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• W1999144365 abstract "The College of American Pathologists offers these templates to assist pathologists in providing clinically useful and relevant information when reporting results of biomarker testing. The College regards the reporting elements in the templates as important elements of the biomarker test report, but the manner in which these elements are reported is at the discretion of each specific pathologist, taking into account clinician preferences, institutional policies, and individual practice.The College developed these templates as educational tools to assist pathologists in the useful reporting of relevant information. It did not issue them for use in litigation, reimbursement, or other contexts. Nevertheless, the College recognizes that the templates might be used by hospitals, attorneys, payers, and others. The College cautions that use of the templates other than for their intended educational purpose may involve additional considerations that are beyond the scope of this document.Completion of the template is the responsibility of the laboratory performing the biomarker testing and/or providing the interpretation. When both testing and interpretation are performed elsewhere (eg, a reference laboratory), synoptic reporting of the results by the laboratory submitting the tissue for testing is also encouraged in order to ensure that all information is included in the patient's medical record and thus readily available to the treating clinical team.Select a single response unless otherwise indicated.Note: Use of this template is optional.**Reporting on the data elements in this template is not required.IDH1/2 Mutation___ Present (specify): ___________________________ Absent___ Cannot be determined (explain): ____________________IDH1 R132H Immunohistochemistry___ Positive___ Negative___ Cannot be determined (explain): ____________________1p/19q Deletion___ 1p/19q codeletion___ 1p only deleted___ 19q only deleted___ Polysomy (specify): ___________________________ Monosomy (specify): ___________________________ None detected___ Cannot be determined (explain): ____________________TP53 Mutation___ Present (specify): ___________________________ Absent___ Cannot be determined (explain): ____________________ATRX Mutation___ Present (specify): ___________________________ Absent___ Cannot be determined (explain): ____________________ATRX Immunohistochemistry___ Loss of nuclear expression___ Intact nuclear expression___ Cannot be determined (explain): ____________________EGFR Amplification___ Present___ Absent___ Cannot be determined (explain): ____________________10q23 (PTEN Locus) Deletion___ Deletion identified___ Polysomy (specify): ___________________________ Monosomy (specify): ___________________________ None detected___ Cannot be determined (explain): ____________________PTEN Mutation___ Present (specify): ___________________________ Absent___ Cannot be determined (explain): ____________________MGMT Promoter Methylation___ PresentIf laboratory reports by level: ___ Low level ___ High level___ Absent___ Cannot be determined (explain): ____________________BRAF Mutation___ BRAF V600E (c.1799T>A) mutation present___ Other BRAF mutation present (specify): _________________ Absent___ Cannot be determined (explain): ____________________BRAF V600E Immunohistochemistry___ Positive___ Negative___ Cannot be determined (explain): ____________________BRAF Rearrangement___ Present___ Absent___ Cannot be determined (explain): ____________________Ki-67Percentage of positive nuclei: ____ %Nuclear β-Catenin Immunohistochemistry___ Positive (nuclear staining in at least 50% of tumor cells)___ Negative (no staining or nuclear staining in <50% of tumor cells)___ Cannot be determined (explain): ____________________Monosomy 6___ Present___ Absent___ Cannot be determined (explain): ____________________GAB1 Immunohistochemistry___ Positive___ Negative___ Cannot be determined (explain): ____________________MYC Amplification___ Present___ Absent___ Cannot be determined (explain): ____________________MYCN Amplification___ Present___ Absent___ Cannot be determined (explain): ____________________Isochromosome 17 (i17q)___ Present___ Absent___ Cannot be determined (explain): ____________________INI1 (BAF47) Immunohistochemistry___ Loss of nuclear expression___ Intact nuclear expression___ Cannot be determined (explain): ____________________SMARCB1/INI1/HNSF5 Mutation___ Present (specify): ___________________________ Absent (wild-type SMARCB1/INI1/HNSF5)___ Cannot be determined (explain): ____________________IDH1/2 Mutational AnalysisTesting Method (select all that apply)___ Direct Sanger sequencing___ Pyrosequencing___Polymerase chain reaction (PCR), allele-specific hybridization___ Real-time PCR___ High-throughput next-generation sequencing___ Other (specify): ______________________Immunohistochemistry for IDH1 R132HPrimary Antibody___ H09___ Other (specify): ________________________1p/19q Deletion AnalysisTesting Method (select all that apply)___ In situ hybridization___ Cytogenomic microarray (CMA)___ Loss of heterozygosity___ Other (specify): __________________________TP53 Mutational AnalysisTesting Method (select all that apply)___ Direct Sanger sequencing___ Pyrosequencing___ PCR, allele-specific hybridization___ Real-time PCR___ High-throughput next-generation sequencing___ Other (specify): ________________________ATRX Mutational AnalysisTesting Method (select all that apply)___ Direct Sanger sequencing___ Pyrosequencing___ PCR, allele-specific hybridization___ Real-time PCR___ High-throughput next-generation sequencing___ Other (specify): ________________________Immunohistochemistry for ATRXPrimary AntibodySpecify: ________________________EGFR Amplification AnalysisTesting Method (select all that apply)___ In situ hybridization___ CMA___ Other (specify): ________________________Chromosome 10q23 (PTEN Locus) Deletion AnalysisTesting Method (select all that apply)___ In situ hybridization___ CMA___ Loss of heterozygosity___ Other (specify): ________________________PTEN Mutational AnalysisTesting Method (select all that apply)___ Direct Sanger sequencing___ Pyrosequencing___ PCR, allele-specific hybridization___ Real-time PCR___ High-throughput next-generation sequencing___ Other (specify): ________________________MGMT Promoter MethylationTesting Method (select all that apply)___ Methylation-specific PCR___ Other (specify): ________________________BRAF V600E Mutational AnalysisMutations Assessed (select all that apply)___ V600E___ Any mutation in exon 15___ Other (specify): ________________________Testing Method (select all that apply)___ Direct Sanger sequencing___ Pyrosequencing___ PCR, allele-specific hybridization___ Real-time PCR___ High-throughput next-generation sequencing___ Other (specify): ________________________Immunohistochemistry for BRAF V600EPrimary Antibody___ VE1___ Other (specify): ________________________BRAF Rearrangement AnalysisTesting Method (select all that apply)___ In situ hybridization___ CMA___ Real-time PCR___ Other (specify): ________________________Immunohistochemistry for Ki-67Primary Antibody___ MIB1___ SP6___ Other (specify): ________________________Immunohistochemistry for β-CateninPrimary Antibody___ E-5___ 14___ β-catenin-1___ Other (specify): ________________________Monosomy 6 AnalysisTesting Method (select all that apply)___ In situ hybridization___ CMA___ Other (specify): ________________________Immunohistochemistry for GAB1Primary AntibodySpecify: ________________________MYC Amplification AnalysisTesting Method (select all that apply)___ In situ hybridization___ CMA___ Other (specify): ________________________MYCN Amplification AnalysisTesting Method (select all that apply)___ In situ hybridization___ CMA___ Other (specify): ________________________Isochromosome 17 (i17q) AnalysisTesting Method (select all that apply)___ In situ hybridization___ CMA___ Other (specify): ________________________Immunohistochemistry for INI1 (BAF47)Primary Antibody___ MRQ-27___ 25/BAF47___ Other (specify): ________________________SMARCB1/INI1/HNSF5 Mutational AnalysisTesting Method (select all that apply)___ Direct Sanger sequencing___ Pyrosequencing___ PCR, allele-specific hybridization___ Real-time PCR___ High-throughput next-generation sequencing___ Other (specify): ______________________COMMENTSThe diagnosis of CNS tumors increasingly relies on molecular genetic applications to aid in classification, offer prognostic value, and predict response to therapy.1–6 These applications may assess