Malignant transformation of fibrous dysplasia into chondroblastic osteosarcoma

Kaushik, Shaifali; Smoker, Wendy R. K.; Frable, William J.

doi:10.1007/s002560100436

Cited by 67 publications

(34 citation statements)

References 17 publications

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“…FD is a benign fibro-osseous lesion in which normal bone is replaced by a proliferation of fibrous connective [1]. The disease may present in a monostotic or polyostotic form, affecting one or multiple bones, respectively.…”

Section: Discussionmentioning

confidence: 99%

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Malignant Sarcomatous Transformation of Fibrous Dysplasia

Mardekian

Tuluc

2014

Head and Neck Pathol

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Section: Discussionmentioning

confidence: 99%

“…The humerus, pelvis, tibia and scapula are less commonly involved [4]. Warning signs that should alert clinicians to consider malignant transformation include rapidly increasing pain without apparent trauma, increase in serum alkaline phosphatase, or a significant rapid change in radiologic appearance [1,7].…”

Section: Discussionmentioning

confidence: 99%

Malignant Sarcomatous Transformation of Fibrous Dysplasia

Mardekian

Tuluc

2014

Head and Neck Pathol

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“…The pituitary gland in MAS patients may show GH-and PRLproducing cell hyperplasia, as in CNC patients [71]. The consequences of hypersomatotropinemia in MAS can be, however, grave since PFD seems to be getting worse in the presence of elevated GH levels [72] which have also been implicated in sarcomatous transformation of these bone tumors [73]. GH-producing tumors in MAS show a consistent but inadequate response to treatment with cabergoline, and an intermediate response to long-acting octreotide; GH-receptor antagonists have recently been proposed as effective medical agents for inoperable MAS pituitary tumors or for simple hypersomatotropinemia without a visible adenoma [74,75].…”

Section: Pituitary Tumors As Part Of Mccune-albright Syndromementioning

confidence: 96%

Clinical and molecular genetics of acromegaly: MEN1, Carney complex, McCune–Albright syndrome, familial acromegaly and genetic defects in sporadic tumors

Horvath

Stratakis

2008

Rev Endocr Metab Disord

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Pituitary tumors are among the most common neoplasms in man; they account for approximately 15% of all primary intracranial lesions (Jagannathan et al., Neurosurg Focus, 19:E4, 2005). Although almost never malignant and rarely clinically expressed, pituitary tumors may cause significant morbidity in affected patients. First, given the critical location of the gland, large tumors may lead to mass effects, and, second, proliferation of hormone-secreting pituitary cells leads to endocrine syndromes. Acromegaly results from oversecretion of growth hormone (GH) by the proliferating somatotrophs. Despite the significant efforts made over the last decade, still little is known about the genetic causes of common pituitary tumors and even less is applied from this knowledge therapeutically. In this review, we present an update on the genetic syndromes associated with pituitary adenomas and discuss the related genetic defects. We next review findings on sporadic, non-genetic, pituitary tumors with an emphasis on pathways and animal models of pituitary disease. In conclusion, we attempt to present an overall, integrative approach to the human molecular genetics of both familiar and sporadic pituitary tumors.

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“…Hypersomatotropinemia in MAS can be associated with significant morbidity due to exacerbation of polyostotic fibrous dysplasia in the presence of elevated GH levels [106,113]. Hypersomatotropinemia has also be implicated in sarcomatous transformation of bone tumors in a MAS patient [114]. Treatment of GH-producing tumors in MAS with cabergoline has consistently shown an inadequate response, while long-acting octreotide has demonstrated an intermediate response.…”

Section: Molecular Genetics Of Pituitary Tumorsmentioning

confidence: 99%

Pituitary tumors in childhood: update of diagnosis, treatment and molecular genetics

Keil

Stratakis

2008

Expert Review of Neurotherapeutics

126

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Pituitary tumors are rare in childhood and adolescence, with a reported prevalence of up to 1 per million children. Only 2 -6% of surgically treated pituitary tumors occur in children. Although pituitary tumors in children are almost never malignant and hormonal secretion is rare, these tumors may result in significant morbidity. Tumors within the pituitary fossa are of two types mainly, craniopharyngiomas and adenomas; craniopharyngiomas cause symptoms by compressing normal pituitary, causing hormonal deficiencies and producing mass effects on surrounding tissues and the brain; adenomas produce a variety of hormonal conditions such as hyperprolactinemia, Cushing disease and acromegaly or gigantism. Little is known about the genetic causes of sporadic lesions, which comprise the majority of pituitary tumors, but in children, more frequently than in adults, pituitary tumors may be a manifestation of genetic conditions such as multiple endocrine neoplasia type 1 (MEN 1), Carney complex, familial isolated pituitary adenoma (FIPA), and McCune-Albright syndrome. The study of pituitary tumorigenesis in the context of these genetic syndromes has advanced our knowledge of the molecular basis of pituitary tumors and may lead to new therapeutic developments.

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Malignant transformation of fibrous dysplasia into chondroblastic osteosarcoma

Cited by 67 publications

References 17 publications

Malignant Sarcomatous Transformation of Fibrous Dysplasia

Malignant Sarcomatous Transformation of Fibrous Dysplasia

Clinical and molecular genetics of acromegaly: MEN1, Carney complex, McCune–Albright syndrome, familial acromegaly and genetic defects in sporadic tumors

Pituitary tumors in childhood: update of diagnosis, treatment and molecular genetics

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