Provided are methods of selecting a patient with cancer and/or treating a patient with cancer that comprises a deleterious alteration in FBXW7 and/or an amplification of CCNL1 for CDK11 inhibitor and/or ATR inhibitor treatment. For example, the method of selecting a patient afflicted with a cancer likely to benefit from a CDK11 inhibitor and/or ATR inhibitor treatment, the method comprising: obtaining a biological sample; testing the sample for i) loss of function FBXW7, optionally for a deleterious mutation in F box WD-repeat containing protein (FBXW7) substrate binding domain and/or ii) upregulated CCNL1, optionally a gain or amplification of CCNL1; and selecting the patient having i) loss of function FBXW7, optionally a deleterious mutation in the FBWX7 substrate-binding domain or ii) upregulated CCNL1, optionally a gain or amplification of CCNL1, as likely to benefit and/or for treatment with the CDK11 inhibitor and/or ATR inhibitor.

Provided are methods of selecting a patient with cancer and/or treating a patient with cancer that comprises a deleterious alteration in FBXW7 and/or an amplification of CCNL1 for CDK11 inhibitor and/or ATR inhibitor treatment. For example, the method of selecting a patient afflicted with a cancer likely to benefit from a CDK11 inhibitor and/or ATR inhibitor treatment, the method comprising: obtaining a biological sample; testing the sample for i) loss of function FBXW7, optionally for a deleterious mutation in F box WD-repeat containing protein (FBXW7) substrate binding domain and/or ii) upregulated CCNL1, optionally a gain or amplification of CCNL1; and selecting the patient having i) loss of function FBXW7, optionally a deleterious mutation in the FBWX7 substrate-binding domain or ii) upregulated CCNL1, optionally a gain or amplification of CCNL1, as likely to benefit and/or for treatment with the CDK11 inhibitor and/or ATR inhibitor.

The present invention provides a mass spectrometry-based method and a kit for genotyping of platelet and neutrophil antigens and glycoproteins, which are used for genotyping of platelet-specific antigens, platelet CD36 glycoproteins and neutrophil antigens; by designing an optimal primer combination, problems such as homologous sequences and rich GC are overcome, moreover, by improving amplification reaction conditions and using nucleic acid mass spectrometry as a platform, 35 platelet-specific antigen polymorphic sites, 10 CD36 polymorphic sites and 8 neutrophil antigen polymorphic sites can be simultaneously detected in 2 reactions. The present invention has the characteristics of high specificity and sensitivity, and fast and high throughput, and can be used in clinic, scientific research, platelet donor routine screening, etc.

The present invention provides a mass spectrometry-based method and a kit for genotyping of platelet and neutrophil antigens and glycoproteins, which are used for genotyping of platelet-specific antigens, platelet CD36 glycoproteins and neutrophil antigens; by designing an optimal primer combination, problems such as homologous sequences and rich GC are overcome, moreover, by improving amplification reaction conditions and using nucleic acid mass spectrometry as a platform, 35 platelet-specific antigen polymorphic sites, 10 CD36 polymorphic sites and 8 neutrophil antigen polymorphic sites can be simultaneously detected in 2 reactions. The present invention has the characteristics of high specificity and sensitivity, and fast and high throughput, and can be used in clinic, scientific research, platelet donor routine screening, etc.

Set forth herein are methods useful for identifying disease biomarkers, particularly for diseases such as clear cell renal cell carcinoma (ccRCC). In some examples, the methods set forth herein are useful for monitoring the prognosis of patients having a disease such as ccRCC.

Set forth herein are methods useful for identifying disease biomarkers, particularly for diseases such as clear cell renal cell carcinoma (ccRCC). In some examples, the methods set forth herein are useful for monitoring the prognosis of patients having a disease such as ccRCC.

Methods for quenching a nuclease digestion of a target nucleic acid prior to downstream analysis of the target nucleic acid are disclosed herein. Particularly, methods for controlling the end point of a nuclease digestion prior to sequence analysis of a target nucleic acid is provided. Quenching of a nuclease digestion in the present disclosure employs at least one non-ionic or anionic denaturant combined with an optional reducing agent. The methods presented in this disclosure aids preserving the sample comprising the target nucleic acid or fragments thereof for long term storage and ensures that the effect of contaminating nucleases is eliminated during pretreatment step.

Methods for quenching a nuclease digestion of a target nucleic acid prior to downstream analysis of the target nucleic acid are disclosed herein. Particularly, methods for controlling the end point of a nuclease digestion prior to sequence analysis of a target nucleic acid is provided. Quenching of a nuclease digestion in the present disclosure employs at least one non-ionic or anionic denaturant combined with an optional reducing agent. The methods presented in this disclosure aids preserving the sample comprising the target nucleic acid or fragments thereof for long term storage and ensures that the effect of contaminating nucleases is eliminated during pretreatment step.

Disclosed is a use of methylation sites as a disease diagnosis marker, in particular relating to a use of methylation sites in a Y chromosome as a prostate cancer diagnosis marker. More particularly, the method and criterion for screening methylation sites in chromosomes associated with a disease are established in the present invention, and using prostate cancer as an example, six methylation sites in the Y chromosome associated with the prostate cancer diagnosis are screened out. Methylation sites in the Y chromosome screened can be used for early and rapid diagnosis of the disease as a prostate cancer diagnosis marker.

Provided herein are compositions and systems for use in polymerase-dependent, nucleotide transient-binding methods. The methods are useful for deducing the sequence of a template nucleic acid molecule and single nucleotide polymorphism (SNP) analyses. The methods rely on the fact that the polymerase transient-binding time for a complementary nucleotide is longer compared to that of a non-complementary nucleotide. The labeled nucleotides transiently-binds the polymerase in a template-dependent manner, but does not incorporate. The methods are conducted under any reaction condition that permits transient binding of a complementary or non-complementary nucleotide to a polymerase, and inhibits nucleotide incorporation.