genetic losses, amplifications, translocations, mutations, or the expression levels of specific gene transcripts or proteins. Molecular diagnostics is quickly transitioning from testing for one biomarker at a time to a panel-based approach and whole-genome analysis. Frequently employed methods for genetic testing are gene sequencing, fluorescence in situ hybridization, and CMA. In some cases, immunohistochemistry can be used as a surrogate for genetic analysis when the marker gene is consistently overexpressed or underexpressed. This template for reporting results of biomarker testing for CNS tumors represents a common framework for the reporting of molecular findings relevant to these diseases and does not advocate their specific application.Isocitrate dehydrogenase (IDH) is an enzyme that exists in 5 isoforms, each of which catalyzes the reaction of isocitrate to α-ketoglutarate.7 The finding of mutations in IDH1 and IDH2 in diffuse gliomas has dramatically changed the practice of neuropathology and neurooncology. Mutations in IDH1 are frequent (70%–80%) in World Health Organization (WHO) grades II and III astrocytomas, oligodendrogliomas, and oligoastrocytomas, as well as glioblastomas (GBMs; WHO grade IV) that have progressed from these lower-grade neoplasms (secondary GBMs).8 Mutations in IDH2 have also been detected in these same tumor types, but much less frequently. IDH mutations are infrequent in de novo GBMs. The mutant forms of IDH1 and IDH2 lead to the production of the oncometabolite 2-hydroxyglutarate, which inhibits the function of numerous α-ketoglutarate–dependent enzymes.9 Inhibition of the family of histone demethylases and the ten-eleven translocation (TET) family of 5-methylcytosine hydroxylases has a profound effect on the epigenetic status of mutated cells and leads directly to a hypermethylator phenotype that has been referred to as the CpG island methylator phenotype (G-CIMP).10 The finding of IDH mutations in an infiltrating glioma is associated with substantially improved prognosis, grade for grade. Indeed, IDH-mutant GBMs, WHO grade IV, are associated with longer survival than IDH wild-type anaplastic astrocytomas, WHO grade III. More than 90% of IDH1 mutations in diffuse gliomas occur at a specific site and are characterized by a base exchange of guanine to adenine within codon 132, resulting in an amino acid change from arginine to histidine (R132H). Because of this consistent protein alteration, a monoclonal antibody has been developed to the mutant protein, allowing its use in paraffin-embedded specimens (mIDH1R132H).11 The ability of the antibody to detect a small number of cells as mutant may make this method more sensitive than sequencing for identifying R132H-mutant gliomas. However, mutations in IDH2 and other mutations in IDH1 will not be detected using immunohistochemistry with this antibody.One of the best-studied relationships between genetic alterations and glioma histology is the strong association of allelic losses on chromosomes 1p and 19q and the oligodendroglioma phenotype.12,13 Approximately 60% to 80% of oligodendroglial neoplasms demonstrate combined 1p and 19q losses, and those oligodendrogliomas that are morphologically classic have even higher frequencies.14 Most studies have indicated that combined losses of 1p and 19q are specific to oligodendrogliomas, with only a few astrocytomas and a small subset of oligoastrocytomas harboring these alterations. Those oligodendrogliomas with 1p/19q loss show enhanced response to chemotherapy and are associated with prolonged survival. Codeletion of 1p/19q occurs by an unbalanced translocation after which only one copy of the short arm of chromosome 1 and one copy of the long arm of chromosome 19 remain and der(1;19)(q10;p10) is produced.15 Solitary losses of 1p or 19q are also occasionally noted within an infiltrating glioma, but they are not as strongly linked to the oligodendroglioma histology and are not predictive of enhanced response to therapy or prolonged survival.13 Polysomy of 1p, 19q, or both is also noted in a subset of oligodendrogliomas and has been associated with a poor prognosis, independent of deletion status.16,17 Codeletion of 1p/19q is highly associated with the IDH1 mutation, with more than 80% of 1p/19q codeleted