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Recently, evidence has revealed that a phenomenon called "chromothripsis" can trigger between tens and hundreds of genomic rearrangements in multiple cancer samples, promoting the development of cancer.

Mutational analysis was performed on multiple cancer samples with MSI-H that expressed the MLH1 and MSH2 proteins, as demonstrated by immunohistochemistry.

Here, we describe multiple cancer samples in which tens to hundreds of genomic rearrangements have been acquired in a single catastrophic event, a phenomenon we have termed chromothripsis (Greek, chromos for chromosome; thripsis, shattering into pieces).

There is still not enough genomic data from multiple cancer samples from the same patient to track somatic mutation patterns from the primary through to metastatic disease and subsequent drug resistance.

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Indeed, more than half (3059/5518 or 55%%) of the germline derived SVs are present in multiple cancer patient samples reflecting naturally occurring variation in the human population.

This isoform was confirmed by direct sequencing on the original cDNA library and was detected by RT-PCR in multiple additional breast cancer samples (Additional file 5).

The results indicated that SRSF9 expression levels, in comparison with corresponding normal tissue, were elevated with high frequency in multiple types of cancer samples including glioblastoma (18/20), colon adenocarcinoma (18/20), squamous cell lung carcinoma (19/20) and malignant melanoma (15/20).

Finally, in Section 4, we discuss limitations to our method and propose future directions for the approach of simultaneous analysis of multiple-related NGS cancer samples.

We expect that until multiple samples from each individual tumor can be obtained in a widespread manner, it will not be feasible to address the problem of estimating multiple cancer profiles for each tumor sample because of the small sample sizes.

We studied approximately 4000 normal and cancer samples with multiple tissue types from diverse studies, and using linear and nonlinear regression models identified reliable tissue type-invariant DNAm age signatures.

Finally, in a pooled analysis of 3947 samples from multiple cancer types, we corroborated the association of the pathway signature with increased proliferation (PCC=0.50, P=2 × 10 6) and the gene signature of Myc targets expression (PCC=0.49, P=2 × 10 6).

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