwannomas from neurofibromas. Of 25 schwannomas, 24 (96%) showed moderate to strong staining for calretinin, with the extent of staining ranging from focal to diffuse. In contrast, only 3 (7%) of 42 neurofibromas displayed focal weak to moderate staining with calretinin. All 42 cases of neurofibromas and all 25 cases of schwannomas showed diffuse moderate to strong staining with S-100 protein. Calretinin also labeled mast cells, whose presence was confirmed further by staining for c-kit, which commonly was present in both tumor types in a scattered individual cell pattern easily differentiated from the clustered pattern of neoplastic spindle cells. Taken together, these results indicate that calretinin is detected in almost all schwannomas and in only a small percentage of neurofibromas, suggesting it is a useful marker for differentiating schwannomas from neurofibromas. Although mast cells present in these 2 neoplasms also react with calretinin, the pattern of staining can be distinguished easily from that of neoplastic cells.

Calbindin 2↗
PubMed1994

Retroperitoneal plexiform neurofibromas: CT findings.

OBJECTIVE: CT findings in retroperitoneal plexiform neurofibromas have been described previously only in a few case reports. This study was performed to characterize the CT features in a larger group of patients with this benign neoplasm and to delineate those findings that suggest the presence of concurrent malignant tumors of the nerve sheath. MATERIALS AND METHODS: From a review of CT scans showing retroperitoneal masses in 25 patients with neurofibromatosis type 1, we identified 16 patients whose clinical and CT features suggested the diagnosis of plexiform neurofibromas. The diagnosis was confirmed by biopsy of the mass in three patients. In the remaining 13 patients, the diagnosis was supported by long-term follow-up in eight and by biopsy confirmation of either a neurofibroma or a plexiform neurofibroma elsewhere in the body in the other five patients. Concurrent retroperitoneal malignant tumors of the nerve sheath were confirmed by biopsy in five patients. RESULTS: CT showed bilateral, remarkably symmetric masses extending along the medial and posterior aspects of the psoas muscles in 15 of the 16 patients. Parapsoas masses tended to be long and cylindrical. In addition to parapsoas masses, eight patients had bilateral, symmetric masses extending along the anterior aspect of the sacrum in a sheetlike fashion. Masses were identified in the region of the celiac axis and the origin of the superior mesenteric artery in four patients. Only one patient had an isolated celiac/superior mesenteric artery mass without associated parapsoas or presacral masses. Retroperitoneal masses were of homogeneous, low attenuation when compared with adjacent muscle on CT images of 14 patients. Two patients had an unusual swirling and serpiginous pattern of increased attenuation superimposed on a low-attenuation background. Asymmetry in size and attenuation was due to malignant nerve sheath tumors in five patients. CONCLUSION: Retroperitoneal plexiform neurofibromas have a characteristic appearance on CT scans. They are typically bilateral, symmetric, low-attenuation masses in a parapsoas or presacral location. Asymmetry in size and attenuation of a larger mass suggests the possibility of a malignant tumor of the nerve sheath. Recognition of the CT features of a retroperitoneal plexiform neurofibroma can obviate the expense, pain, and risk of an unnecessary biopsy. Conversely, detection of findings suggestive of malignant tumor can lead to appropriate recommendation of biopsy.

Adult↗
PubMed2004

Perineurial cells and nerve axons in gastrointestinal schwannomas: a similarity with neurofibromas. An immunohistochemical study of eight cases.

