Clinicopathological features and global genomic copy number alterations of pilomyxoid astrocytoma in the hypothalamus/optic pathway: comparative analysis with pilocytic astrocytoma using array-based comparative genomic hybridization

Jeon, Yung Jin; Cheon, Jung Hee; Kim, Seung-Ki; Wang, Kyu-Chang; Cho, Byung-Kyu; Park, Sung Sup

doi:10.1038/modpathol.2008.88

Cited by 36 publications

(20 citation statements)

References 40 publications

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“…Amplification of 8q24.3 occurs commonly in sporadic breast cancer (45) and squamous cell cervical carcinoma (46), two types of carcinomas that display a tendency toward SIPL1 expression with PTEN positivity. Increases in the copy number at the 8q24.3 locus were also observed in astrocytoma (47), gastroesophageal junction cancer (48), prostate cancer (49), chemoresistant ovarian cancer (50), larynx and pharynx squamous cell carcinoma (51), liver cancer (52,53), and colorectal cancer (54,55). Taken together, these observations suggest that amplification of SIPL1 facilitates the tumorigenesis of multiple human cancers.…”

Section: Discussionmentioning

confidence: 98%

Shank-interacting protein–like 1 promotes tumorigenesis via PTEN inhibition in human tumor cells

He¹,

Ingram²,

Rybak³

et al. 2010

J. Clin. Invest.

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Inactivation of phosphatase and tensin homolog (PTEN) is IntroductionWhile PTEN displays phosphatase activity for both protein and lipid substrates (1), accumulating evidence reveals that its lipid phosphatase activity, which dephosphorylates the 3ʹ-position phosphate from the inositol ring of phosphatidylinositol 3,4,5-triphosphate (PIP 3 ) (2, 3), contributes to PTEN's tumor suppression activities. Thus, PTEN directly antagonizes a critical oncogenic activity mediated by PI3K (4, 5).Consistent with its biochemical functions, inactivation of PTEN is a critical step during tumorigenesis. Typical mechanisms responsible for PTEN inactivation in human cancers include genetic and epigenetic events. The PTEN gene is frequently mutated in human cancers (6-8), including more than 50% of glioblastomas and melanomas, 30%-50% of endometrial carcinomas, and 10% of breast cancers (4, 9, 10). A missense mutation, PTEN/G129E, leading to loss of PTEN's PIP 3 phosphatase activity (4, 11), was detected in Cowden disease (12), a multiple hamartoma syndrome with predisposition to multisystemic malignant tumors (13). Hypermethylation of the PTEN promoter in sporadic colorectal cancers and reduction of PTEN protein without mutations in the PTEN gene in prostate and cervical cancers have also been observed (14-16).Inactivation of PTEN is known to contribute to cervical tumorigenesis. Low levels (2%-16%) of mutations in the PTEN gene as well as the loss of heterozygosity of PTEN have been reported in cervical cancer (17)(18)(19)(20). Consistent with the hypermethylation of PTEN in cervical cancer, reduction in the PTEN protein was observed in approximately 15% of cervical squamous cell carcinomas (21,22). Furthermore, essential pathways that promote cervical tumorigenesis have been shown to inhibit PTEN function. The E6 and E7

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Section: Discussionmentioning

confidence: 98%

Shank-interacting protein–like 1 promotes tumorigenesis via PTEN inhibition in human tumor cells

He¹,

Ingram²,

Rybak³

et al. 2010

J. Clin. Invest.

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“…Furthermore, results of a recent genome-wide gene copy number analysis provided additional argument for the "spectrum disease" thesis (Jeon et al, 2008). Interestingly, the same study reported worse survival of patients with the above mentioned mixed-form PMA/PA in comparison to classical chiasmatic-hypothalamic PAs and also observed one PMA that transferred into a PA after recurrence.…”

Section: Discussionmentioning

confidence: 79%

“…Most studies underline the histological resemblance of PMA to PA and propose a similar astrocytic origin, however, the cell origin and exact pathogenesis of the PMA are still unclear (Fuller et al, 2001;Chikai et al, 2004;Jeon et al, 2008). Growing evidence suggests that the two tumor types are pathologically and genetically related.…”

