The authors provide an unique aetiology for pulmonary lymphangioleiomyomatosis (PLAM), which includes a review of clinical and pathology data on the condition, as well as a review of senescence research. PLAM is more like a progressive chronic interstitial pneumonia than a metastatic neoplasm in terms of clinical and radiographic progression. This pathogenesis model proposes that: 1) the primary site of origin for this disease is the Mullerian smooth muscle in the female reproductive tract, which accounts for the disease's striking female predominance; 2) the tumour spreads to the lungs via a mechanism similar to lymphangitic carcinomatosis, which accounts for the disease's universal symmetric and bilateral distribution; and 3) there is a mutational basis for a senescence-associated growth arrest. PLAM cells' secretory phenotype is examined, and the overlap with known senescent cells' senescence-associated secretory phenotype products is established. PLAM cells' role in switching to glycolytic metabolism (Warburg state) is discussed. Finally, the "contradictory signals" hypothesis for senescence induction is discussed, as well as its role in PLAM.
Author(S) Details
Charles Michael Lombard
Department of Pathology, Stanford University School of Medicine, Stanford, California, The United States and Department of Pathology, El Camino Hospital, Mountain View, California, The United States.
View Book:- https://stm.bookpi.org/IDMMR-V4/article/view/5545
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