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My group is focused on understanding pathogenic and drug resistance mechanisms in hematological malignancies. Working closely with the clinic, we apply research tools to patient samples for better understanding of inter- and intra-disease heterogeneity and translation of basic research findings to patient care.
Although precision treatment strategies have been achieved with cancers such as chronic myeloid leukemia, which develop and can be targeted through a single driver event, most cancers are extremely heterogeneous and result from complex genetic changes. Thus, newer, targeted therapies often have limited efficacy in broader patient populations, or the duration of response is short, as drug resistant subclones are selected for and eventually cause disease recurrence. Future cancer drug development is therefore dependent on being able to identify responding and non-responding patients, and effectively monitor and change treatment as the patient’s disease evolves.
For our research, we use a systems-wide approach to analyze samples from individual patients diagnosed with a hematological malignancy. By combining genomic, transcriptomic, proteomic and functional ex vivo drug sensitivity testing of the patient’s tumor cells and comparing these data to that of normal cells, we get a broad view of genomic and phenotypic changes that have occurred in the tumor and which could potentially be therapeutically targeted. In addition, we analyze samples acquired at different stages of the patient’s disease (e.g. diagnosis, during treatment response and relapse) for better insight of disease progression mechanisms and understanding the impact of therapy on the patient’s tumor. Working closely with the FIMM Technology Centre and our collaborators, we quickly return our results to the clinic to maximize the amount of data available for guiding treatment decision of patients with relapsed or refractory disease.
Although precision treatment strategies have been achieved with cancers such as chronic myeloid leukemia, which develop and can be targeted through a single driver event, most cancers are extremely heterogeneous and result from complex genetic changes. Thus, newer, targeted therapies often have limited efficacy in broader patient populations, or the duration of response is short, as drug resistant subclones are selected for and eventually cause disease recurrence. Future cancer drug development is therefore dependent on being able to identify responding and non-responding patients, and effectively monitor and change treatment as the patient’s disease evolves.
For our research, we use a systems-wide approach to analyze samples from individual patients diagnosed with a hematological malignancy. By combining genomic, transcriptomic, proteomic and functional ex vivo drug sensitivity testing of the patient’s tumor cells and comparing these data to that of normal cells, we get a broad view of genomic and phenotypic changes that have occurred in the tumor and which could potentially be therapeutically targeted. In addition, we analyze samples acquired at different stages of the patient’s disease (e.g. diagnosis, during treatment response and relapse) for better insight of disease progression mechanisms and understanding the impact of therapy on the patient’s tumor. Working closely with the FIMM Technology Centre and our collaborators, we quickly return our results to the clinic to maximize the amount of data available for guiding treatment decision of patients with relapsed or refractory disease.
Research Interests
Papers共 335 篇Author StatisticsCo-AuthorSimilar Experts
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Sari Kytola,Ida Vaenttinen,Tanja Ruokoranta,Anu Partanen,Annasofia Holopainen,Joseph Saad,Milla E. L. Kuusisto,Sirpa Koskela,Riikka Raty,Maija Itala-Remes,Imre Vastrik,Minna Suvela,Alun Parsons,Kimmo Porkka,Krister Wennerberg,Caroline A. Heckman, Tero Jalkanen,Teppo Huttunen,Pia Ettala,Johanna Rimpilainen,Timo Siitonen,Marja Pyorala,Heikki Kuusanmaki,Mika Kontro
BLOODno. 4 (2025)
Tero Satomaa,Henna Pynnönen, Olli Aitio,Jukka O. Hiltunen,Virve Pitkänen,Tuula Lähteenmäki,Titta Kotiranta,Annamari Heiskanen,Anna-Liisa Hänninen, Ritva Niemelä, Jari Helin,Heikki Kuusanmäki,Ida Vänttinen, Ramji Rathod, Anni I. Nieminen,Emrah Yatkin,Caroline A. Heckman,Mika Kontro,Juhani Saarinen
crossref(2024)
Jessica R. Koski, Laura Langohr, Tuulia Raisanen,Atte Lahtinen,Marja Hakkarainen,Caroline A. Heckman,Ulla Wartiovaara-Kautto,Esa Pitkanen,Outi Kilpivaara
medrxiv(2024)
Tero Satomaa,Henna Pynnönen, Olli Aitio,Jukka O. Hiltunen,Virve Pitkänen,Tuula Lähteenmäki,Titta Kotiranta,Annamari Heiskanen,Anna-Liisa Hänninen, Ritva Niemelä, Jari Helin,Heikki Kuusanmäki,Ida Vänttinen, Ramji Rathod, Anni I. Nieminen,Emrah Yatkin,Caroline A. Heckman,Mika Kontro,Juhani Saarinen
crossref(2024)
Tero Satomaa,Henna Pynnönen, Olli Aitio,Jukka O. Hiltunen,Virve Pitkänen,Tuula Lähteenmäki,Titta Kotiranta,Annamari Heiskanen,Anna-Liisa Hänninen, Ritva Niemelä, Jari Helin,Heikki Kuusanmäki,Ida Vänttinen, Ramji Rathod, Anni I. Nieminen,Emrah Yatkin,Caroline A. Heckman,Mika Kontro,Juhani Saarinen
crossref(2024)
Mahesh Tambe, Sarah Unterberger,Mette C. Kriegbaum,Ida Vanttinen, Ezgi June Olgac,Markus Vaha-Koskela,Mika Kontro,Krister Wennerberg,Caroline A. Heckman
CELL DEATH & DISEASEno. 10 (2024)
biorxiv(2024)
Bloodno. Supplement 1 (2024): 6928-6928
EUROPEAN JOURNAL OF HUMAN GENETICS (2024): 786-786
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Tero Satomaa,Henna Pynnönen, Olli Aitio,Jukka O. Hiltunen,Virve Pitkänen,Tuula Lähteenmäki,Titta Kotiranta,Annamari Heiskanen,Anna-Liisa Hänninen, Ritva Niemelä, Jari Helin,Heikki Kuusanmäki,Ida Vänttinen, Ramji Rathod, Anni I. Nieminen,Emrah Yatkin,Caroline A. Heckman,Mika Kontro,Juhani Saarinen
crossref(2024)
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Author Statistics
#Papers: 335
#Citation: 6679
H-Index: 39
G-Index: 79
Sociability: 7
Diversity: 3
Activity: 90
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