A mechanism for asymmetric cell division resulting in proliferative asynchronicity

Molecular Cancer Research

Volumn 13, Issue 2, 2015, Pages 223-230

  Dey Guha, Ipsita ^a,b   Alves, Cleidson P ^a,b   Yeh, Albert C ^b   Salony, ^a,b   Sole, Xavier ^a,b   Darp, Revati ^a   Ramaswamy, Sridhar ^a,b,c,d,e  

^a HARVARD MEDICAL SCHOOL   (United States)

^b BROAD INSTITUTE OF MIT AND HARVARD   (United States)

^c HARVARD STEM CELL INSTITUTE   (United States)

^d HARVARD UNIVERSITY   (United States)

^e MASSACHUSETTS GENERAL HOSPITAL CANCER CENTER   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

BETA1 INTEGRIN; BUPARLISIB; EVEROLIMUS; FOCAL ADHESION KINASE; MAMMALIAN TARGET OF RAPAMYCIN COMPLEX 2; PF 562271; PROTEASOME; PROTEIN KINASE B; RAPAMYCIN; AKT1 PROTEIN, HUMAN; AKT2 PROTEIN, HUMAN;

ARTICLE; ASYMMETRIC CELL DIVISION; CANCER CELL; CANCER GROWTH; CANCER RESISTANCE; CELL POPULATION; CELL PROLIFERATION; CONTROLLED STUDY; HUMAN; HUMAN CELL; PRIORITY JOURNAL; PROTEIN DEGRADATION; SIGNAL TRANSDUCTION; CLONAL EVOLUTION; GENETIC HETEROGENEITY; GENETICS; HCT 116 CELL LINE; MCF-7 CELL LINE; METABOLISM; NEOPLASM; PATHOLOGY; TUMOR MICROENVIRONMENT;

ASYMMETRIC CELL DIVISION; CLONAL EVOLUTION; GENETIC HETEROGENEITY; HCT116 CELLS; HUMANS; MCF-7 CELLS; NEOPLASMS; PROTO-ONCOGENE PROTEINS C-AKT; SIGNAL TRANSDUCTION; TUMOR MICROENVIRONMENT;

EID: 84923935202     PISSN: 15417786     EISSN: 15573125     Source Type: Journal    
DOI: 10.1158/1541-7786.MCR-14-0474     Document Type: Article

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