oligodendrogliomas also carrying the IDH1 mutation.18 Oligodendrogliomas of grades II and III that have 1p/19q codeletion also have a high frequency of TERT promoter mutations, CIC mutations on the remaining chromosome 1p allele, and FUBP1 mutation on the remaining 19q allele.18,19Mutations of TP53 are found in more than 60% to 80% of infiltrative astrocytomas, anaplastic astrocytomas, and secondary GBMs, yet are rare in oligodendrogliomas.8,20,21 The vast majority of diffuse astrocytomas that have IDH mutations also harbor a TP53 mutation.22 In one study, 80% of anaplastic astrocytomas and GBMs that had an IDH1 or IDH2 mutation also carried a TP53 mutation. Conversely, TP53 mutations were identified in only 18% of high-grade astrocytomas that lacked an IDH1 or IDH2 mutation.8 Thus, there is a strong association between IDH1 mutation and TP53 mutation in diffuse astrocytomas, and this combination of mutations is helpful in distinguishing astrocytomas from oligodendroglimas. Immunohistochemical reactivity for the p53 protein is often used as a marker for astrocytic differentiation in diffuse gliomas, because the mutant protein is degraded more slowly and accumulates in the nucleus of tumor cells. This immunostain reacts with both the normal and mutant forms of p53 and therefore is not entirely specific for TP53 mutations.23IDH1 mutation and TP53 mutation in infiltrating gliomas are strongly associated with inactivating alterations in alpha thalassemia/mental retardation syndrome X-linked (ATRX), a gene that encodes a protein involved in chromatin remodeling.22,24 ATRX mutations are a marker of astrocytic lineage among the IDH-mutant gliomas and are mutually exclusive with 1p/19q codeletion. Mutations are most frequent in grade II (67%) and grade III (73%) astrocytomas and secondary GBMs (57%), whereas they are uncommon in primary GBMs and oligodendrogliomas. Nearly all diffuse gliomas with IDH and ATRX mutations also harbor TP53 mutation and are associated with the alternative lengthening of telomeres (ALT) phenotype.24 Immunohistochemistry for ATRX demonstrates a loss of protein expression in neoplastic cells that harbor inactivating mutations, whereas expression is retained in nonneoplastic cells within the sample (eg, endothelial cells).25,26Epidermal growth factor receptor (EGFR) is a transmembrane receptor tyrosine kinase, the ligands of which include EGF and transforming growth factor α (TGF-α). EGFR is the most frequently amplified oncogene in astrocytic tumors, being amplified in more than 40% of all GBMs and less frequently in anaplastic astrocytomas (5%–10%).27 EGFR amplification is much more frequent in de novo (primary) GBMs than in secondary GBMs.28 Approximately one-half of those GBMs with EGFR amplification also have specific EGFR mutations (the vIII mutant), which produce a truncated transmembrane receptor with constitutive activity. Both EGFR amplification and the EGFRvIII mutant are mutually exclusive with IDH mutations. EGFR amplification is specific to those gliomas that are astrocytic in differentiation and of higher grade, such as anaplastic astrocytoma, WHO grade III, and GBM, WHO grade IV.29 This molecular finding can be useful in distinguishing the morphologically similar small-cell GBMs, which harbor the amplification, from anaplastic oligodendrogliomas, which do not.30Loss of the entire chromosome (monosomy), deletions, and copy-neutral loss of heterozygosity (LOH) of chromosome 10 occur in 60% to 95% of GBMs and less frequently in grade II or III diffuse astrocytomas.28 Loss of large regions at 10p, 10q23, and 10q25-26 loci, or loss of an entire copy of chromosome 10 are the most frequent genetic alterations in GBMs.1 Loss of the long arm, which occurs more frequently than the short arm in GBMs, occurs equally in primary and secondary GBMs. The PTEN gene at 10q23.3 has been most strongly implicated as a glioma-related tumor suppressor on chromosome 10q, with PTEN mutations identified in about 25% of GBMs and less frequently in anaplastic astrocytomas, WHO grade III.29 PTEN mutations are more common in primary GBMs than secondary GBMs. Losses on chromosome 10 and mutations in PTEN are considered to be specific for astrocytic differentiation and are rare in oligodendrogliomas. They are also markers of