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SUMMARY:Title to be confirmed - Roger Gomis\, ICREA Research Professor\, I
 RB Barcelona
DTSTART:20171107T113000Z
DTEND:20171107T123000Z
UID:TALK93865@talks.cam.ac.uk
CONTACT:Mala Jayasundera
DESCRIPTION:_Roger R. Gomis*_\n\n_*Oncology Program\, Institute for Resear
 ch in Biomedicine (IRB Barcelona)\, The Barcelona Institute of Science and
  Technology\, Barcelona\, Spain and ICREA\, Institució Catalana de Recerc
 a i Estudis Avançats\, Barcelona\, Spain_\n\nAlthough breast cancer (BCa)
  can relapse to bones\, lungs and liver as well as brain\, metastasis freq
 uently becomes prevalent in one organ long before it does in others\, and 
 brain metastasis tends to be a late event. The ability to metastasize to a
  secondary site can be stochastic\, owing to new interactions between the 
 tumor cell and the target microenvironment\, or can be encoded by the arri
 ving tumor cell. The slow progression of certain subtypes of BC under thes
 e different selective conditions gives rise to metastatic speciation\, as 
 suggested by the different kinetics of BC relapse to different sites in th
 e same patient\, and by the coexistence of malignant cells with different 
 organ tropisms in patient-derived samples. We aimed to set the stage for t
 he detailed study of the mechanisms of metastasis and their potential valu
 e as therapeutic targets.\n\nFor many BCa patients\, symptomatic bone meta
 stases appear after years or even decades of la¬tency. How metastatic cel
 ls disseminate\, and how micromet¬astatic lesions remain dormant and unde
 tectable yet initiate colonization\, are major questions in cancer researc
 h. We identify and func¬tionally analyse a molecular mechanism involved i
 n bone metastatic latency of estrogen receptor–positive (ER)+ BCa. We de
 veloped an in vivo loss-of-function\, genome-wide shRNA screening to ident
 ify genes relevant for long-latent relapse in BCa. This screen revealed an
  important regulator of metastatic dormancy. Notably\, low expression asso
 ciates with early metastasis in ER+ BCa patients and reduced levels impair
 ed cellular differentiation of metastatic cells. These effects are mediate
 d through modulation of chromatin status at promoters to regulate the expr
 ession of luminal differentiation genes\, which prevent the progression of
  ER+ BCa towards metastasis. Our results identify the regulation of lumina
 l cell differentiation via modulation of chromatin remodelling to be a key
  mechanism for controlling metastatic dormancy in BCa. 
LOCATION:Sackler Lecture Theatre (Level 7)\, Cambridge Institute for Medic
 al Research
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