Section: Discussionmentioning

confidence: 99%

Differential imaging characteristics and dissemination potential of pilomyxoid astrocytomas versus pilocytic astrocytomas

et al. 2015

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“…Pilocytic astrocytoma and pilomyxoid astrocytoma have signifi cant overlap in clinical and radiographic features, histologic features [ 126 ], and genetic aberrations [ 127 ]. Tumors with intermediate features are typically found in older patients, and cases of "maturation" of pilomyxoid astrocytoma into pilocytic astrocytoma [ 126 ] have been documented.…”

Section: Pilocytic-pilomyxoid Spectrummentioning

confidence: 99%

Tumors of the Central Nervous System

Fung

Petropoulou

2014

Pediatric Malignancies: Pathology and Imaging

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Knowledge of normal neuroanatomy and neurodevelopment is critical to proper diagnosis. A few normal structures may be mistaken as tumor particularly on frozen sections.The external granular layer (Fig. 6.1a ) is a layer of small neurons that covers the external surface of fetal/infant cerebellum. It is quite prominent at the time of birth but is almost completely regressed by the ninth postnatal month. It should not be misinterpreted as medulloblastoma or lymphocytic infi ltration in younger infants. The internal granular layer is also composed of small neurons. Without a size comparison, these cells may be mistaken for medulloblastoma or other small blue cell tumors in minute specimens or cytologic preparations. Conversely medulloblastoma cells, particularly those with smaller nuclei, can be mistaken as internal granular cells. Purkinje cells are rather large and should not be mistaken as rhabdoid cells (Fig. 6.1b ). Other normal structures that can be mistaken for neoplastic tissue include the posterior pituitary and the pineal gland which may be mistaken as glial neoplasm and normal choroid plexus being mistaken as choroid plexus papilloma. These misinterpretations are likely to be committed when the specimen is minute and communication between the pathologist and the neurosurgeon is poor. Overview and Classifi cationTumor of the CNS is not uncommon in the pediatric age group and some of these entities occur only rarely in adults (Table 6.1 ). While meningiomas are very common in adults, it is uncommon in children and almost nonexistent in infants. The most common pediatric tumors in descending order of frequency are pilocytic astrocytoma, diffuse astrocytomas, medulloblastomas, and craniopharyngiomas. Ependymal neoplasms and schwannomas are the most frequent infratentorial tumors. Most tumors occur in the brain with a supratentorial-to-infratentorial ratio of approximately 2-to-1. Malignant CNS neoplasms represent 16.6 % of all malignancies in the pediatric age group. In general, the incidence is higher in males than females and among white compared to black children. The incidence is 36.2 per million between infancy and 7 years of age and 21.0 per million between 7 and 10 years of age. As a group, they are the second most frequent malignancy and most common solid tumor in pediatric patients. About 2,200 new cases are diagnosed annually in the United States. Among CNS malignancies, astrocytic tumors account for 52 %, while medulloblastoma and primitive neuroectodermal tumor (PNET), other gliomas, and ependymomas accounted for 21, 15, and 9 %, respectively [ 2 ].In contrast to adults, there is a high occurrence of malignancies in the cerebellum and brain stem in young children. About 40 % of all thalamic tumors arise in patients under 18 years old and account for 2-5 % of all intracranial tumors in children [ 3 ]. About two third or pediatric thalamic tumors are high grade in histology [ 4 ]. Tumor of the spinal cord represents about 9.9 % and extramedullary tumors are slightly more common than intramedullary...

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Clinicopathological features and global genomic copy number alterations of pilomyxoid astrocytoma in the hypothalamus/optic pathway: comparative analysis with pilocytic astrocytoma using array-based comparative genomic hybridization

Cited by 36 publications

References 40 publications

Shank-interacting protein–like 1 promotes tumorigenesis via PTEN inhibition in human tumor cells

Shank-interacting protein–like 1 promotes tumorigenesis via PTEN inhibition in human tumor cells

Differential imaging characteristics and dissemination potential of pilomyxoid astrocytomas versus pilocytic astrocytomas

Tumors of the Central Nervous System

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