Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Chondrosarcoma”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 289 records · Page 16Linked to original sources
PubMed2002

Radiotherapy for chordomas and low-grade chondrosarcomas of the skull base with carbon ions.

PURPOSE: Compared to photon irradiation, carbon ions provide physical and biologic advantages that may be exploited in chordomas and chondrosarcomas. METHODS AND MATERIALS: Between August 1998 and December 2000, 37 patients with chordomas (n = 24) and chondrosarcomas (n = 13) were treated with carbon ion radiotherapy within a Phase I/II trial. Tumor conformal application of carbon ion beams was realized by intensity-controlled raster scanning with pulse-to-pulse energy variation. Three-dimensional treatment planning included biologic plan optimization. The median tumor dose was 60 GyE (GyE = Gy x relative biologic effectiveness). RESULTS: The mean follow-up was 13 months. The local control rate after 1 and 2 years was 96% and 90%, respectively. We observed 2 recurrences outside the gross tumor volume in patients with chordomas. Progression-free survival was 100% for chondrosarcomas and 83% for chordomas at 2 years. Partial remission after carbon ion radiotherapy was observed in 6 patients. Treatment toxicity was mild. CONCLUSION: These are the first data demonstrating the clinical feasibility, safety, and effectiveness of scanning beam delivery of ion beams in patients with skull base tumors. The preliminary results in patients with skull base chordomas and low-grade chondrosarcomas are encouraging, although the follow-up was too short to draw definite conclusions concerning outcome. In the absence of major toxicity, dose escalation might be considered.

Adolescent↗
PubMed2001

Alterations in the regulatory pathway involving p16, pRb and cdk4 in human chondrosarcoma.

The G1 regulatory pathway involving p16, pRb and cdk4 in the cell cycle has been investigated in human chondrosarcoma. The protein expression of p16, pRb and cdk4 was analyzed by Western blot in cultured cells from eight chondrosarcomas and in two chondrosarcoma cell lines. Both cell lines and one other sample were negative for p16. Moreover, one of the cell lines was pRb-negative and showed a high expression of cdk4 as well. In the other cell line and in three other samples pRb of expected size were detected in addition to a shorter form of the protein. To further investigate the reasons for down-regulation of the p16 protein, the p16-coding gene CDKN2 was analyzed by polymerase chain reaction (PCR), methyl-specific PCR (MSP) and sequencing in all tumor samples as well as in corresponding tumor tissues from three of the samples. The p16-negative samples were all found to have homozygous deletion of CDKN2. Another sample showed partial gene methylation and a heterozygous position in codon 148 was detected in one sample. The same base substitution was also found in two of the tissue samples. Finally, cytogenetic analysis of the samples with homozygously deleted CDKN2 revealed multiple structural abnormalities in all three cases. In conclusion, the p16/pRb/cdk4 pathway may play an important role in the pathogenesis of some chondrosarcomas.

Bone Neoplasms↗
PubMed2002

Serum cartilage-derived retinoic acid-sensitive protein (CD-RAP) levels in swarm rat chondrosarcoma.

Cartilage-derived retinoic acid-sensitive protein (CD-RAP) is a new protein that was isolated from bovine articular chondrocytes and human melanoma cell lines (melanoma inhibitory protein or MIA). In normal tissue its expression is limited to cartilage, and in morbid tissue to melanoma, chondrosarcoma, and breast cancer. Serum levels of CD-RAP/MIA correlate with the progression of malignant melanoma, but there have been no reports on chondrosarcoma. Here, it was first demonstrated by RT-PCR and immunohistological methods that CD-RAP was expressed in tissue from a Swarm rat chondrosarcoma that was used as an experimental model. The course following tumor transplantation and changes in serum CD-RAP after tumor excision were then observed to investigate whether serum CD-RAP could be used as a marker of tumor activity. Consequently, serum CD-RAP in control rats tended to decrease as the animal grew, whereas it rose in proportion to tumor proliferation in rats that had received a tumor graft. Serum CD-RAP levels dropped rapidly following excision of the tumor in a group of tumor-excised rats. In those rats which had a recurrence following excision of the tumor, serum CD-RAP rose prior to the appearance of the tumor. Serum CD-RAP thus sensitively reflected tumor onset and proliferation, so that it appeared to be an effective marker of tumor activity for Swarm rat chondrosarcoma.

