Inflammatory Pathways to Carcinogenesis: Deciphering the Rheumatoid Arthritis–Lung Cancer Connection

Rheumatoid arthritis (RA) is the most common chronic autoimmune arthropathy. If the disease is aggressive or left untreated, it becomes debilitating, affects a patient’s functionality, and reduces the quality of life. Disease-modifying anti-rheumatic drugs (DMARDs), both conventional, targeted, and...

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Published inCancers Vol. 17; no. 8; p. 1330
Main Authors Abou Hjeily, Boushra, Nevaneeth, Briana Candace, Samborski, Włodzimierz, Szekanecz, Zoltán, Grygiel-Górniak, Bogna
Format Journal Article
LanguageEnglish
Published Switzerland MDPI AG 15.04.2025
MDPI
Subjects
Adalimumab
Antiarthritic agents
Apoptosis
Arthritis
Cancer
Cancer therapies
Carcinogenesis
Carcinogens
Care and treatment
Case reports
Cell growth
Cell proliferation
Development and progression
Diagnosis
Enzymes
Fibroblasts
Gene regulation
Inflammation
Interleukin 6
Kinases
Lung cancer
Molecular modelling
Oncology, Experimental
Prevention
Quality of life
Respiratory agents
Review
Rheumatic diseases
Rheumatoid arthritis
Rheumatoid factor
Risk factors
Smoking
Stat3 protein
Transcription factors
Up-regulation
Wnt protein
Womens health
lung cancer
iatrogenic effect of DMARDs
lung cancer risk factors
rheumatoid arthritis
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Abstract Rheumatoid arthritis (RA) is the most common chronic autoimmune arthropathy. If the disease is aggressive or left untreated, it becomes debilitating, affects a patient’s functionality, and reduces the quality of life. Disease-modifying anti-rheumatic drugs (DMARDs), both conventional, targeted, and biological, decrease the disease progression and are key components of effective treatment. Recently, there has been a continuous debate about the possible carcinogenicity of various DMARDs. Lung cancer is a leading cause of cancer death worldwide. The available data show an increased risk of lung cancer in RA patients, but the link between RA and cancer is poorly understood. Carcinogenesis in RA seems to be related to chronic inflammation, familial predisposition, risky behaviors (e.g., smoking), and iatrogenic complications. The main mechanisms of carcinogenic processes in patients with RA are the up-regulation of interleukin-6 (IL-6) cytokine production and wingless/integrated WNT signaling. Up-regulation of WNT5A is an important mechanism that links chronic inflammatory pathways to carcinogenesis observed in RA patients. Concomitant up-regulation of transcription factor STAT3 promotes cell proliferation and inhibits apoptosis. Conversely, suppressed inflammatory processes by DMARDs may decrease the risk of lung cancer. In this article, we discuss the molecular mechanisms of lung cancer in RA and the role of DMARDs in this process. Furthermore, we analyze the molecular effect of drug-induced cancer, which affects transcription factors and thus modulates carcinogenic processes. Finally, we describe risk factors and present preventive and therapeutic approaches.
AbstractList Lung cancer is a well-known long-term complication of rheumatoid arthritis (RA). However, the management of lung cancer concerning RA has been poorly studied and managed without a focused set of guidelines. In this extensive review, we have discussed the carcinogenic impact of using disease-modifying anti-rheumatic drugs (DMARDs), the molecular processes involved in the carcinogenic mechanisms of DMARDs, the factors involved in the development of lung cancer in RA patients, and the prevention and treatment of lung cancer associated with RA. Future long-term studies must be conducted to establish guidelines on the screening and treatment of cancers in RA patients. It should also focus on setting guidelines for the prevention of lung cancer in RA patients on long-term DMARD therapy, as well as determine the carcinogenic potential of new DMARDs on the market.
