0000000000150134

AUTHOR

Raju Kandimalla

showing 3 related works from this author

A multidimensional network approach reveals microRNAs as determinants of the mesenchymal colorectal cancer subtype

2016

Colorectal cancer (CRC) is a heterogeneous disease posing a challenge for accurate classification and treatment of this malignancy. There is no common genetic molecular feature that would allow for the identification of patients at risk for developing recurrences and thus selecting patients who would benefit from more stringent therapies still poses a major clinical challenge. Recently, an international multicenter consortium (CRC Subtyping Consortium) was established aiming at the classification of CRC patients in biologically homogeneous CRC subtypes. Four consensus molecular subtypes (CMSs) were identified, of which the mesenchymal CMS4 presented with worse prognosis signifying the impor…

0301 basic medicineMaleCancer ResearchEpithelial-Mesenchymal TransitionGene regulatory networkComputational biologyBiologymedicine.disease_causeEpigenesis Genetic03 medical and health sciencesMolecular Biology; Cancer Research; GeneticsCell Line TumormicroRNAmedicineGeneticsHumansGene Regulatory NetworksEpigeneticsPromoter Regions GeneticMolecular BiologyRegulation of gene expressionCancerComputational BiologyDNA Methylationmedicine.diseasePrognosisSubtyping3. Good healthGene Expression Regulation NeoplasticMicroRNAs030104 developmental biologyPhenotypeMultigene FamilyDNA methylationCancer researchFemaleOriginal ArticleCarcinogenesisColorectal NeoplasmsTranscriptomeOncogene
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Consensus molecular subtypes of colorectal cancer are recapitulated in in vitro and in vivo models

2018

Colorectal cancer (CRC) is a highly heterogeneous disease both from a molecular and clinical perspective. Several distinct molecular entities, such as microsatellite instability (MSI), have been defined that make up biologically distinct subgroups with their own clinical course. Recent data indicated that CRC can be best segregated into four groups called consensus molecular subtypes (CMS1-4), each of which has a unique biology and gene expression pattern. In order to develop improved, subtype-specific therapies and to gain insight into the molecular wiring and origin of these subtypes, reliable models are needed. This study was designed to determine the heterogeneity and identify the prese…

0301 basic medicineStromal cellColorectal cancerCellMice NudeAntineoplastic AgentsApoptosisComputational biologyBiologyModels BiologicalArticle03 medical and health sciencesMiceStructure-Activity Relationship0302 clinical medicineIn vivomedicineBiomarkers TumorTumor Cells CulturedAnimalsHumansMolecular BiologyCell ProliferationRegulation of gene expressionDose-Response Relationship DrugGene Expression ProfilingMesenchymal stem cellMicrosatellite instabilityCell DifferentiationNeoplasms ExperimentalCell Biologymedicine.diseaseGene expression profilingGene Expression Regulation NeoplasticOxaliplatin030104 developmental biologymedicine.anatomical_structure030220 oncology & carcinogenesisFluorouracilDrug Screening Assays AntitumorColorectal NeoplasmsCell death and differentiation
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ΔNp63 drives metastasis in breast cancer cells via PI3K/CD44v6 axis

2016

P63 is a transcription factor belonging to the family of p53, essential for the development and differentiation of epithelia. In recent years, it has become clear that altered expression of the different isoforms of this gene can play an important role in carcinogenesis. The p63 gene encodes for two main isoforms known as TA and ΔN p63 with different functions. The role of these different isoforms in sustaining tumor progression and metastatic spreading however has not entirely been clarified. Here we show that breast cancer initiating cells express ΔNp63 isoform that supports a more mesenchymal phenotype associated with a higher tumorigenic and metastatic potential. On the contrary, the ma…

0301 basic medicineGene isoformEpithelial-Mesenchymal TransitionBreast Neoplasmsmedicine.disease_causeMetastasisMicePhosphatidylinositol 3-Kinases03 medical and health sciencesBreast cancerTumor MicroenvironmentmedicineAnimalsHumansmetastasisEpithelial–mesenchymal transitionNeoplasm MetastasisPI3K/AKT/mTOR pathwayAgedAged 80 and overTumor microenvironmentp63breast cancer initiating cellsbusiness.industryMembrane ProteinsCD44v6Middle Agedmedicine.diseasePI3K/AKT pathwayHyaluronan Receptors030104 developmental biologyOncologyDrug Resistance NeoplasmTumor progressionImmunologyCancer researchFemalebreast cancer initiating cellmetastasibusinessCarcinogenesisProto-Oncogene Proteins c-aktSignal TransductionPriority Research Paper
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