Gastrointestinal schwannoma (GIS) is a distinctive and extremely rare lesion showing some differences from conventional soft tissue schwannoma and some similarities with common soft tissue neurofibroma. Soft tissue neurofibromas and schwannomas differ by contents of specific types of nerve sheath cells, such as Schwann cells, perineurial cells and CD34+ cells. To compare GIS with these soft tissue lesions, eight cases of typical GIS were studied immunohistochemically to evaluate their nerve sheath cell types. Epithelial membrane antigen (EMA) and claudin-1 as perineurial cell markers, and neurofilament protein as a marker for intratumoral axons were used. In addition, the tumors were stained for cytokeratin, CD117 (C-KIT), alpha-muscle specific actin, S100 protein and CD34. EMA- and claudin-positive cells were seen in 2 (25%) and one lesion, respectively, thus resembling cellular composition of neurofibroma. Intratumoral neurofilament protein positive axons otherwise typical of neurofibroma were found inside 4 tumors (50%). CD34 positivity was found in 6 tumors (75%) and often revealed a diffuse pattern as seen in neurofibroma and not a zonal pattern as described in schwannomas. These results show that GIS has some features that are more typical for neurofibroma than for conventional schwannoma. In surgical pathology practice, a finding of intratumoral axons and positivity for claudin-1 and especially for EMA should not preclude diagnosis of GIS.

Adult↗
PubMed2004

A solitary laryngeal neurofibroma ina pediatric patient.

A neurofibroma of the larynx is a rare disease that usually involves the arytenoids and the aryepiglottic fold. Pediatric patients with a laryngeal neurofibroma often present with progressive dyspnea. A definitive diagnosis of a laryngeal neurofibroma is based on the histopathologic demonstration of the characteristic spindle cells, and a positive result in immunohistochemical staining for S-100 protein. Tumor excision of laryngeal neurofibromas by an external approach was formerly common. We present a case of a solitary laryngeal neurofibroma in a 4-year-old child that was completely excised using direct laryngoscopy and a CO2 laser. There has been no recurrence after a follow-up of 4 years. For pediatric patients with an isolated laryngeal neurofibroma, endoscopic surgery provides an alternative approach due to its safety, effectiveness, and minimal invasiveness.

Child, Preschool↗
PubMed1990

Immunohistochemical demonstration of factor XIIIa expression in neurofibromas. A practical means of differentiating these tumors from neurotized melanocytic nevi and schwannomas.

Neurofibromas, schwannomas, and neurotized melanocytic nevi may closely resemble one another at the light microscopic level. We studied 10 neurofibromas, 10 schwannomas, and 10 partially neurotized melanocytic nevi immunohistochemically using an antibody directed against factor XIIIa to determine if this antibody might provide a useful method of differentiating these lesions. The cases were also stained with S100 protein. All of the neurofibromas stained intensely for factor XIIIa. The proportion of cells staining within the tumors varied from 30% to 70%. In contrast, none of the schwannomas and neurotized nevi studied demonstrated staining of tumor cells with this antibody. S100 protein was expressed by 100% of neurofibromas, schwannomas, and melanocytic nevi. Our findings suggest that factor XIIIa may provide a reliable and practical means of differentiating cutaneous neurofibromas from neurotized nevi and cutaneous schwannomas. Distinguishing between these different tumor types may be important in some clinical situations, particularly with respect to rendering a diagnosis of von Recklinghausen's neurofibromatosis. The differences in the immunohistochemical profiles of neurofibromas and neurotized nevi support the concept that these tumors are histogenetically distinct, despite their similar histologic appearances.

Antigens, Neoplasm↗
PubMed1984

Type IV and V collagens in von Recklinghausen's neurofibromas. An immunohistochemical and electrophoretical study.

Type IV and V collagens were localized in neurofibromas from six patients with von Recklinghausen's neurofibromatosis (NF) using the peroxidase anti-peroxidase (PAP) technique. The collagens were also isolated from neurofibromas by pepsin digestion and fractionating salt precipitations and demonstrated with sodium dodecyl sulphate polyacrylamide gel electrophoresis (SDS-PAGE). Staining reactions for both collagens were detected in most of the cells in the disorganized NF tumor tissue. These cells also were S-100 protein-positive and were considered to be of Schwannian cell origin, while the type IV collagen-negative cells showed fibroblastoid, mast cell and histiocytic characteristics. Type IV collagen detection was also used to study the structure of a neurofibroma after 3 weeks in tissue culture. The proportion of fibroblastoid, type IV collagen-negative cells increased significantly in the cultured neurofibromas and "buds" containing solely fibroblastoid cells were seen at the periphery of the tumor fragments. Cultured 6th passage tumor cells produced type V but no type IV collagen as estimated with SDS-PAGE. Further, two malignant Schwannomas from a patient with NF were stained with antibodies to type IV collagen. A positive staining reaction was associated only with the vascular walls in the malignant Schwannomas suggesting that type IV collagen expression is linked with cell differentiation. The present data show that the detection of type IV collagen using the PAP-method is useful in studying the organization of tumors with mixed cell populations such as neurofibromas. Large neurofibromas might also serve as a source for the isolation of human type IV and V collagens.

