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MPM is characterized by a long latency period from the time of asbestos exposure to clinical diagnosis, suggesting that multiple somatic changes may be required for the tumorigenic conversion of normal mesothelial cells [8].
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In aposporic gametogenesis, one or multiple somatic cells belonging to the ovule nucellus change their fate by dividing mitotically and developing functionally unreduced embryo sacs by mimicking sexual gametogenesis.
In the upper aerodigestive tract, significant exposure of the mucosa surface to the same carcinogens or stimulants (such as alcohol or cigarettes) may lead to a multitude of somatic changes that are susceptible to the development of multiple primary cancers.
The change from a normal to a cancer cell requires acquisition of multiple somatic mutations that collectively impart the malignant phenotype.
The prevalence of multiple somatic symptoms is high in primary and hospital outpatient populations.
Large-scale genomic studies have identified multiple somatic aberrations in breast cancer, including copy number alterations and point mutations.
Pediatric osteosarcoma is characterized by multiple somatic chromosomal lesions, including structural variations (SVs) and copy number alterations (CNAs).
Since multiple somatic and psychological symptoms frequently coexist in OFP and TMD patients, case-finding instruments have been developed for initiating diagnostic procedures that facilitate optimized treatment.
In the meantime, patients with chronic, multiple somatic symptoms who are still waiting for a diagnosis would be vulnerable to misdiagnosis as psychiatrically ill.
A principle difference exists between single vs. multiple somatic alleles.
Although their disease has features shared with single somatic allele patients, most notably the preferential enrichment of somatic alleles in memory T cells [9], [10], other important features of their phenotype are specific to multiple somatic alleles.
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