Rheumatoid arthritis (RA) is the most common chronic autoimmune arthropathy. If the disease is aggressive or left untreated, it becomes debilitating, affects a patient’s functionality, and reduces the quality of life. Disease-modifying anti-rheumatic drugs (DMARDs), both conventional, targeted, and biological, decrease the disease progression and are key components of effective treatment. Recently, there has been a continuous debate about the possible carcinogenicity of various DMARDs. Lung cancer is a leading cause of cancer death worldwide. The available data show an increased risk of lung cancer in RA patients, but the link between RA and cancer is poorly understood. Carcinogenesis in RA seems to be related to chronic inflammation, familial predisposition, risky behaviors (e.g., smoking), and iatrogenic complications. The main mechanisms of carcinogenic processes in patients with RA are the up-regulation of interleukin-6 (IL-6) cytokine production and wingless/integrated WNT signaling. Up-regulation of WNT5A is an important mechanism that links chronic inflammatory pathways to carcinogenesis observed in RA patients. Concomitant up-regulation of transcription factor STAT3 promotes cell proliferation and inhibits apoptosis. Conversely, suppressed inflammatory processes by DMARDs may decrease the risk of lung cancer. In this article, we discuss the molecular mechanisms of lung cancer in RA and the role of DMARDs in this process. Furthermore, we analyze the molecular effect of drug-induced cancer, which affects transcription factors and thus modulates carcinogenic processes. Finally, we describe risk factors and present preventive and therapeutic approaches.
Rheumatoid arthritis (RA) is the most common chronic autoimmune arthropathy. If the disease is aggressive or left untreated, it becomes debilitating, affects a patient's functionality, and reduces the quality of life. Disease-modifying anti-rheumatic drugs (DMARDs), both conventional, targeted, and biological, decrease the disease progression and are key components of effective treatment. Recently, there has been a continuous debate about the possible carcinogenicity of various DMARDs. Lung cancer is a leading cause of cancer death worldwide. The available data show an increased risk of lung cancer in RA patients, but the link between RA and cancer is poorly understood. Carcinogenesis in RA seems to be related to chronic inflammation, familial predisposition, risky behaviors (e.g., smoking), and iatrogenic complications. The main mechanisms of carcinogenic processes in patients with RA are the up-regulation of interleukin-6 (IL-6) cytokine production and wingless/integrated WNT signaling. Up-regulation of WNT5A is an important mechanism that links chronic inflammatory pathways to carcinogenesis observed in RA patients. Concomitant up-regulation of transcription factor STAT3 promotes cell proliferation and inhibits apoptosis. Conversely, suppressed inflammatory processes by DMARDs may decrease the risk of lung cancer. In this article, we discuss the molecular mechanisms of lung cancer in RA and the role of DMARDs in this process. Furthermore, we analyze the molecular effect of drug-induced cancer, which affects transcription factors and thus modulates carcinogenic processes. Finally, we describe risk factors and present preventive and therapeutic approaches.Rheumatoid arthritis (RA) is the most common chronic autoimmune arthropathy. If the disease is aggressive or left untreated, it becomes debilitating, affects a patient's functionality, and reduces the quality of life. Disease-modifying anti-rheumatic drugs (DMARDs), both conventional, targeted, and biological, decrease the disease progression and are key components of effective treatment. Recently, there has been a continuous debate about the possible carcinogenicity of various DMARDs. Lung cancer is a leading cause of cancer death worldwide. The available data show an increased risk of lung cancer in RA patients, but the link between RA and cancer is poorly understood. Carcinogenesis in RA seems to be related to chronic inflammation, familial predisposition, risky behaviors (e.g., smoking), and iatrogenic complications. The main mechanisms of carcinogenic processes in patients with RA are the up-regulation of interleukin-6 (IL-6) cytokine production and wingless/integrated WNT signaling. Up-regulation of WNT5A is an important mechanism that links chronic inflammatory pathways to carcinogenesis observed in RA patients. Concomitant up-regulation of transcription factor STAT3 promotes cell proliferation and inhibits apoptosis. Conversely, suppressed inflammatory processes by DMARDs may decrease the risk of lung cancer. In this article, we discuss the molecular mechanisms of lung cancer in RA and the role of DMARDs in this process. Furthermore, we analyze the molecular effect of drug-induced cancer, which affects transcription factors and thus modulates carcinogenic processes. Finally, we describe risk factors and present preventive and therapeutic approaches.