Collagen↗
PubMed1992

Effects of several growth factors on cultured neurofibroma cells.

Neurofibromatosis type 1 (NF1) is a common autosomal dominant disorder characterized by abnormalities affecting multiple tissues derived from the neural crest. The peripheral neurofibromas are numerous and sometimes reach several hundred in number. In this study, the possible involvement of several growth factors in neurofibroma growth was investigated in vitro. When explants of neurofibroma tissue were cultured, macrophage-like cells with pseudopodia migrated out first, and later took on a slender fusiform shape. These cells contained S-100 protein and were identified as Schwann cells. They did not proliferate under standard culture conditions. Nerve growth factor (NGF) was helpful in maintaining the differentiated phenotype of Schwann cells, but did not stimulate their proliferation. Immunohistochemical staining for type IV collagen revealed that some large flattened polygonal cells had a mesh of type IV collagen on the surface. These cells were perineurial cells. The proliferation of cells derived from neurofibroma was stimulated by basic fibroblast growth factor (bFGF), epidermal growth factor (EGF), and transforming growth factor alpha (TGF-alpha). In comparison with skin fibroblasts, the cells derived from neurofibroma responded to these growth factors at considerably lower concentrations. Stimulation by EGF at physiological concentrations indicated the possible involvement of EGF in the development of neurofibromas.

Cell Division↗
PubMed1996

Identification of NF1 mutations in both alleles of a dermal neurofibroma.

A hallmark clinical feature of neurofibromatosis 1 (NF1) is multiple dermal neurofibromas, benign tumours that typically appear in early adolescence and increase in numbers throughout life. The pathogenesis of these tumours is not known. One domain of the NF1 gene product, neurofibromin, stimulates the intrinsic GTPase of Ras, and inactivation of both NF1 alleles has been demonstrated in specific malignancies. These observations support the contention that the NF1 gene product is a tumour suppressor that is involved in the Ras signal transduction pathway. Even though accumulating evidence demonstrates that NF1 acts as a tumour suppressor in some cells, mutations have not been identified in both NF1 alleles in dermal neurofibromas. Using standard techniques to analyse DNA extracted from benign neurofibromas, numerous investigators failed to identify loss of heterozygosity (LOH) in multiple tumours. In contrast to these reports, Colman et al. demonstrated NF1 LOH of dermal neurofibromas derived from 2 of 5 NF1 patients, yet the constitutional NF1 mutations in these patients were not identified, and the extent of the somatic deletions beyond the NF1 locus were not established. In this study, we show that a dermal neurofibroma from an NF1 individual who has a constitutional deletion of the entire NF1 locus harbours a 4-bp deletion of NF1 exon 4b in the other allele. This is the first definitive identification of a somatic mutation which is limited to the NF1 locus in a benign neurofibroma from an NF1 individual in whom the constitutional NF1 mutation is known.

Alleles↗
PubMed2003

A possible paracrine hedgehog signalling pathway in neurofibromas from patients with neurofibromatosis type 1.

