Methods are provided for treating a cancer patient suffering from a glioblastoma (GBM) by administering to the patient an effective amount of temozolomide, wherein a mass spectrometry analysis of a protein digest of a formalin-fixed tumor sample from the patient evidences an amount of a MGMT fragment peptide less than or substantially equal to 150 amol/g.

One embodiment is a method of treating cancer. The method includes administering a therapeutically effective amount of a compound to a patient. The compound is represented by Formula I: ##STR00001##

The present invention relates to an in vitro method for determine the prognosis of the survival time of a patient suffering from a cancer comprising the steps consisting of i) determining the expression level of the couple DNMT3A/ISGF3 in a sample from said patient, ii) comparing said expression level with a predetermined reference value and iii) providing a good prognosis when the expression level is lower than the predetermined reference value and a poor prognosis when the expression level is higher than the predetermined reference value. The invention also relates a compound which is a DNMT3A/ISGF3 antagonist or a compound which is a DNMT3A/ISGF3 gene expression inhibitor for use in the treatment and prevention of cancer.

The present invention relates to clonal expansion of somatic cells in subjects, and acquired selective advantage of cell clones during the lifetime of a subject. In particular, the invention relates to methods for predicting the development of cancer based on the observation of specific genetic mutations in somatic cell clones, as well as to methods for treating or preventing cancer in a subject, in which clonal expansion of cells comprising specific modifications is observed.

Methods are provided for identifying whether a lung tumor will be responsive to treatment with the combination of the therapeutic agents cisplatin and pemetrexed. Specified ERCC1, TS, p16, and FR fragment peptides are precisely detected and quantitated by SRM-mass spectrometry directly in lung tumor cells collected from lung tumor tissue that was obtained from a cancer patient and compared to reference levels in order to determine if the lung cancer patient will positively respond to treatment with the combination of cisplatin and pemetrexed therapeutic agents.

The invention relates to inhibition of wild-type and certain mutant forms of human histone methyltransferase EZH2, the catalytic subunit of the PRC2 complex which catalyzes the mono- through tri-methylation of lysine 27 on histone H3 (H3-K27). In one embodiment the inhibition is selective for the mutant form of the EZH2, such that trimethylation of H3-K27, which is associated with certain cancers, is inhibited. The methods can be used to treat cancers including follicular lymphoma and diffuse large B-cell lymphoma (DLBCL). Also provided are methods for identifying small molecule selective inhibitors of the mutant forms of EZH2 and also methods for determining responsiveness to an EZH2 inhibitor in a subject.

The present disclosure relates to acetaminophen protein adducts and methods of diagnosing acetaminophen toxicity using the acetaminophen protein adducts.

Methods are provided for treating a cancer patient suffering from a glioblastoma (GBM) by administering to the patient an effective amount of temozolomide, wherein a mass spectrometry analysis of a protein digest of a formalin-fixed tumor sample from the patient evidences an amount of a MGMT fragment peptide less than or substantially equal to 150 amol/g.

The present disclosure relates to acetaminophen protein adducts and methods of diagnosing acetaminophen toxicity using the acetaminophen protein adducts.

The present disclosure relates to acetaminophen protein adducts and methods of diagnosing acetaminophen toxicity using the acetaminophen protein adducts. The present disclosure provides acetaminophen (APAP)-protein adducts and methods of detecting acetaminophen-induced toxicity in a subject using APAP-protein adducts. One aspect of the present disclosure provides an APAP-protein adduct for diagnosing acetaminophen-induced toxicity. According to the present disclosure, the inventors have identified proteins that are modified by N-acetyl-pbenzoquinoneimine (NAPQI) in subjects with acetaminophen-induced toxicity. Non-limiting examples of proteins modified by NAPQI include betaine-homocysteine S-methyltransferase 1, cytoplasmic aspartate aminotransferase, 1,4-alpha-glucan branching enzyme, formimidoyltransferase-cyclodeaminase, and dystrophin.