Animals↗
PubMed2003

Inhibition of MMP-1 expression by antisense RNA decreases invasiveness of human chondrosarcoma.

We previously reported that an elevated level of matrix metalloproteinase-1 (MMP-1) gene expression in patients with chondrosarcoma has a strong statistical correlation with recurrence and in vitro invasion. In the present study, we used an antisense RNA strategy for MMP-1 inhibition to determine if this would affect the invasive characteristics of the cells. We transfected a human chondrosarcoma cell line with a retroviral plasmid expressing a 770 bp genomic fragment of the human MMP-1 gene in the sense or antisense orientation. The results show that cells transfected with the MMP-1 antisense fragment had a significant decrease in both MMP-1 protein and enzyme activity (p<0.05) as compared to cells transfected with an empty plasmid or the parental cells. Cells transfected with the MMP-1 antisense fragment demonstrated a significant decrease in their ability to invade the collagen I barrier (p<0.05). The gene expression for MMP-8 and MMP-13 were unaffected in cells transfected with the MMP-1 antisense fragment, MMP-1 sense fragment, or empty plasmid. These results support the hypothesis that MMP-1 facilitates tumor cell egress from chondrosarcoma tissue and demonstrate the potential of MMP-1 as a promising target for a novel biologic therapy in chondrosarcoma.

Cell Movement↗
PubMed1997

Chondrosarcomas of the skull base: review of the literature and report of two cases.

Chondrosarcomas are malignant mesenchymal tumours occurring only rarely in the bones of the cranium. Less than 5% of all chondrosarcomas are located in the head and neck area and their commonest location is the ethmoids and the sphenoid sinus. They are slow-growing tumours with low malignancy rate and unclear histopathogenesis. The prevailing hypothesis is that they arise from cartilaginous remnants in the petro-clival, spheno-occipital and fronto-nasal synchondroses. Diagnosis is only made after biopsy since clinical signs and symptoms and radiological findings are not pathognomonic. Symptomatology mainly derives from tumour encroachment and infiltration of adjacent intracranial structures. Surgery is the treatment of choice, while radiotherapy has an adjunctive role. Chemotherapy is not effective. Partial tumour excision to alleviate symptoms is an acceptable surgical technique since diagnosis is usually late, but treatment can be repeated when recurrence occurs. During the last year, two cases of chondrosarcoma of the skull base were treated in our institution. Both patients were female, aged 62 and 73, respectively. Computerized Tomography and Magnetic Resonance Imaging were inconclusive and diagnosis was established after biopsy. Treatment for both cases was surgical, with partial excision due to intracranial involvement of the internal carotid artery. In one case, a temporal approach was used, whereas the other patient was operated on via a naso-orbital approach. One patient received postoperative radiotherapy. The postoperative course was uneventful in both patients and marked clinical improvement was noted 18 months and 1 year after surgery. We support the view that partial resection of chondrosarcomas of the base of the skull to alleviate symptoms is an acceptable surgical treatment.

Aged↗
PubMedDate not supplied

Chondrosarcoma of the proximal phalanx.

An 87-year-old male presented with a painless, large mass on the dorsum of the left foot. He reported that the mass had first appeared 10 years ago and now had become so large that he could no longer tie his shoe. The mass originated from the proximal aspect of the second digit, encompassing the second web space and distal one third of the second and third metatarsals. Surgical excision of the mass was performed and pathologic diagnosis of the specimen confirmed a grade 1 chondrosarcoma. As expected with a lower grade chondrosarcoma, the patient did not have metastasis and fully recovered. While the occurrence of chondrosarcoma is not uncommon, it rarely affects the foot. This appears to be the third case of chondrosarcoma appearing in the proximal phalanx second digit of the foot.

Aged↗
PubMed1979

Chondrosarcoma of the larynx.

A chondrosarcoma arising in the posterior cricoid plate is presented. The tumour gave rise to increasing inspiratory stridor: laryngectomy was performed. The tumour consisted of loose cartilaginous tissue with great predominance of highly differentiated cartilage cells and only small areas with nuclear polymorphism. This complicated the differential diagnosis between chondroma and highly differentiated chondrosarcoma. From the fact that the patient died from massive pulmonary metastases 3 1/2 years later, it is evident that the degree of malignancy of cartilaginous tumours should be determined even on small polymorphic foci. The DNA histogram for the foci of the laryngeal tumour with atypia differed distinctly from those for benign chondroma and normal cartilage, but resembled those of the pulmonary and splenic metastases and of a nasal chondrosarcoma. Photometric examination may provide an aid in the difficult differential diagnosis between chondroma and highly differentiated chondrosarcoma.