BACKGROUND: Hedgehogs (Hhs) and their receptors are involved in organ development as well as in tumorigenesis observed in basal cell carcinoma. Among Hhs, Desert hedgehog secreted from Schwann cells mediates the formation of peripheral nerve sheaths. However, there has been no study on the role of Hhs and their receptors in tumorigenesis of neurofibromas in neurofibromatosis type 1 (NF1). OBJECTIVES: To clarify the expression and localization of Hhs and their receptors in neurofibromas of NF1 patients. METHODS: Expression of Hhs and their receptors was studied by immunohistochemistry using neurofibromas from NF1 patients and control normal skin samples. RESULTS: In neurofibromas, CD57-positive tumour cells with delicate elongated processes were positive for the receptor PTCH2. Perineurial cells of involved nerves within neurofibromas as well as those of normal cutaneous nerves expressed Indian hedgehog and Sonic hedgehog. Schwann cells of normal cutaneous nerves were positive for PTCH2. CONCLUSIONS: Our study suggests that a paracrine Hh signalling pathway may be involved in tumorigenesis of neurofibromas in NF1.

CD57 Antigens↗
PubMed1986

Growth-promoting factors in neurofibroma crude extracts.

Crude extracts of neurofibromas from two unrelated neurofibromatosis (NF) patients were prepared by mincing, homogenizing, and ultracentrifugation in the absence of added solvents. Explant cultures of neurofibromas from other NF patients were grown at low density in culture medium with and without neurofibroma extract supplementation. Differences in growth were monitored by comparing monolayer densities, colony counts, or uptake of [3]H-thymidine. A consistent enhancement of growth rate was demonstrated, and titration curves showed an increasing effect with increasing dosage (ranging from 1.5 microliter/ml to 25 microliters/ml). However, the extract could not substitute for fetal bovine serum. As determined by microscopic examination of Giemsa-stained petri dishes, small spindle-shaped cells, distinct in morphology from ordinary fibroblasts, were the overwhelmingly predominant cell type in most extract-treated cultures. While the specific identity of the growth factor(s) involved is unknown, the following may be stated: The presence of one or more growth factors that may act in an autocrine or paracrine manner in neurofibromas in vivo is demonstrated. There is a preferential effect of such a factor on spindle-shaped cells (presumably Schwann cells), allowing for the selective enrichment of these cells in vitro. There is an enhanced yield of clones derived from single cells, allowing further analysis of the cellular heterogeneity of neurofibromas at the biochemical and molecular levels. These considerations should help to distinguish between those models for neurofibroma growth that emphasize secondary somatic mutations (including allelic exclusion) on the one hand, and cellular interaction on the other hand.

Cell Division↗
PubMed1986

Schwann-like cells cultured from human dermal neurofibromas. Immunohistological identification and response to Schwann cell mitogens.

Primary cultures prepared from dermal and plexiform neurofibromas contain Schwann-like cells and fibroblast-like cells. SLC are elongated and bipolar or multipolar. By indirect immunofluorescence light microscopy, living SLC bind antibodies against laminin and against nerve growth factor receptor to their surface, but not antibodies against fibronectin. In these respects, cultured SLC are indistinguishable from cultured human adult Schwann cells. FLC are flat and pleomorphic. By indirect immunofluorescence light microscopy, living FLC bind antibodies against fibronectin but not against laminin or NGFR. In these respects, cultured FLC are indistinguishable from cultured human adult endoneurial fibroblasts. Considerable purification of viable SLC from SLC/FLC mixed cultures can be achieved by flow cytofluorometry using a monoclonal anti-NGFR antibody. Tritiated thymidine radioautography indicated that mitosis of SLC in mixed SLC/FLC cultures prepared from dermal neurofibromas is infrequent in MEM with 10% calf serum, more frequent in RPMI 1640 medium with 15% fetal calf serum. Central nervous system axolemmal fragments (rat or human) elicited a greater than 10-fold SLC proliferative response in mixed SLC/FLC cultures from three of seven dermal neurofibromas (from six patients with neurofibromatosis), but had no effect on SLC mitosis in cultures from the other four dermal neurofibromas. SLC mitosis was inhibited by concentrations of cyclic adenosine 3',5'-monophosphate analogues known to stimulate proliferation of normal rat Schwann cells. Glial growth factor partially purified from bovine pituitaries stimulated SLC mitosis both in SLC/FLC mixed cultures and in cultures of purified SLC. The studies we have described indicate that neurofibroma SLC can be cultured, unequivocally identified in culture by morphological and immunohistological criteria, purified, and stimulated to proliferate by several Schwann cell mitogens. Further quantitative comparisons of the baseline and mitogen-stimulated rates of proliferation of SLC and age-matched control human Schwann cells are needed, however, to determine which of the two alternate pathogenetic mechanisms for formation of neurofibromas mentioned in the introduction is correct.

