About this Research Topic
The initial discovery that epigenetic reprogramming was critical for chronic myeloid leukemia development implied that leukemia stem cells were not oncogene addicted, consequently the therapies that biochemically target the oncogene did not eliminate the leukemia stem cells. These findings were corroborated later in human patients. Those studies revealed that leukemia stem cells are much more heterogeneous and versatile than has been previously thought, supporting the notion that whilst cells that initiate leukemia have multi-lineage potential, leukemia stem cells are reprogrammed by further oncogenic insults to restrict their lineage decision-making. Accordingly, evolution of a sub-clone of lineage-restricted malignant cells is a key feature of overt leukemia.
These new notions and concepts seem to be applicable to many cancer types. Thus, in the recent years it has been shown that stem cell epigenetic reprogramming seems represent a potentially important mechanism of tumour development for many types of cancer. In this regard, new additional published data show that i) epigenetic reprogramming can drive development of other hematopoietic cancers, ii) chondroblastomas, iii) lung carcinomas, iv) breast carcinomas; v) pancreatic carcinomas; and vi) skin carcinomas etc.
These findings revealed that the contribution of oncogenes to cancer development is mediated mainly through epigenetic priming of cancer-initiating cells, suggesting that genetic lesions that initiate the cancer process might be dispensable for the posterior tumor progression and maintenance. This epigenetic priming may remain latent until it is later triggered by endogenous or environmental stimuli. In addition, this epigenetic priming is being exploited in the development of new therapeutic approaches.
Finally, although differentiation of hematopoietic stem cells into distinct cell types was thought to occur through a series of discrete, stable progenitor states, recent work now shows that hematopoietic cells differentiate via a mechanism of continuous lineage priming.
In this Research Topic, we welcome contributions examining the relevance and implications of epigenetic priming in both normal and cancer development and in the development of new therapeutic approaches.
These new notions and concepts seem to be applicable to many cancer types. Thus, in the recent years it has been shown that stem cell epigenetic reprogramming seems represent a potentially important mechanism of tumour development for many types of cancer. In this regard, new additional published data show that i) epigenetic reprogramming can drive development of other hematopoietic cancers, ii) chondroblastomas, iii) lung carcinomas, iv) breast carcinomas; v) pancreatic carcinomas; and vi) skin carcinomas etc.
These findings revealed that the contribution of oncogenes to cancer development is mediated mainly through epigenetic priming of cancer-initiating cells, suggesting that genetic lesions that initiate the cancer process might be dispensable for the posterior tumor progression and maintenance. This epigenetic priming may remain latent until it is later triggered by endogenous or environmental stimuli. In addition, this epigenetic priming is being exploited in the development of new therapeutic approaches.
Finally, although differentiation of hematopoietic stem cells into distinct cell types was thought to occur through a series of discrete, stable progenitor states, recent work now shows that hematopoietic cells differentiate via a mechanism of continuous lineage priming.
In this Research Topic, we welcome contributions examining the relevance and implications of epigenetic priming in both normal and cancer development and in the development of new therapeutic approaches.
Keywords: cancer, oncogenes, reprogramming, stem cells, cancer therapy
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