Chondrosarcoma↗
PubMed2000

Intracranial low-grade chondrosarcoma with hyperostosis of the skull: a case report.

We describe a case of intracranial chondrosarcoma in a 46-year-old woman. The preoperative diagnosis was meningioma as plain radiography and computed tomography of the head revealed a tumor with discrete calcifications predominantly in the right frontoparietal region and hyperostosis of the inner table of the skull overlying the tumor. However, the tumor was histologically composed of cartilaginous tissue without meningiomatous differentiation and the final diagnosis was a low-grade chondrosarcoma based on its histological appearance and size, together with the radiologic images. Intracranial chondrosarcoma occurring above the skull base is extremely rare and 19 cases were found in our literature review. Intracranial chondrosarcoma showing hyperostosis of the skull has not been reported in the cases. The discussion includes its differential diagnosis, origin, and clinical behavior.

Chondrosarcoma↗
PubMed2002

Inhibition of human chondrosarcoma cell growth via apoptosis by peroxisome proliferator-activated receptor-gamma.

A rare immunohistochemical study using 28 surgical sections of human chondrosarcoma revealed that 67.9% of tumour cells had weak (10-40%) or strong (>40%) positive immunoreaction for peroxisome proliferator-activated receptor-gamma. The expression of peroxisome proliferator-activated receptor-gamma mRNA and protein in human chondrosarcoma cell line OUMS-27 was also determined by reverse transcription-polymerase chain reaction and immunocytochemistry, respectively. Furthermore, the effects of peroxisome proliferator-activated receptor-gamma ligands on cell proliferation and survival were investigated in OUMS-27 cells. Pioglitazone, a selective ligand for peroxisome proliferator-activated receptor-gamma, and 15-deoxy-Delta(12,14)-prostaglandin J(2) (15d-PGJ(2)), a putative endogenous ligand for peroxisome proliferator-activated receptor-gamma, inhibited the proliferation of OUMS-27 cells in a dose-dependent manner. The mechanism of cytotoxic effects of 15d-PGJ(2) was via apoptosis as shown by DNA fragmentation using TUNEL stain and DNA ladder formation, and by ultrastructural analysis using transmission electron microscopy. Flow-cytometric analysis using annexin-V-fluorescein and propidium iodide detected the early change of apoptosis, as well as necrosis of OUMS-27 cells at 4 h after co-incubation with 15d-PGJ(2). These results suggest that peroxisome proliferator-activated receptor-gamma may play a significant role in the pathogenesis of chondrosarcoma, and peroxisome proliferator-activated receptor-gamma ligands, especially 15d-PGJ(2), may be of therapeutic value in the treatment of human chondrosarcoma.

Apoptosis↗
PubMed2004

p38 MAP kinase signaling is necessary for rat chondrosarcoma cell proliferation.

Chondrosarcomas represent the second most frequent class of primary skeletal malignancies. This tumor type is highly resistant to radiation therapy and currently available chemotherapies, thereby limiting treatment choice to surgical resection. Identifying the mechanisms responsible for chondrosarcoma cell proliferation is therefore crucial for the development of new treatment strategies. Here, we demonstrate a significant reduction in rat chondrosarcoma cell proliferation following treatment with pharmacological inhibitors (SB202190 and PD169316) of p38 mitogen-activated protein (MAP) kinases. In an attempt to dissect possible mechanisms, we investigated the effect of p38 inhibition on promoter activity of cell-cycle genes. Surprisingly, p38 inhibition resulted in upregulation of the activities of all three D-type cyclin promoters. In addition, p38 inhibitors induced increased transcription of the cell-cycle inhibitor p21(waf1/cip1). As expected, promoter activity of the cyclin A gene, which lies downstream of D-type cyclins and p21 in cell-cycle progression, was strongly reduced by p38 inhibitors. These effects were independent of a cyclic AMP response element and conferred by the proximal 150 nucleotides of the cyclin A promoter. Decreased transcription was accompanied by greatly reduced cyclin A protein levels upon p38 inhibition. These observations indicate complex regulation of chondrosarcoma cell-cycle progression by p38 signaling, and suggest that components of p38 MAP kinase pathways may be effective targets in the treatment of these tumors.

