Monday, January 26, 2026
Lung cancer Impact of Food Nutrtion Microbiota
Abstract
Lung cancer still represents the leading cause of cancer-related death, globally. Likewise,
malnutrition and inactivity represent a major risk for loss of functional pulmonary capacities influencing overall lung cancer severity.
Therefore, the adhesion to an appropriate
health lifestyle is crucial in the management of lung cancer patients despite the subtype of cancer.
This review aims to summarize the available knowledge about dietary approaches as well as physical activity as the major factors that decrease the risk towards lung cancer,
and improve the response to therapies.
We discuss the most significant dietary schemes positively associated to body composition and prognosis of lung cancer and the main molecular processes regulated by specific diet schemes, functional foods and physical activity, i.e., inflammation and oxidative stress.
Finally, we report evidence demonstrating that dysbiosis of lung and/or gut microbiome, as well as their interconnection (the gut–lung axis), are strictly related to dietary patterns and regular physical activity playing a
key role in lung cancer formation and progression, opening to the avenue of modulating the microbiome as coadjuvant therapy. Altogether, the evidence reported in this review highlights the necessity to consider non-pharmacological interventions (nutrition and physical activity) as effective adjunctive strategies in the management of lung cancer.
Ref
Int J Environ Res Public Health. 2021 Mar 1;18(5):2399. doi: 10.3390/ijerph18052399
Food, Nutrition, Physical Activity and Microbiota: Which Impact on Lung Cancer?
Ersilia Nigro 1,2, Fabio Perrotta 3, Filippo Scialò 2,4, Vito D’Agnano 3, Marta Mallardo 1,2, Andrea Bianco 2,4,*, Aurora Daniele 1,2,*
Editor: Dagrun Engeset
Sunday, January 25, 2026
Lung cancer Genetic and Racial Disparities
2.3. Genetic and Racial
Disparities and Lung Cancer Susceptibility
Lung cancer risk is influenced significantly by
different racial and ethnic disparities.
Individuals with African ancestry (AA) have
higher mortality rates and incidence of lung cancer development at an earlier age compared to individuals with European ancestry (EA) due to disparities in preventive screening monitoring and treatment disparities [39,40].
In addition, there is a significant disparity in the metabolic pathways and how the body processes nicotine between AA and EA groups, as AA has lower levels of cotinine glucuronidation [41].
Non-Hispanic AA males show the highest rates of mortality and lung cancer incidence compared to all race-ethnicities [42,43].
Similarly, Primm et al. showed persistent disparities in NSCLC incidence between AA and EA men [44].
Interestingly, despite disparities in diagnosis and treatment, AA and Asian NSCLC patients demonstrate better outcomes for the same-stage cancer compared to EA patients [45].
The cause for disparities is genetic ancestry, as AA populations with LUSC have more genomic instability and aggressive molecular traits, while AA patients with LUAD have a higher frequency of PTPRT and JAK2 gene mutations [46,47].
Additionally, the Asian population demonstrates a higher frequency of STK11, TP53, and EGFR gene mutation [48],
but they have longer survival rates and higher chemotherapy responses in comparison to EA patients [49].
Ok Another study linked TP53, KRAS, and KEAP1 gene mutations with worse overall survival, whereas EGFR gene mutations are associated with a higher chance of survival [50].
Recent studies found that EA patients have higher mortality rates compared to Hispanics and Asians, and they have a higher susceptibility to lung cancer due to higher frequencies in smoking-related loci [51,52].
Many studies have revealed racial disparities in the genetic mutation profile of lung cancer patients. Compared to Japanese patients, EA-LUSC patients present a higher frequency of mutations in TP53, PIK3CA, KEAP1, and NFE2L2 genes [53].
On the contrary, EA-LUAD patients exhibit a significantly lower occurrence of EGFR mutation but an increased frequency of mutation in the PIK3CA, KEAP1, KRAS, TP53, BRAF, NF1, STK11, RBM10, and MET genes.
Weiner and Winn reported a higher prevalence
of EGFR gene mutation in the East Asian population and more predominant KRAS and STK11 gene alterations in EA and AA populations [54].
Generally, the disparities in survival rates between EA and AA populations are noticeable in patients who are young and have localized tumors [55].
The disparities also exist in histological subtype, stage, and tumor grade. Asian or Pacific Islander (API) exhibit a higher frequency of adenocarcinoma (ADC) compared to AA, EA, and American Indian/Alaska Native (AIAN) patients [56].
