Women's Lung Cancer: Recognizing Signs and Symptoms
In a groundbreaking review of lung cancer research, a significant gender disparity has been uncovered, with females exhibiting higher mortality rates compared to their male counterparts. This discrepancy is attributed to both hormonal and genetic factors that influence susceptibility, tumor biology, and treatment responses.
Hormonal influences play a crucial role in lung cancer development and progression. Estrogen, a female sex hormone, and its receptors are widely expressed in lung tissue. Estrogen can promote tumor growth through these receptors, particularly in women, affecting the susceptibility to lung adenocarcinoma, the most common lung cancer subtype among females, especially non-smokers.
Women may also be more sensitive to carcinogens due to hormonal regulation affecting DNA repair and carcinogen metabolism. Estrogen-related pathways can interact with genetic mutations and environmental carcinogens, potentially enhancing tumor growth and influencing prognosis.
Genetic factors also contribute to the increased lung cancer mortality rate in females. Women exhibit a higher prevalence of certain genetic mutations associated with lung cancer, notably mutations in the EGFR (epidermal growth factor receptor) and KRAS genes. EGFR mutations are more common in female, non-smokers and younger patients, driving cancer growth and offering therapeutic opportunities but also indicating a distinct tumor biology in women.
Moreover, women have been shown to have higher DNA adducts and reduced DNA repair capacity when exposed to tobacco carcinogens. This means that even equivalent levels of smoking can cause more DNA damage in females than males. Additionally, women overexpress enzymes like cytochrome CYP1A1 that bioactivate tobacco carcinogens, increasing lung cancer risk even at lower tobacco exposures.
Certain gene polymorphisms may also influence lung cancer risk differently in females. For instance, the MTHFR C677T TT genotype increases lung cancer risk among some female populations.
The incidence and mortality rates for lung cancer in women, particularly younger women and never-smokers, are rising and in some age groups have exceeded those of men. This suggests that factors beyond smoking, including hormonal and genetic influences, contribute significantly to risk and outcomes.
Women’s lung cancers often have distinct molecular and histological profiles compared to men, influencing both prognosis and response to targeted therapies. The review identifies KRAS as a gene that may explain the differing lung cancer rates among females and males, with mutations making cancerous tumors grow more quickly and more likely to spread.
It is essential to note that smoking and exposure to secondhand smoke remain the most significant risk factors for lung cancer. However, the findings of this review suggest that a better understanding of hormonal and genetic aspects of lung cancer could lead to new therapies that may be more effective in females than males.
For both sexes, maintaining a healthful lifestyle and avoiding exposure to smoke can help reduce the risk of developing lung cancer. Symptoms of lung cancer in females include shortness of breath, wheezing, hoarseness, fatigue, persistent cough, difficulty swallowing, loss of appetite, weight loss, ongoing chest pain, coughing up blood, recurrent lung infections, and recurrent pneumonia or bronchitis.
The review also associates gastric-releasing peptide receptor (GRPR) activity with cancer cell growth, which is more active in females. Long-term exposure to estrogen may also affect lung cancer risk in females. Lung cancer is the second most common type of cancer in both males and females, excluding skin cancer.
In summary, the combination of estrogen’s growth-promoting effects, higher susceptibility to tobacco carcinogens via genetic and enzymatic pathways, and a higher frequency of actionable driver mutations like EGFR contribute to the increased lung cancer mortality rates observed in women compared to men. These hormonal and genetic factors also imply different disease mechanisms and may necessitate gender-specific approaches in lung cancer prevention, screening, and treatment.
- Estrogen, expressed widely in lung tissue, can promote tumor growth in women, particularly affecting the susceptibility to lung adenocarcinoma, a common subtype among females, especially non-smokers.
- Women may be more sensitive to carcinogens due to hormonal regulation affecting DNA repair and carcinogen metabolism, potentially enhancing tumor growth and influencing prognosis.
- Genetic mutations in EGFR and KRAS genes are more prevalent in females and are linked to lung cancer, with EGFR mutations being more common in non-smoking, younger women.
- Women have higher DNA adducts and reduced DNA repair capacity when exposed to tobacco carcinogens, causing more DNA damage at similar smoking levels as men.
- The MTHFR C677T TT genotype increases lung cancer risk among some female populations.
- Distinct molecular and histological profiles of lung cancers in women may influence both prognosis and response to targeted therapies, with mutations in genes like KRAS making cancerous tumors grow more quickly and spread more readily.