Animals↗
PubMed1990

Purification and characterization of a hyaluronan-binding protein from rat chondrosarcoma.

Swarm rat chondrosarcoma contains a hyaluronan-binding protein of molecular mass 102 kDa (HABP102). The protein is present in 4 M-guanidinium chloride extracts of the chondrosarcoma and can be incorporated into reconstituted proteoglycan aggregates, but it is not present in native proteoglycan aggregates or in 0.5 M-guanidinium chloride extracts. HABP102 is unlikely to be an integral membrane protein, as it does not require detergent for extraction, is not enriched in hydrophobic amino acids and does not bind avidly to octyl-Sepharose. The protein stains poorly with Coomassie Blue and is only visible on PAGE gels after staining with silver. Disulphide bonds are essential for the binding of HABP102 to hyaluronan, and bivalent cations are not required for this interaction. HABP102 can be purified from dissociative chondrosarcoma extracts by sequential density-gradient centrifugation, hyaluronan-Sepharose affinity chromatography and hydrophobic-interaction chromatography. The amino acid composition is similar to that of domains 1-4 of the chondrosarcoma proteoglycan core protein, but peptide analysis after digestion with Staphylococcus aureus V8 proteinase and chymotrypsin and different immunoreactivity suggest that HABP102 is not closely related to proteoglycan hyaluronan-binding region. HABP102 is a glycoprotein containing N-acetylgalactosamine, N-acetylglucosamine, mannose and galactose.

Amino Acids↗
PubMed1999

High-grade extraskeletal myxoid chondrosarcoma: a high-grade epithelioid malignancy.

AIMS: Extraskeletal myxoid chondrosarcoma is typically a low-to-intermediate grade sarcoma that is associated with a prolonged clinical course. High-grade forms are rare and not well characterized. In this series we report the clinicopathological, immunohistochemical and ultrastructural findings in four cases of high-grade extraskeletal myxoid chondrosarcoma. METHODS AND RESULTS: The patients were three men and one woman (ages 34-73 years) with tumours located in the thigh (two cases), paraspinal soft tissue and perineum. Three patients had metastases, one at 12 weeks, one at 10 months, and one at presentation of recurrent tumour. In the latter case the original tumour was low grade and became high grade when it recurred 3.5 years later. All three patients died of disease. One patient was lost to follow-up. The most striking histological feature in all four tumours was the presence of numerous large epithelioid cells. These cells were arranged in cords within myxoid matrix and in sheets devoid of matrix. Two tumours had areas of conventional extraskeletal myxoid chondrosarcoma intermixed with the high-grade areas. One tumour showed transition to high-grade spindle cell sarcoma. One tumour had cells with rhabdoid features. Immunohistochemically, two tumours focally expressed S100 protein, and one focally expressed EMA. All were negative with cytokeratin, desmin, smooth muscle actin, HMB45, CD31 and CD34. Ultrastructural features in three cases were compatible with chondrosarcoma; one tumour had aggregates of microtubules within rough endoplasmic reticulum, a characteristic feature of this tumour. CONCLUSIONS: High-grade extraskeletal myxoid chondrosaroma is a rare and aggressive soft tissue sarcoma, and should be included in the differential diagnosis of other epithelioid malignancies.

Adult↗
PubMed2003

Sox9, a master regulator of chondrogenesis, distinguishes mesenchymal chondrosarcoma from other small blue round cell tumors.

