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ABSOLUTE

Infers tumor purity and malignant cell ploidy directly from analysis of somatic DNA alterations. ABSOLUTE can detect subclonal heterogeneity, somatic homozygosity, and calculate statistical sensitivity to detect specific aberrations. It provides a foundation for integrative genomic analysis of cancer genome alterations on an absolute (cellular) basis. It may be possible to extend ABSOLUTE to other types of genomic alterations, such as structural rearrangements and small insertions/deletions.

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1 user review

1 user review

Calvi. C.'s avatar image Calvi. C.'s country flag

Calvi. C.

Only having problems with this tool. (bunch of errors) .. there is no source code to check what could be wrong and not enough support for users

ABSOLUTE forum

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ABSOLUTE classification

  • Animals
    • Homo sapiens

ABSOLUTE specifications

Software type:
Package/Module
Restrictions to use:
None
Programming languages:
R
Stability:
Stable
Interface:
Command line interface
Operating system:
Unix/Linux, Mac OS, Windows
Computer skills:
Advanced
Maintained:
Yes

ABSOLUTE distribution

versioning

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No versioning.

ABSOLUTE support

Maintainer

  • Scott L. Carter <>

Additional information

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Credits

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Publications

Institution(s)

The Broad Institute of Harvard and MIT, Cambridge, MA, USA; Division of Health Sciences and Technology, MIT, Cambridge, MA, USA; USC Epigenome Center, Keck School of Medicine, University of Southern California, Los Angeles, CA, USA; Biophysics Program, Harvard University, Cambridge, MA, USA; Divisions of Medical Oncology and Cancer Biology and Center for Cancer Genome Discovery, Dana-Farber Cancer Institute, Boston, MA, USA; Department of Medicine, Brigham and Women's Hospital, Boston, MA, USA; Howard Hughes Medical Institute, Department of Pediatric Oncology, Dana-Farber Cancer Institute, Children's Hospital, Department of Cell Biology, Harvard Medical School, Boston, MA, USA; Gynecology Service, Department of Surgery, Memorial Sloan-Kettering Cancer Center, New York, NY, USA; Whitehead Institute for Biomedical Research, Cambridge, MA, USA; Department of Systems Biology, Harvard Medical School, Boston, MA, USA; MIT Department of Biology, Cambridge, MA, USA

Funding source(s)

This work was supported by grants from the National Cancer Institute as part of The Cancer Genome Atlas project [U24CA126546, U24CA143867, and U24CA143845]; the National Human Genome Research Institute (NHGRI) [grant T32 HG002295]; the NIH [5R01 GM083299-14, K08CA122833 and U54CA143798]; the DoD [W81XWH-10-1-0222]; the NIH/NIGMS [5 T32 GM008313] and the NRSA [grant F32CA113126].

Link to literature

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