Ref
International Journal of Molecular Sciences logo
Int J Mol Sci. 2025 Apr 17;26(8):3818. doi: 10.3390/ijms26083818
The Current Roadmap of Lung Cancer Biology, Genomics and Racial Disparity
Enas S Alsatari 1,2, Kelly R Smith 1,2, Sapthala P Loku Galappaththi 1,2, Elba A Turbat-Herrera 1,2, Santanu Dasgupta 1,2,3,*
Editor: Robert Arthur Kratzke
Lung Cancer and Risk Factors
Ref
International Journal of Molecular Sciences logo
Int J Mol Sci. 2025 Apr 17;26(8):3818. doi: 10.3390/ijms26083818
The Current Roadmap of Lung Cancer Biology, Genomics and Racial Disparity
Enas S Alsatari 1,2, Kelly R Smith 1,2, Sapthala P Loku Galappaththi 1,2, Elba A Turbat-Herrera 1,2, Santanu Dasgupta 1,2,3,*
Editor: Robert Arthur Kratzke
2.2. Environmental and Lifestyle Risk Factors
Epidemiology and risk factors involve a complex interaction of environmental, genetic mutations, and lifestyle factors that contribute to susceptibility to lung cancer and its outcomes [16,17].
However, these interactions become more significant when considering ethnic and ancestor differences.
Although smoking is the predominant cause of lung cancer, another study revealed that 10–25% of all lung cancer patients have never smoked [18].
This disparity underscores the need to investigate additional risk factors other than smoking, especially in populations where lung cancer is not related to smoking [19].
Cigarette smoking remains a major risk factor for lung cancer development. The initiation of smoking habits is mediated by peer pressure, family habits, and psychological distress [20,21].
Interestingly, Harrell et al. reported that demographic factors such as race, socioeconomic status, and pubertal development were significant predictors of early smoking initiation among schoolchildren [22].
Additionally, preventative measures for air pollution include techniques like urea-selective catalytic reduction (SCR), diesel particulate filters, and NOx storage-reduction catalysts approved to enhance air quality to avoid additional health effects from gaseous as well as particulate air pollution pollutants [23].
As a reason, there were substantial declines in lung cancer incidence in the USA from 2007 to 2018. On the other hand, there has been little change in rates among never-smokers, though rates increased significantly in Asian and Pacific Islander populations [24].
In Denmark, lung cancer trends are influenced by historical smoking patterns, where a decline in male smoking rates led to reduced incidence. In contrast, the prevalence of smoking in women remained stable for longer, contributing to a later increase in lung cancer incidence [25].
Existing evidence suggests that passive smoke is the cause of a significant proportion of lung cancer in women.
For instance, Du et al. reported that passive smoking accounts for about 17.9% of lung cancer cases among never-smoking women, most of them exposed to household smoking [26]
. Moreover, a study of Moroccan women showed that 75% of lung cancer cases were recorded in never-smokers, and LUAD was the most common subtype among passive smokers [27].
Zhu et al. reported that non-smoking people who drink tea ≥ 2 cups/day have a greater risk of lung cancer [28].
At the population level, cigarette smoking is the primary determinant of the occurrence of lung cancer [29].
Environmental factors increase the risk of developing lung cancer, such as air pollution, occupational exposure, secondhand smoke, and radiation exposure [30,31].
In China, a study by Liu et al. observed that occupational environment and meteorological conditions synergistically affect lung cancer development [32].
Furthermore, Chinese-style cooking increases lung cancer risk [33].
Moreover, long-term exposure to air pollutants such as PM2.5, NO2, and NOx significantly increases the risk of developing lung cancer [34]. The World Cancer Research Fund (WCRF) reported that drinking water with high concentrations of arsenic increases lung cancer risk, and the evidence was reported as “convincing” [35]. Additional interaction of these air pollutants with poor lifestyle and high genetic risk dramatically raises the likelihood of lung cancer occurrence [35]. Similarly, Huang et al. showed the same results [36]. However, predicting cancer associated with environmental factors like alcohol consumption and smoking can alter based on the variation in polymorphism of xenobiotic metabolizing enzymes (XME) genes [37]. Pettit et al. studied the genetic correlation between various traits and lung cancer risk, indicating a negative genetic correlation between lung cancer risk and some traits, including dietary behaviors, fitness metrics, educational attainment, and other psychosocial characteristics. On the contrary, the body mass index (BMI) showed a positive genetic correlation with the likelihood of lung cancer [38].