Lung cancer is a well-known long-term complication of rheumatoid arthritis (RA). However, the management of lung cancer concerning RA has been poorly studied and managed without a focused set of guidelines. In this extensive review, we have discussed the carcinogenic impact of using disease-modifying anti-rheumatic drugs (DMARDs), the molecular processes involved in the carcinogenic mechanisms of DMARDs, the factors involved in the development of lung cancer in RA patients, and the prevention and treatment of lung cancer associated with RA. Future long-term studies must be conducted to establish guidelines on the screening and treatment of cancers in RA patients. It should also focus on setting guidelines for the prevention of lung cancer in RA patients on long-term DMARD therapy, as well as determine the carcinogenic potential of new DMARDs on the market. Rheumatoid arthritis (RA) is the most common chronic autoimmune arthropathy. If the disease is aggressive or left untreated, it becomes debilitating, affects a patient’s functionality, and reduces the quality of life. Disease-modifying anti-rheumatic drugs (DMARDs), both conventional, targeted, and biological, decrease the disease progression and are key components of effective treatment. Recently, there has been a continuous debate about the possible carcinogenicity of various DMARDs. Lung cancer is a leading cause of cancer death worldwide. The available data show an increased risk of lung cancer in RA patients, but the link between RA and cancer is poorly understood. Carcinogenesis in RA seems to be related to chronic inflammation, familial predisposition, risky behaviors (e.g., smoking), and iatrogenic complications. The main mechanisms of carcinogenic processes in patients with RA are the up-regulation of interleukin-6 (IL-6) cytokine production and wingless/integrated WNT signaling. Up-regulation of WNT5A is an important mechanism that links chronic inflammatory pathways to carcinogenesis observed in RA patients. Concomitant up-regulation of transcription factor STAT3 promotes cell proliferation and inhibits apoptosis. Conversely, suppressed inflammatory processes by DMARDs may decrease the risk of lung cancer. In this article, we discuss the molecular mechanisms of lung cancer in RA and the role of DMARDs in this process. Furthermore, we analyze the molecular effect of drug-induced cancer, which affects transcription factors and thus modulates carcinogenic processes. Finally, we describe risk factors and present preventive and therapeutic approaches.
Audience Academic
Author Szekanecz, Zoltán
Nevaneeth, Briana Candace
Grygiel-Górniak, Bogna
Abou Hjeily, Boushra
Samborski, Włodzimierz
AuthorAffiliation 2 Department of Rheumatology, Rehabilitation and Internal Diseases, Poznan University of Medical Science, 61-701 Poznan, Poland; wlodzimierz.samborski@ump.edu.pl
3 Division of Rheumatology, Faculty of Medicine, University of Debrecen, 4032 Debrecen, Hungary; szekanecz.zoltan@med.unideb.hu
1 Rheumatology Research Group, Department of Rheumatology, Rehabilitation and Internal Diseases, Poznan University of Medical Science, 61-701 Poznan, Poland
AuthorAffiliation_xml – name: 2 Department of Rheumatology, Rehabilitation and Internal Diseases, Poznan University of Medical Science, 61-701 Poznan, Poland; wlodzimierz.samborski@ump.edu.pl
– name: 1 Rheumatology Research Group, Department of Rheumatology, Rehabilitation and Internal Diseases, Poznan University of Medical Science, 61-701 Poznan, Poland
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  surname: Abou Hjeily
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  givenname: Briana Candace
  orcidid: 0000-0001-9585-9448
  surname: Nevaneeth
  fullname: Nevaneeth, Briana Candace
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Keywords lung cancer
iatrogenic effect of DMARDs
lung cancer risk factors
rheumatoid arthritis
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Snippet Rheumatoid arthritis (RA) is the most common chronic autoimmune arthropathy. If the disease is aggressive or left untreated, it becomes debilitating, affects a...
Lung cancer is a well-known long-term complication of rheumatoid arthritis (RA). However, the management of lung cancer concerning RA has been poorly studied...
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SubjectTerms Adalimumab
Antiarthritic agents
Apoptosis
Arthritis
Cancer
Cancer therapies
Carcinogenesis
Carcinogens
Care and treatment
Case reports
Cell growth
Cell proliferation
Development and progression
Diagnosis
Enzymes
Fibroblasts
Gene regulation
Inflammation
Interleukin 6
Kinases
Lung cancer
Molecular modelling
Oncology, Experimental
Prevention
Quality of life
Respiratory agents
Review
Rheumatic diseases
Rheumatoid arthritis
Rheumatoid factor
Risk factors
Smoking
Stat3 protein
Transcription factors
Up-regulation
Wnt protein
Womens health
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Title Inflammatory Pathways to Carcinogenesis: Deciphering the Rheumatoid Arthritis–Lung Cancer Connection
URI https://www.ncbi.nlm.nih.gov/pubmed/40282506
https://www.proquest.com/docview/3194505744
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https://pubmed.ncbi.nlm.nih.gov/PMC12026397
Volume 17
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