high-grade progression and aggressive clinical behavior in astrocytomas.4,31 The clinical significance of polysomy involving chromosome 10 is not fully understood.The current standard therapy for GBM includes radiation and chemotherapy with temozolomide, which acts by crosslinking DNA by alkylating multiple sites, including the O6 position of guanine.32 DNA crosslinking at the O6 position of guanine is reversed by the DNA repair enzyme MGMT (O6-methylguanine-DNA methyltransferase). Thus, low levels of MGMT expression by GBM cells would be expected to be associated with an enhanced response to alkylating agents. The expression level of MGMT is determined in large part by the methylation status of the gene's promoter. This “epigenetic silencing” of MGMT occurs in 40% to 50% of GBMs and can be assessed by its promoter methylation status on PCR-based tests of genomic DNA. Some laboratories report the promoter methylation statuses as “low level” and “high level,” or indicate that “partial methylation” is present, yet the clinical implications of this distinction are not fully understood. Most investigations have shown that epigenetic gene silencing of MGMT is a strong predictor of prolonged survival, independent of other clinical factors or treatment.33 It has also been demonstrated that MGMT promoter methylation is associated with prolonged progression-free and overall survival in patients with GBM treated with chemotherapy and radiation therapy.33,34Genomic alterations involving BRAF are common in sporadic cases of pilocytic astrocytoma and result in the downstream activation of the ERK/MAPK pathway.2 BRAF activation in pilocytic astrocytoma occurs most commonly through a gene fusion between KIAA1549 and BRAF, producing a fusion protein that lacks the BRAF regulatory domain and demonstrates constitutive activity.35 This fusion is seen in most cerebellar and midline pilocytic astrocytomas, but it is present at a lower frequency in cerebral tumors.36 Cerebral hemispheric pilocytic astrocytomas are more likely to harbor activating BRAF V600E point mutations. Other genomic alterations in pilocytic astrocytomas include other BRAF gene fusions, RAF1 rearrangements, and RAS mutations, but these are less common. Given the role of neurofibromatosis 1 (NF1) deficiency in activating the ERK/MAPK pathway, BRAF genomic alterations are uncommon in pilocytic astrocytomas associated with NF1. BRAF point mutations (V600E) are also observed in other low-grade gliomas and glioneuronal neoplasms, including approximately two-thirds of pleomorphic xanthoastrocytomas and lower percentages of ganglioglioma, desmoplastic infantile ganglioglioma, and dysembryoplastic neuroepithelial tumor.37 Although these tumor types are most frequently encountered in children, they are also occasionally seen in adults and have similar BRAF mutations. Although less common, diffusely infiltrative gliomas, including GBM, particularly the epithelioid variant, may also demonstrate the V600E mutation.27,38–40 More recently, BRAF mutations have been identified in papillary craniopharyngiomas.41The most reliable and technically feasible marker of proliferation for gliomas is Ki-67, a nuclear antigen expressed in cells actively engaged in the cell cycle but not expressed in the resting phase, G0.5 Results are expressed as a percentage of positively staining tumor cell nuclei (Ki-67 labeling index). Numerous investigations have demonstrated a positive correlation between Ki-67 indices and histologic grade for astrocytomas, oligodendrogliomas, and oligoastrocytomas.42,43 Among grades II and III diffuse gliomas, the Ki-67 index provides prognostic value because there is a strong inverse relation with survival on multivariate analysis.42 In contrast, investigations of Ki-67 proliferation on patient outcome for GBM, WHO grade IV, have consistently concluded that it does not provide prognostic value in this set of tumors.44 One potential shortcoming of Ki-67 as a marker is the high degree of variability in tissue processing, immunohistochemical staining, and quantization techniques between laboratories, making it difficult to standardize proliferation indices.45 Large variations in proliferation rates within a single tumor may also be noted. Nonetheless, when interpreted uniformly within a