Patrik Ernfors Group
Two main directions of research are conducted in my group - understanding how complex sets of modality specific sensory neurons codes for somatic sensation and understanding the biology of glioblastoma.
Program 1: Somatic sensation
The problem of pain continues to grow as population age, but there has been a difficulty to develop new useful analgesic drugs. Almost 1 in 5 of the population has an ongoing pain problem, with 7% suffering debilitating pain. Little remains known regarding the actual cellular and molecular complexity during pain transduction, simply because of lack of knowledge on the sensory neuron types conducting somatosensation and pain. A major focus of the lab is to determine the full cellular and molecular complexity of pain and unravel the critical cell types driving pain in particular types of pain disorders.
For this purpose we are using unbiased identification and classification of sensory cell types in rodents and non-human primates and exploit this knowledge to reveal their participation in acute, inflammatory and neuropathic pain using mouse genetics. Hence, the overall aim is to provide knowledge on the existence of defined types of nociceptive cells and assign their participation to particular types of pain states.
Program 2: Glioblastoma
High-grade gliomas are the most common and lethal types of the primary malignant brain tumors with a median survival in patient obtaining the most aggressive treatment strategy of around 15 month from diagnosis. Glioblastoma (GBM) are caused by mutations which have been extensively characterized genetically using whole genome sequencing approaches. A few main pathways are affected in nearly all primary glioblastoma subtypes, including TKR/RAS/PI3K, p53 and Rb signaling, and these seem to be drivers of glioma initiation. However, another common feature of glioblastoma cells is the re-expression of a neurodevelopmental (stem-like) core transcription factor gene program. Intriguingly, removal of specific transcription factors in this program results in loss of tumor initiating properties, despite that cells carry genetic alterations supposedly underlying tumor initiation and propagation. Our aim is to understanding how the variety of mutations causing GBM converges on expression of core stem-associated genes in the diversity of cell types present in tumors, with the hope that such knowledge will explain how tumor initiating properties are acquired.