Validation of the Myelofibrosis Secondary to PV and ET-Prognostic Model in Newly Diagnosed Patients with Post-Polycythemia Vera and Post-Essential Thrombocythemia Myelofibrosis: MD Anderson Cancer Center

The recently proposed Myelofibrosis Secondary to PV and ET-Prognostic Model (MYSEC-PM) (Passamonti, Leukemia 2017) refines overall survival in patients with post-polycythemia vera and post-essential thrombocythemia myelofibrosis (PPV, PET-MF) molecularly annotated for JAK2, CALR, and MPL mutations. We aimed to validate the prognostic utility of MYSEC-PM for PET / PPV-MF patients at MD Anderson Cancer Center (MDACC).
Source: Clinical Lymphoma, Myeloma and Leukemia - Category: Hematology Authors: Source Type: research

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The presence of recurrent genetic mutations in the myeloblasts of patients with acute myeloid leukemia (AML) are prognostic and incorporated into risk stratification systems of both the National Comprehensive Cancer Network and European Leukemia Network.1 In patients with FLT3-internal tandem duplications (FLT3-ITD) or tyrosine kinase domain mutations (TKD) small molecule inhibitors of the resultant mutant proteins in combination with cytotoxic chemotherapy can improve overall survival in newly diagnosed AML patients with a FLT3 mutation.
Source: Clinical Lymphoma, Myeloma and Leukemia - Category: Hematology Authors: Tags: Review Article Source Type: research
Conditions:   Cancer;   Breast Cancer;   Lung Cancer;   Colon Cancer;   Ovarian Cancer;   Melanoma;   Lymphoma;   Leukemia;   Mutation;   Lynch Syndrome;   Cowden Syndrome;   BRCA1 Mutation;   BRCA2 Mutation;   Uterine Cancer;   Myeloma;   Kidney Cancer;   Head and Neck Cancer;   Meningioma Intervention:   Sponsor:   University Health Network, Toronto Recruiting
Source: ClinicalTrials.gov - Category: Research Source Type: clinical trials
Emergency general surgery (EGS) in cancer patients is high risk. Solid organ and liquid (lymphoma, leukemia and multiple myeloma) cancers are fundamentally different, which may impact presentation and outcomes.
Source: Journal of the American College of Surgeons - Category: Surgery Authors: Tags: Scientific poster presentations Source Type: research
ConclusionOur proposed nomogram based on Eastern Cooperative Oncology Group performance status, Ann Arbor stage, albumin-to-globulin ratio, and platelet count provides an individualized risk estimate of OS in patients with ENKTL.
Source: Clinical Lymphoma Myeloma and Leukemia - Category: Cancer & Oncology Source Type: research
This study reveals important areas of progress in cancer outcomes in Canada since the early 1990s. It also sheds light on cancers for which there has seemingly been no improvement in five-year net survival over a 20-year period. PMID: 30230521 [PubMed - in process]
Source: Health Reports - Category: International Medicine & Public Health Tags: Health Rep Source Type: research
ConclusionIncidental findings are common, but the majority are of no clinical consequence. No additional cancers were noted in our series. DWI and CE T1-W sequences increased diagnostic confidence in 50% of indeterminate findings and may reduce the need for further investigation.
Source: Clinical Lymphoma Myeloma and Leukemia - Category: Cancer & Oncology Source Type: research
tam Sethi Signal transducer and activator of transcription 3 (STAT3), a member of the STAT protein family, can be phosphorylated by receptor-associated Janus kinases (JAKs) in response to stimulation by cytokines and growth factors. It forms homo- or heterodimers that can translocate to the cell nucleus where they act as transcription activators. Constitutive activation of STAT3 has been found to be associated with initiation and progression of various cancers. It can exert proliferative as well as anti-apoptotic effects. This review focuses on the role of STAT3 in pathogenesis i.e., proliferation, differentiation, mig...
Source: Cancers - Category: Cancer & Oncology Authors: Tags: Review Source Type: research
Type 2 diabetes mellitus and cancer are correlated with changes in insulin signaling, a pathway that is frequently upregulated in neoplastic tissue but impaired in tissues that are classically targeted by insulin in type 2 diabetes mellitus. Many antidiabetes treatments, particularly metformin, enhance insulin signaling, but this pathway can be inhibited by specific cancer treatments. The modulation of cancer growth by metformin and of insulin sensitivity by anticancer drugs is so common that this phenomenon is being studied in hundreds of clinical trials on cancer. Many meta-analyses have consistently shown a moderate but...
Source: Clinics - Category: General Medicine Source Type: research
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