given laboratory, the Ki-67 proliferation index provides prognostic value to clinicians and can be helpful in histologically borderline cases, such as those that are at the grades II to III and III to IV border. A high labeling index in this setting may indicate a more aggressive neoplasm.Medulloblastomas are primitive embryonal neoplasms of the cerebellum, generally arising in childhood, whose molecular genetic alterations have now been well defined. Four subgroups have been described based on gene expression profiles: wingless (WNT), sonic hedgehog (SHH), “group 3,” and “group 4.”3,46 WNT medulloblastomas display monosomy 6, and most also show nuclear accumulation of the WNT pathway protein β-catenin, the latter serving as a useful immunohistochemical screen for this group.47 Medulloblastomas with more than 50% nuclear staining for β-catenin have been shown to have WNT pathway activation, CTNNB1 mutations, and monosomy 6, whereas those with only focal nuclear staining do not.48 The overall survival rates for WNT pathway medulloblastomas are dramatically longer than those of the other subtypes, and clinical practices are changing in light of this.49 SHH medulloblastomas often show a nodular/desmoplastic histology and are associated with a better prognosis in younger children and infants. The 9q deletion is characteristic of the SHH group, and MYCN amplifications are occasionally noted. GAB1 is expressed in the cytoplasm of nearly all SHH medulloblastomas but not in other groups, and can be detected immunohistochemically, making it a valuable SHH-group marker.47 Targeted therapies directed at this subgroup have been established and are entering clinical practice.50,51 Group 3 has the worst overall prognosis and contains the vast majority of MYC-amplified tumors. MYC and MYCN amplifications are strong negative prognostic factors, although they occur in only a small percentage of cases.49 Approximately 30% to 40% of all medulloblastomas have i(17q), making it the most common genetic defect. Those tumors with i(17q) have a worse prognosis than those that do not. Among the genetic markers for medulloblastoma, monosomy 6 (or nuclear β-catenin immunoreactivity), GAB1 expression, MYC or MYCN amplification, and i(17q) appear to be the most reliable and carry the strongest prognostic and therapeutic implications.The atypical teratoid/rhabdoid tumor (AT/RT) is a clinically aggressive embryonal tumor of infancy that occurs in the posterior fossa and cerebral hemispheres.6 The tumor is characterized by deletions and mutations of SMARCB1/INI1 (HSNF5) (22q11.2).52,53 Immunohistochemical evaluation of AT/RT for the INI1 protein (using the BAF47 antibody) shows a loss of labeling in tumor cell nuclei but retention of nuclear labeling in nonneoplastic cells, such as endothelial cells. The recognition of AT/RT is important for clinical management because AT/RTs have morphologic overlap with medulloblastoma, CNS primitive neuroectodermal tumor, choroid plexus carcinoma, GBM, and other malignant tumors of childhood.54 The diagnosis of AT/RT and the finding of SMARCB1/INI1 loss or mutation also carry potential implications for inheritance. These tumors are often a component of the rhabdoid tumor predisposition syndrome, characterized by germline mutations of SMARCB1/INI1 and manifested by a marked predisposition to the development of malignant rhabdoid tumors of infancy and early childhood.52,55 Up to one-third of AT/RTs arise in the setting of rhabdoid tumor predisposition syndrome, and most of these occur within the first year of life.56 The diagnosis of rhabdoid tumor predisposition syndrome is established with certainty by sequencing of SMARCB1/INI1 on tissue representing the patient's germline. Because of the risk associated with the rhabdoid tumor predisposition syndrome, the germline status of SMARCB1/INI1 is typically assessed for each new case of AT/RT." @default.
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• W1999144365 title "Template for Reporting Results of Biomarker Testing of Specimens From Patients With Tumors of the Central Nervous System" @default.
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• W1999144365 doi "https://doi.org/10.5858/arpa.2014-0588-cp" @default.
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