Tumorigenesis: Developmental and Homeostatic Signaling Gone Awry!

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Background

Pioneering work of Dr. Mina J. Bissell and Dr. Robert A. Weinberg have illustrated some very fundamental conceptual frameworks in cancer research.

The naturally occurring nuts and bolts that make-up the machinery supporting development and tissue repair/regeneration become dilapidated or incur errors to result in aging and tumorigenesis.

Identification of the precise nuts and bolts making up the machinery in development and tissue repair/regeneration is context specific and give us clues as to how we can intervene to remedy/fix aging and tumorigenesis.

Interestingly, it was Dr. Mina J. Bissell who demonstrated the significance of context in which studies are conducted and the importance of tissue microenvironment, niche, extracellular matrix, and biophysical cues and nuclear environment for gene expression. Dr. Robert A. Weinberg has conducted exemplary studies in support of the significance of Cancer Stem Cells (CSC) and the significance of the Epithelial Mesenchymal Transition (EMT) in cancer metastasis.

Identification and targeting of key signaling molecules in development, homeostasis, and tumorigenesis are important.
Currently, efforts have culminated in generation of tissue-specific organoid platforms for genome-wide screening to identify developmental and disease-related targets in nephrogenesis and development of therapies or combination therapies in ovarian cancer. Targets may also be utilized for diagnosis, prognosis, therapy, prediction of response to therapy, and follow-up. This is evident in the 2021 EANO guidelines on the diagnosis and treatment of diffuse gliomas of adulthood. CSC and their vesicles affect generation of distinct cell subtypes, proliferation, differentiation, progression, formation of metastasis, immune and therapy resistance, and cancer relapse.

Epigenetic and transcriptome profiling for key regulatory elements in development, homeostasis, and tumor formation. Identification, characterization and possible expansion of the functional genome in development, homeostasis, and tumorigenesis (e.g. CancerMIRNome, Chimeric RNAs) and analysis across multiple cancer types.

Senescence is evolving from an aging phenomenon to a cellular defense mechanism in response to stress, implicated in a wide spectrum of biological processes like tissue remodeling, injury and cancer.

Regulation of EMT mediated immunosuppression. Myc enables tumor cells to dysregulate their microenvironment and evade host immune response. MGMT low gliomas are Temozolomide resistant. Signaling factors contributing to therapeutic resistance and relapse.
GLI3, a mediator of genetic diseases, development, and cancer, is now implicated in immune cell development and other similar molecules. Cell–extracellular matrix dynamics: The sites of interaction between a cell and its surrounding microenvironment serve as dynamic signaling hubs that regulate cellular adaptations during developmental processes, immune functions, wound healing, cell migration, cancer invasion, and metastasis, as well as in many other disease states.

The cytoskeleton/cell infrastructure controls many phenotypes like polarity, movement, invasion, endocytosis, cell division, and trafficking. A cytoskeleton regulator AVIL drives tumorigenesis in glioblastoma and Calcium signaling is disrupted in GBM. Calcium channels play critical roles in nervous system development. STIM1 splice variant, STIM1B, is increased in glioma, promotes GBM growth, and perturbs calcium signaling.

Quiescent disseminated tumor cells (DTCs) reside on the astrocyte endfeet. Astrocyte-deposited laminin-211 drives DTC quiescence by inducing the dystroglycan receptor to associate with yes-associated protein, thereby sequestering it from the nucleus and preventing its prometastatic functions.

Manuscripts consisting solely of bioinformatics, computational analysis, or predictions of public databases which are not accompanied by validation (independent cohort or biological validation in vitro or in vivo) will not be accepted in any of the sections of Frontiers in Oncology.

Keywords: signaling, (epi)genome, tumor, diagnostic, therapeutic

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