Dually Efficacious Medicine Against Fibrosis and Cancer

Abstract

Although there is a contemporary consensus of managing a severe disease with multi-targeted approach-based therapeutic combinations, it should not be ignored that certain patho-biological pathways are shared by distinct medical conditions and can be exploited to develop an exceptional type of medication conferring a dual efficacy. This article thus presents a spectrum of emerging molecular targets that substantially contribute to the pathogenesis of both fibrotic and neoplastic disorders, including kinase activities, cytokine cascades, and protein dynamics among others. Moreover, recently approved therapeutic agents in this regard have been sorted out to corroborate the drug’s ability upon targeting each one of these molecular pathways to treat fibrosis and cancer simultaneously. It not only streamlines an overlapping mechanistic profile in the pathogenesis across these two medical conditions, but also inspires clinicians and pharmaceutical innovation to tackle concomitant diseases, such as fibrosis and cancer, with an optimally efficacious medication.

Obesity-Activated Lung Stromal Cells Promote Myeloid Lineage Cell Accumulation and Breast Cancer Metastasis

“…However, other studies have suggested that weight loss may not reverse epigenetic changes induced in obese adipose tissue [ 71 ], and the impact of weight loss on the function of lung stromal cells needs to be investigated. Given the similarities that we observed among lung stromal cells in obesity- and cancer-associated fibroblasts, therapeutics in development to target inflammatory characteristics of fibroblasts as well as antifibrotic agents may also have efficacy to limit metastasis in obese breast cancer patients [ 72 , 73 ]. Further studies are necessary to determine how obesity alters stromal cells in the microenvironment of other frequent sites of breast cancer metastases, such as liver and bone.…”

Inhibition of Autotaxin with GLPG1690 Increases the Efficacy of Radiotherapy and Chemotherapy in a Mouse Model of Breast Cancer

“…1A, IC 50 $130-220 nmol/L; Ki $15 against human ATX), succeeded in halting the progression of idiopathic pulmonary fibrosis in phase IIa clinical trials (31,32), and it is now being tested in a phase III trial (33). Significantly, many therapeutics that are effective against fibrosis are also used to improve cancer treatments (34). It was, therefore, important to establish if an ATX inhibitor that is in clinical trials for fibrosis has positive effects on the treatment of cancers.…”

Obesity-Activated Lung Stomal Cells Promote Myeloid-Lineage Cell Accumulation and Breast Cancer Metastasis

“…However, other studies have suggested that weight loss may not reverse epigenetic changes induced in obese adipose tissue (Rossi et al, 2016), and the impact of weight loss on the function of lung stromal cells needs to be investigated. Given the similarities that we observed among lung stromal cells in obesity and cancer-associated fibroblasts, therapeutics in development to target inflammatory characteristics of fibroblasts as well as anti-fibrotic agents may also have efficacy to limit metastasis in obese breast cancer patients (Chen, 2019;Liu et al, 2019). Further studies are necessary to determine how obesity alters other frequent sites of breast cancer metastases.…”