Spawned from science, growing from science

Our aim is to make an impact on human lives by developing new approach methodologies that will help shape and define the future technologies for precision medicine and toxicology research. By converting our own science into novel technologies we shape our own research and services and mediate scientific progress in global scale.

Our team has been involved in the development of high-throughput screening as we now know it since the beginning and our laboratory is built around a state-of-art high-throughput screening setup incorporating also industrial scale microarray production capabilities.

Our services are products of our own research and designed to support coordinated measurement science research programs encompassing advanced multi-parameter measurement technologies, general cell biology assays, custom reporter assays and miniaturized array technologies.

We also specialize in computational biology related to high-throughput screening, predictive toxicogenomics, cancer genetics and translational medicine. Integration of cell based in vitro modelling and genetic profiling can be used to address strategic biomedical questions in the areas of cancer, toxicology, nanotoxicology and basic cell biology.

Small but mighty

Our research and development efforts are guided by our talented team of scientists who focus on researh quality over quantity, and who shape the innovativeness of our R&D activities and our business. As a demonstration of the high level of our research achievements, Misvik Biology’s research team has participated in ten European commission funded research consortia, second most of all Finnish life science, biotech or health tech companies.

Our expertise areas

Discovery services

Built on more than two decades of experience on contract research for target discovery and technology development, we apply deep technical expertise in specialist technologies to support target discovery and cell biological research projects. Combining novel approach methodologies and integrated omics technologies including genomics and proteomics with advanced cell models we can deliver new insights to any project focused on human health and disease.

Precision medicine

Our dream is to start a new chapter in rare cancer care and transform patients’ lives by developing a diagnostic platform that will allow tissue agnostic personalized treatment guidance for rare cancers. In context of this effort, we can serve as a partner to find exceptional responders to experimental therapeutic molecules and match early pipeline drugs and treatments to patients most likely to benefit. Our ex vivo drug screening pipeline is built around state-of-the-art high-content microcopy setup, propietary image cytometry pipelines, versatile panels of off-the-shelf phenotypic assays, drug libraries covering all FDA approved drugs, thousands of experimental drug molecules and genome-wide siRNA and miRNA libraries.

Let the science speak for itself

Publications from collaborative research projects

Defined extracellular matrix compositions support stiffness-insensitive cell spreading and adhesion signaling. Conway JRW, Isomursu A, Follain G, Härmä V, Jou-Ollé E, Pasquier N, Välimäki EPO, Rantala JK, Ivaska J.  Proc Natl Acad Sci U S A. 2023 Oct 24;120(43):e2304288120. doi: 10.1073/pnas.2304288120.

FBXL12 degrades FANCD2 to regulate replication recovery and promote cancer cell survival under conditions of replication stress. Brunner A, Li Q, Fisicaro S, Kourtesakis A, Viiliäinen J, Johansson HJ, Pandey V, Mayank AK, Lehtiö J, Wohlschlegel JA, Spruck C, Rantala JK, Orre LM, Sangfelt O. Mol Cell. 2023 Aug 9:S1097-2765(23)00599-3. doi: 10.1016/j.molcel.2023.07.026

Precision oncology using ex vivo technology: a step towards individualised cancer care? Williams ST, Wells G, Conroy S, Gagg H, Allen R, Rominiyi O, Helleday T, Hullock K, Pennington CEW, Rantala J, Collis SJ, Danson SJ.  Expert Rev Mol Med. 2022;24:e39.

Cisplatin overcomes radiotherapy resistance in OCT4-expressing head and neck squamous cell carcinoma. Routila J, Qiao X, Weltner J, Rantala JK, et al. Oral Oncol. 2022;127:105772.

FBXO44 promotes DNA replication-coupled repetitive element silencing in cancer cells. Shen JZ, Qiu Z, Wu Q, Finlay D, Garcia G, Sun D, Rantala J et al.  Cell. 2021;184(2):352-369.e23.

Substrate-biased activity-based probes identify proteases that cleave receptor CDCP1. Kryza T, Khan T, Lovell S, Harrington BS, Yin J, Porazinski S, Pajic M, Koistinen H, Rantala JK et al. Nat Chem Biol. 2021;Apr 15.

PTEN and DNA-PK determine sensitivity and recovery in response to WEE1 inhibition in human breast cancer. Brunner A, Suryo Rahmanto A, Johansson H, Franco M, Viiliäinen J, Gazi M, Frings O, Fredlund E, Spruck C, Lehtiö J, Rantala JK, Larsson LG, Sangfelt O.  Elife. 2020;9:e57894.

Clonal Evolution of MEK/MAPK Pathway Activating Mutations in a Metastatic Colorectal Cancer Case. Lehtomaki KI, Lahtinen LI, Rintanen N, Kuopio T, Kholova I, Mäkelä R, Rantala JK, Kellokumpu-Lehtinen PL, Kononen J.  Anticancer Res. 39(11):5867-5877, 2019.

Personalized Drug Sensitivity Screening for Bladder Cancer Using Conditionally Reprogrammed Patient-derived Cells. Kettunen K, Boström PJ, Lamminen T, Heinosalo T, West G, Saarinen I, Kaipio K, Rantala J, Albanese C, Poutanen M, Taimen P.  Eur. J. Urol. 76(4):430-434, 2019.

Combined prognostic value of CD274 (PD-L1)/PDCDI (PD-1) expression and immune cell infiltration in colorectal cancer as per mismatch repair status. Ahtiainen M, Wirta EV, Kuopio T, Seppälä T, Rantala JK, Mecklin JP, Böhm J. Modern Pathology. 6:866-883. 2019.

Differentiation-state plasticity is a targetable resistance mechanism in basal-like breast cancer. Risom T, Langer EM, Chapman MP, Rantala J, Fields AJ, Boniface C, Alvarez MJ, Kendsersky ND, Pelz CR, Johnson-Camacho K, Dobrolecki LE, Chin K, Aswani AJ, Wang NJ, Califano A, Lewis MT, Tomlin CJ, Spellman PT, Adey A, Gray JW, Sears RC.  Nat Commun. 9(1):3815, 2018.

High-throughput RNAi screen in Ewing sarcoma cells identifies leucine rich repeats and WD repeat domain containing 1 (LRWD1) as a regulator of EWS-FLI1 driven cell viability.He T, Surdez D, Rantala JK, Haapa-Paananen S, Ban J, Kauer M, Tomazou E, Fey V, Alonso J, Kovar H, Delattre O, Iljin K.  Gene. S0378-1119(16)30827-7, 2016.