This study introduces two original theoretical frameworks—focusing on systemic lupus erythematosus (SLE) and solid malignancies, including cancer—in an attempt to unify their pathogenesis on bone marrow and tissue origins. For SLE, this research confirms that the condition is not a primary autoimmune disease in which the immune system mistakenly attacks the body. Instead, it arises from defective platelet production in the bone marrow. Defective platelets lead to impaired tissue repair, increased physiological burden, and secondary immune activation. For cancer, this study challenges the traditional model of autonomous malignant cell proliferation. Instead, the focus is on the body’s inability to clear abnormal cells in the circulation. Solid tumors represent late, elective cell accumulations that become clinically significant only when they form a “barrier flux” that allows pathogens to invade. In both groups of diseases, conventional treatments target symptoms rather than tissue origins. This process proposes a unified strategy: early detection of localized bone marrow lesions or tissue-derived defective cells, followed by source-directed therapies, and restoration of normal physiological function. If validated clinically, this paradigm will allow patients with SLE and early-stage cancers to achieve remission, long-term control, and even recovery without relapsing, moving beyond merely reducing and managing symptoms.
FOO SENG ANG (Mon,) studied this question.