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Clone 6h2

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The Clone 6H2.1 is a laboratory equipment product offered by Agilent Technologies. It is designed to perform a specific core function, but a detailed and unbiased description cannot be provided without the risk of extrapolation or interpretation.

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Lab products found in correlation

Iplex system, by Labcorp (2 mentions) Ki 67 clone mib 1, by Agilent Technologies (1 mentions) Clone 6f11, by Leica (1 mentions) Phospho s6, by Cell Signaling Technology (1 mentions)

Close spelling variants of this product

PTEN (clone 6H2.1,

4 protocols using clone 6h2

1

Immunohistochemical Biomarker Analysis

Cited 2 times
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IHC staining for ER (clone 6F11, Novocastra, Leica Biosystems), PgR (clone 1A6, Novocastra), Ki67 (clone MIB-1, Dako, Glostrup, Denmark) and c-erbB2 (HER2/neu, A0485 polyclonal antibody, Dako) on each slide was performed as previously described,14 (link) while detection of cyclin D1 (clone SP4, Spring Bioscience, USA), phosphatase and tensin homolog (PTEN) (clone 6H2.1, code M3627, Dako) and mammalian target of rapamycin (mTOR) (clone 49F9, code 2976, Cell Signaling Technology, Danvers, Massachusetts, USA) proteins was performed as mentioned in earlier published studies.2 15 (link)
Mountzios G., Kotoula V., Kolliou G.A., Papadopoulou K., Lazaridis G., Christodoulou C., Pentheroudakis G., Skondra M., Koutras A., Linardou H., Razis E., Papakostas P., Chrisafi S., Aravantinos G., Nicolaou I., Goussia A., Kalogeras K., Pectasides D, & Fountzilas G. (2019). Cyclin D1 differential activation and its prognostic impact in patients with advanced breast cancer treated with trastuzumab. ESMO Open, 4(2), e000441.
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2

Genetic Characterization of PTEN-Altered Tumors

Cited 2 times
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Enrollment in cohort B required a documented genetic alteration (inactivating mutation or homozygous deletion) in the PTEN gene identified by the clinically validated, custom hybrid capture targeted next generation sequencing (NGS) assay, MSK-IMPACT, using methods previous described. [24 (link)]
Archival formalin-fixed paraffin-embedded (FFPE) tumor specimens were collected from patients in cohort A (where available) and subjected to mass spectrometry genotyping using the iPLEX system (Sequenom, San Diego, CA) using a multiplexed system for genotyping PIK3CA, AKT1, KRAS, NRAS, and BRAF.[25 (link)–27 (link)] For patients in cohort A and B, tumor PTEN expression was scored as 0, 1+, or 2+, according to previously described immunohistochemistry (IHC) methods (Dako, clone 6H2.1).[28 ] For Cohort A only, to characterize the drug elimination phase, plasma levels of buparlisib were determined from samples collected at the following time points on cycle 1/day 1: 0, 15, 30, and 60 min; 2, 3, 4.5, 6, and 8 h. On cycle 1/day 8, an additional PK blood sample was collected prior to treatment with buparlisib. Day 8, 0 h was considered as 168-h post-dose to perform the PK analysis for AUC0–168 h. The area under the curve (AUC0→∞), half-life (t½), and maximum concentration (Cmax) for buparlisib were determined by noncompartmental analysis, as previously described.[11 (link),18 (link)]
Smyth L.M., Monson K.R., Jhaveri K., Drilon A., Li B.T., Abida W., Iyer G., Gerecitano J.F., Gounder M., Harding J.J., Voss M.H., Makker V., Ho A.L., Razavi P., Iasonos A., Bialer P., Lacouture M.E., Teitcher J.B., Erinjeri J.P., Katabi N., Fury M.G, & Hyman D.M. (2017). A phase 1b dose expansion study of the pan-Class I PI3K inhibitor buparlisib (BKM120) plus carboplatin and paclitaxel in PTEN deficient tumors and with dose intensified carboplatin and paclitaxel. Investigational new drugs, 35(6), 742-750.
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3

Mutational Analysis of Oncogenic Drivers

Cited 1 time
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Formalin-fixed paraffin-embedded (FFPE) tumor specimens, obtained as part of standard oncologic management, were subjected to mass spectrometry genotyping using the iPLEX system (Sequenom, San Diego, CA) using a multiplexed system for genotyping PIK3CA, AKT1, KRAS, NRAS, and BRAF [11 (link)–13 (link)]. Additionally, tumor PTEN expression was scored as 0, 1+, or 2+, according to previously described immunohistochemistry (IHC) methods (Dako, clone 6H2.1) [14 (link)].
Hyman D.M., Snyder A.E., Carvajal R.D., Gerecitano J.F., Voss M.H., Ho A.L., Konner J., Winkelmann J.L., Stasi M.A., Monson K.R., Iasonos A., Spriggs D.R., Bialer P., Lacouture M.E., Teitcher J.B., Katabi N, & Fury M.G. (2015). Parallel phase Ib studies of two schedules of buparlisib (BKM120) plus carboplatin and paclitaxel (q21 days or q28 days) for patients with advanced solid tumors. Cancer chemotherapy and pharmacology, 75(4), 747-755.
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4

Immunohistochemical Analysis of Molecular Markers

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Immunohistochemical analyses were carried out with antibodies specific for ATRX (n = 31) (Clone BSB108, 1:200; Bio SB, Santa Barbara, USA), MIB-1 labeling index (n = 31) (Clone M7240, 1:200; Aligent-Dako, Les Ulis, France), monoclonal mouse anti-human PTEN (n = 31) (Clone 6H2.1, 1:100; Dako, Les Ulis, France), Phospho-S6 (n = 31) (Ser235/236, 1:400; Cell Signaling Technology Inc, Leiden, The Netherlands), H3K27me3 (n = 31) (Clone A0821D, 1:1250; Diagenode, Seraing, Belgium), and BRAFV600E (n = 18) (Clone VE1, 1:100; Spring Biosciences, Pleasanton, USA) on the Benchmark XT immunostainer.
Gareton A., Tauziède-Espariat A., Dangouloff-Ros V., Roux A., Saffroy R., Castel D., Kergrohen T., Fina F., Figarella-Branger D., Pagès M., Bourdeaut F., Doz F., Puget S., Dufour C., Lechapt E., Chrétien F., Grill J, & Varlet P. (2019). The histomolecular criteria established for adult anaplastic pilocytic astrocytoma are not applicable to the pediatric population. Acta Neuropathologica, 139(2), 287-303.
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