The relationship between lung cancer risk and dietary items like fruits, vegetables, micronutrients, phytochemicals, fat, and beverages has been studied. An increased intake of fruits, vegetables, and carotenoid-rich foods is associated with a reduced risk of developing lung cancer [35].
On the contrary, higher intake of retinol, red meat intake, processed meat intake, alcohol drinking, and dietary fat have been associated with an increased risk of lung cancer.
However, no link has been reported between the phytochemical “bioflavonoid” and lung cancer risk
Lung cancer Types
2.1. Histological Subtypes of Lung Cancer
Ref
Int J Mol Sci. 2025 Apr 17;26(8):3818. doi: 10.3390/ijms26083818
The Current Roadmap of Lung Cancer Biology, Genomics and Racial Disparity
Enas S Alsatari 1,2, Kelly R Smith 1,2, Sapthala P Loku Galappaththi 1,2, Elba A Turbat-Herrera 1,2, Santanu Dasgupta 1,2,3,*
Editor: Robert Arthur Kratzke
Lung cancer is divided into two major groups: small-cell lung cancer
(SCLC) and non-small-cell lung cancer (NSCLC).
SCLC is aggressive and has a high risk for distant metastasis at initial diagnosis [11] and accounts for 12% of all lung cancer cases [12].
NSCLC is, conversely, the most common group, representing 80% to 85% of the lung cancer cases [13].
Among the NSCLC, adenocarcinoma (LUAD) is the most common histologic subtype, accounting for 45% of all cases,
followed by squamous cell carcinoma (LUSC) at 21% of cases,
while 23% attributed to unclassified histologic subtypes [12]. Notably, LUAD is more common in never-smokes with a predominant EGFR gene mutation, whereas LUSC is more common among smokers with a predominant TP53 gene mutation [14,15].
Saturday, January 24, 2026
फुफ्फुसाच्या कर्करोगाचे जीवशास्त्र
इंट जे मोल सायन्स. २०२५ एप्रिल १७;२६(८):३८१८. doi: १०.३३९०/ijms२६०८३८१८
फुफ्फुसाच्या कर्करोगाचे जीवशास्त्र, जीनोमिक्स आणि वांशिक विषमतेचा सद्यस्थितीतील आराखडा
एनास एस अलसातारी १,२, केली आर स्मिथ १,२, सप्तला पी लोकू गलापथी १,२, एल्बा ए टर्बट-हेरेरा १,२, सांतनु दासगुप्ता १,२,३,*
संपादक: रॉबर्ट आर्थर क्रॅट्झके
Ref
Int J Mol Sci. 2025 Apr 17;26(8):3818. doi: 10.3390/ijms26083818
The Current Roadmap of Lung Cancer Biology, Genomics and Racial Disparity
Enas S Alsatari 1,2, Kelly R Smith 1,2, Sapthala P Loku Galappaththi 1,2, Elba A Turbat-Herrera 1,2, Santanu Dasgupta 1,2,3,*
Editor: Robert Arthur Kratzke
प्रस्तावना
फुफ्फुसाचा कर्करोग हा दुसऱ्या क्रमांकाचा सर्वात सामान्य कर्करोग आहे, ज्याचा घटना दर ११.४% आहे [१].
२०१८ मध्ये युनायटेड स्टेट्समध्ये २,३०,००० हून अधिक नवीन प्रकरणे आढळली, ज्यामुळे स्तन, कोलन आणि प्रोस्टेट कर्करोगासह इतर सर्व कर्करोगांच्या एकत्रित प्रकरणांपेक्षा जास्त मृत्यू झाले [२].
ग्लोबोकॅन २०२० च्या आकडेवारीनुसार, २०२० मध्ये फुफ्फुसाच्या कर्करोगाची अंदाजे २.३ दशलक्ष नवीन प्रकरणे (११.४%) आणि जवळपास १.८ दशलक्ष मृत्यू नोंदवले गेले [३].
आयुष्याच्या पाचव्या दशकापूर्वी फुफ्फुसाचा कर्करोग असामान्य आहे, परंतु वयानुसार त्याचा घटना दर वाढतो [३].