Axons↗
PubMed2005

Do hormonal contraceptives stimulate growth of neurofibromas? A survey on 59 NF1 patients.

BACKGROUND: Neurofibromas are benign tumors of the peripheral nerves and hallmark of neurofibromatosis type 1 (NF1), a tumor suppressor gene syndrome. Neurofibromas mostly start developing at puberty and can increase in size and number during pregnancy. Expression of progesterone receptors has been found in 75% of the tumors. Many female NF1 patients are thus concerned about the possibility that hormonal contraceptives may stimulate the growth of their neurofibromas. METHODS: A survey was carried out on 59 female NF1 patients who are practicing or have practiced hormonal contraception to examine the effect of the various contraceptives on the growth of neurofibromas. RESULTS: Majority (53 out of 58) of patients who received oral estrogen-progestogen or pure progestogen preparations reported no associated tumor growth. In contrast, significant tumor growth was reported by two patients who received depot contraceptive containing high dose of synthetic progesterone. CONCLUSIONS: Oral contraceptives do not seem to stimulate the growth of neurofibromas in NF1 patients. High doses of progesterone might stimulate the growth of neurofibromas and deserve more caution.

Adolescent↗
PubMed1987

Mast-cell stabilization to decrease neurofibroma growth. Preliminary experience with ketotifen.

Based on (1) the large numbers of mast cells present in neurofibromas, (2) the possibility that these mast cells contribute directly to neurofibroma growth, and (3) the ability of ketotifen therapy to stabilize (ie, block) mast-cell secretion, treatment with ketotifen was started in a patient with severe neurofibromatosis (NF) in August 1983. Subsequently, ten additional patients with one or more symptomatic neurofibromas were treated with comparable doses of ketotifen, 2 to 4 mg/d, orally administered for 30 to 43 months. This represents a total of 389 patient-months or 32.4 patient-years. All of these patients showed an unequivocal decrease in neurofibroma-associated pruritus and/or pain and tenderness; a consistent, but less-uniform, decrease in the rate of neurofibroma growth; and an unexpected improvement in overall sense of well-being, productivity, and general performance. It appears likely that mast-cell secretions do contribute to the growth and associated symptoms of neurofibromas, and that mast-cell blockers, such as ketotifen therapy, can retard this growth.

Adolescent↗
PubMed1993

Possible involvement of c-kit receptor and its ligand in increase of mast cells in neurofibroma tissues.

Many mast cells are present in the tumor tissues of neurofibromatosis 1. We investigated the mechanism of the mast cell increase. Since the stem cell factor (SCF) induces development of mast cells and since the receptor of SCF is encoded by the c-kit gene, we examined the expression of SCF mRNA and c-kit mRNA in neurofibroma tissues. In situ hybridization demonstrated strong expression of c-kit messenger RNA in mast cells in the neurofibroma, but the expression of SCF mRNA was not demonstrable by in situ hybridization in either neurofibroma tissues or control normal skin tissues. When RNA extracted from neurofibroma tissues or normal skin tissues was reverse transcribed and then amplified by the polymerase chain reaction, the amount of SCF cDNA was greater in neurofibroma tissues than in normal skin tissues. The results suggest that SCF and the c-kit receptor are associated with the increase of mast cells in neurofibroma tissues.

Adolescent↗