Over the last decade, a number of "master regulator" genes that control distinct pathways of mesenchymal differentiation have been discovered. These genes are expressed early during embryogenesis and initiate a cascade of gene expression responsible for specific cell lineage commitment. Thus, identification of their products may allow the classification of seemingly primitive, morphologically uncommitted tumors such as small blue round cell tumors. The transcription factor Sox9 has been demonstrated to be a master regulator of the differentiation of mesenchymal cells into chondrocytes. For this reason, we examined the utility of Sox9 in distinguishing mesenchymal chondrosarcoma (a small cell malignancy thought to be derived from primitive chondroprogenitor cells) from other primitive small cell malignancies. Representative sections from 90 cases of small blue round cell tumors (22 mesenchymal chodrosarcoma, 10 neuroblastomas, 11 rhabdomyosarcomas, 9 Ewing's sarcomas/primitive neuroectodermal tumors, 5 desmoplastic small round cell tumors, 7 small cell carcinomas, 6 Merkel cell carcinomas, 6 small cell osteosarcomas, 7 diffuse large B-cell lymphomas, 7 lymphoblastic leukemias/lymphomas, and 5 extraskeletal myxoid chondrosarcomas) were immunohistochemically stained with antibodies to Sox9 protein. All but 1 mesenchymal chondrosarcoma showed positive nuclear staining in both primitive mesenchymal and cartilaginous components of the tumor. All other types of small blue round cell tumors, as well as the lymphomas and leukemias, were negative for Sox9 protein. These findings confirm that mesenchymal chondrosarcoma has phenotypic features corresponding to the early condensational phase of cartilaginous differentiation. More important, Sox9 may serve as a useful tool in the differentiation of small cell malignancies.

Adolescent↗
PubMed1996

Chondrosarcoma of the skull base: CT, MR and pathological features.

We report on CT and MR image findings of a skull base chondrosarcoma. Chondroid mineralisation, a histological feature of chondrosarcoma, can be recognised on CT and is, together with the off-midline position of the tumour, the most characteristic finding. Differentiation is usually made by histological and immunocytochemical staining. Surgery, proton radiation therapy and stereotactic single high-dose irradiation have been used to treat patients with chondrosarcoma. It is worth mentioning that it was likely that the chondrosarcoma in our patient represented a malignant degeneration of an enchondroma that had been resected 30 years earlier.

Aged↗
PubMed1983

Inhibition of growth of the transplantable rat chondrosarcoma by analogs of hypothalamic hormones.

The Swarm chondrosarcoma is a hormone-responsive tumor whose growth is dependent on growth hormone, somatomedins, and glucocorticoids. Our previous work showed that partial functional hypophysectomy can be achieved by chronic administration of the luteinizing hormone-releasing hormone (LH-RH) analog [D-Trp(6)]LH-RH, which lowers blood levels of LH and follicle-stimulating hormone. We have also demonstrated that somatostatin (SS)-28 or analogs of SS-14 depress serum prolactin, growth hormone, and corticotropin (ACTH) levels. Consequently, we investigated the effect of subcutaneous injection of these analogs on the growth of Swarm chondrosarcoma 3 days after transplanting it into male Sprague-Dawley rats. At autopsy, tumor volume was measured and tumors and various organs were weighed. In rats treated with three different analogs of SS-14, [p-NH(2)-Phe(4)]SS, [D-5-F-Trp(8)]SS, and [D-5-MeO-Trp(8)]SS, in doses of 30 mug once or twice daily for 14-30 days, there was a significant reduction in tumor volume and/or weight as compared with control rats. The longer acting SS-28 or its analog Val-Gly-Tyr-Val-Ile-Leu-Gly-SS-28, given in doses of 30 mug/day for 22-30 days, also significantly decreased tumor weight and/or volume. In three experiments, [D-Trp(6)]LH-RH (30-60 mug/day), administered alone or together with analogs of SS-14, decreased tumor weight and/or volume. Serum growth hormone and prolactin levels in rats bearing the tumors were significantly decreased after treatment with [D-5-F-Trp(8)]SS or with [D-Trp(6)]LH-RH. The inhibition of growth of the Swarm chondrosarcoma in rats by these analogs suggests that they might lead to a new endocrine therapy for chondrosarcomas, osteosarcomas, and related hormone-dependent neoplasias.

Animals↗
PubMed2002

Endostatin inhibits adhesion of endothelial cells to collagen I via alpha(2)beta(1) integrin, a possible cause of prevention of chondrosarcoma growth.

