{'fraction_non_alphanumeric': 0.015317286652078774, 'fraction_numerical': 0.0, 'mean_word_length': 5.596153846153846, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Multiple myeloma may include microvessel endothelial cells of malignant origin

Multiple myeloma (MM) comprises B and plasma cell compartments that originate from the same parent B cell and share as a cancer signature the same clonotypic IgH VDJ gene rearrangement. Here, we hypothesize that functional interactions between MM plasma cells (MM-PC) and their sister population of MM monocytoid B cells lead to the generation of microvessel endothelium of malignant origin from the monocytoid B cell progenitors. Published reports confirm that endothelial cells can harbor a molecular cancer signature characteristic of a given malignancy. We predict that MM monocytoid B cells—in response to both paracrine and autocrine pathways—contribute to tumor neovascularization in the bone marrow of MM patients. Our hypothesis further predicts that in MM, endothelial cells of malignant origin coexist with those of normal origin. We speculate that malignant development of MM incorporates functionally distinct sister lineages arising from the same MM progenitor that—by working together—ensure survival of the MM clone. We hypothesize that these two arms of the malignant MM clone are functionally interlinked to promote growth of the MM-PC compartment; by providing its own microenvironment, MM clonal evolution may ensure neovascularization to support an expanding malignancy.