Endostatin derived from collagen XVIII is a potent endogenous anti-angiogenic factor that induces regression of various tumors of epithelial origin. Endostatin has been shown to inhibit endothelial cell functions, however, its effect remains controversial. We first attempted here to apply the inhibitory effect of recombinant human endostatin on chondrosarcomas, which originate from the mesenchyme, in nude mice. Endostatin induced reduction of chondrosarcoma growth and tumor angiogenesis in vivo. However, endostatin showed no effect on the proliferation and migration of chondrosarcoma cells in vitro. Next, we investigated the interactions between endostatin and endothelial cells in detail. Endostatin inhibited the migration on and attachment to collagen I but did not affect the proliferation of endothelial cells. Although the migration of endothelial cells was stimulated by angiogenic factors such as basic fibroblast growth factor and vascular endothelial growth factor, endostatin showed similar inhibitory effects on it in the presence and absence of the stimulants. Moreover, the inhibitory effect against endothelial cell attachment to collagen I was attenuated or modulated in the presence of neutralizing antibodies of alpha(2), alpha(5)beta(1), and alpha(V)beta(3) integrins but not that of alpha(1) integrin. Our results suggest that endostatin might suppress the alpha(2)beta(1) integrin function of endothelial cells via alpha(5)beta(1) or alpha(V)beta(3) integrin. We propose here that endostatin might be effective for anti-angiogenic therapy for human chondrosarcomas through the suppression of alpha(2)beta(1) integrin functions in endothelial cells.

Animals↗
PubMed1992

Chondroid chordomas and low-grade chondrosarcomas of the craniospinal axis. An immunohistochemical analysis of 17 cases.

The classification of cartilaginous neoplasms of the craniospinal axis is controversial. Indeed, the very existence of chondroid chordomas has recently been questioned. In an effort to clarify the direction of differentiation of cartilaginous neoplasms of this region, 17 neoplasms obtained from 17 patients with cartilaginous tumors of the craniospinal axis were examined by immunohistochemistry with a panel of antibodies. The panel included antibodies to cytokeratin (CK), epithelial membrane antigen (EMA), vimentin (VIM), S-100 protein, carcinoembryonic antigen (CEA), and type II collagen. Areas with cartilaginous differentiation were present in all 17 neoplasms. These areas were characterized by a matrix of amorphous blue ground substance with lacunae that contained enlarged and slightly atypical cells. This cartilaginous matrix stained strongly for type II collagen. Thirteen of the 17 neoplasms had a biphasic growth pattern in which areas with conventional chordoma were admixed with areas with cartilaginous differentiation. The cells within the cartilaginous components of these 13 neoplasms stained for CK (10 of 12 cases), EMA (10 of 13 cases), VIM (12 of 12 cases), S-100 protein (seven of 12 cases), and CEA (two of nine cases). Similarly, the conventional chordoma components of these same 13 neoplasms stained for CK (12 of 12 cases), EMA (13 of 13 cases), VIM (12 of 12 cases), S-100 protein (nine of 12 cases), and CEA (two of nine cases). The hyaline-appearing areas between the cords and sheets of cells of the conventional chordoma components of these 13 tumors also stained with type II collagen. These 13 tumors with both neoplastic cartilage and conventional chordoma were classified as chondroid chordomas. One of the 17 cases was composed entirely of neoplastic cartilage; however, the cells within the matrix of the cartilage of this neoplasm stained with the epithelial markers (CK and EMA). Based on the presence of epithelial differentiation within this otherwise cartilaginous neoplasm, it was also classified as a chondroid chordoma. In contrast, the remaining three cases without histologic evidence of chordoma differentiation did not stain for CK or EMA, but they did stain for S-100 protein (three of three cases) and VIM (three of three cases). These three tumors were therefore classified as chondrosarcomas. For purposes of comparison, 19 conventional chordomas without cartilage and 29 peripheral chondrosarcomas were also stained. The 19 conventional chordomas stained in a pattern similar to the conventional chordoma components of the chondroid chordomas, whereas the 29 peripheral chondrosarcomas stained in a pattern similar to the three chondrosarcomas of the craniospinal axis.(ABSTRACT TRUNCATED AT 400 WORDS)

Adolescent↗
PubMedDate not supplied

Chondrosarcoma of the hand arising from a pre-existent benign solitary enchondroma.

Chondrosarcomas of the hand are relatively rare. Chondrosarcomas may arise by malignant transformation of a pre-existing enchondroma, but this causal relationship has been difficult to establish in solitary enchondroma. This is a case report of a chondrosarcoma of the proximal phalanx of the right index finger in a 66-year-old woman demonstrating histologic evidence of malignant transformation of a pre-existent benign solitaary enchondroma. Careful analysis of the preoperative X-ray for punctate endosteal calcification or cortical expansion and ample histologic sampling of the endosteal component of chondrosarcomas arising from within bone may demonstrate a greater incidence of preexistent enchondroma.

Aged↗