अमेरिकेत, पुरुषांमध्ये फुफ्फुसाच्या कर्करोगाचा घटना दर कमी होत आहे, तर महिलांमध्ये सुरुवातीला वाढ आणि नंतर घट दिसून आली.
हे विशेषतः तरुण स्त्रियांमध्ये अधिक ठळकपणे दिसून येते, ज्यांच्यामध्ये अलीकडे पुरुषांपेक्षा जास्त घटना दर दिसून आले आहेत, विशेषतः नॉन-हिस्पॅनिक श्वेतवर्णीय आणि आशियाई/पॅसिफिक बेटांवरील लोकांमध्ये [४].
त्याचप्रमाणे, नोलेन आणि इतरांच्या एका अभ्यासात असे दिसून आले की, युनायटेड स्टेट्समध्ये तरुण स्त्रियांमध्ये समान वयाच्या पुरुषांपेक्षा फुफ्फुसाच्या कर्करोगाचे प्रमाण जास्त आहे, जे ५०-५४ वयोगटापर्यंत दिसून येते [५].
एका अगदी अलीकडील अभ्यासात असे दिसून आले आहे की फुफ्फुसाच्या कर्करोगाच्या मृत्यू दरातील घट ही घटना दरातील घटीपेक्षा जास्त आहे, विशेषतः पुरुष (वार्षिक ५.०% विरुद्ध २.६%) आणि महिलांमध्ये (वार्षिक ४.३% विरुद्ध १.१%) [६].
दुसरीकडे, विविध वांशिक आणि जातीय गटांमध्ये फुफ्फुसाच्या कर्करोगाच्या घटना दरामध्ये अजूनही विषमता अस्तित्वात आहे। मूळ अमेरिकन लोकांमध्ये या रोगाचे प्रमाण सर्वाधिक आणि घट सर्वात कमी दिसून आली, आणि मिसिसिपी आणि केंटकीसह विविध राज्यांमध्ये, ऐतिहासिक धूम्रपान प्रसारामुळे बहुतेक पाश्चात्य राज्यांपेक्षा दोन ते तीन पट जास्त मृत्यू दर अनुभवला जात आहे [६].
याव्यतिरिक्त, इतर हिस्पॅनिक गटांच्या तुलनेत क्यूबन पुरुषांमध्ये या रोगाचे प्रमाण अधिक आहे, तर अमेरिकेत जन्मलेल्या कृष्णवर्णीय पुरुषांमध्ये कॅरिबियनमध्ये जन्मलेल्या कृष्णवर्णीयांपेक्षा हे प्रमाण जास्त आहे [७].
महिलांमध्ये, अमेरिकेत जन्मलेल्या कृष्णवर्णीय महिलांमध्ये या रोगाचे प्रमाण सर्वाधिक आहे [७].
असे असले तरी, फुफ्फुसाचा कर्करोग हा जगाच्या सर्व भागांमध्ये कर्करोगामुळे होणाऱ्या मृत्यूचे सर्वात सामान्य कारण आहे [८].
२०२० मध्ये, फुफ्फुसाच्या कर्करोगामुळे सुमारे १.८ दशलक्ष मृत्यू झाले, जे सर्व कर्करोगाच्या मृत्यूंपैकी १८% होते.
वय-मानक मृत्यू दर (ASMR) प्रति १,००,००० लोकांमागे १८.० होता (पुरुषांमध्ये २५.९ आणि महिलांमध्ये ११.२) [९,१०].
मृत्यू दरामध्ये प्रादेशिक स्तरावर लक्षणीय फरक दिसून येतो. सर्वाधिक मानवी विकास निर्देशांक (HDI) असलेल्या देशांमध्ये, प्रामुख्याने युरोप आणि उत्तर अमेरिकेत, हे दर सर्वाधिक आहेत, तर उप-सहारा आफ्रिकेत असलेल्या देशांमध्ये हे दर सर्वात कमी आहेत [९].
या समीक्षा लेखात, आम्ही फुफ्फुसाच्या कर्करोगाचे आणि वांशिक विषमतेचे सध्याचे ज्ञान सारांशित केले आहे, ज्यामध्ये जीनोमिक्स, जीवशास्त्र आणि सूक्ष्मजीव परिसंस्था यासह विविध पैलूंवर लक्ष केंद्रित केले आहे.
आम्ही फुफ्फुसाच्या कर्करोगाच्या निर्मितीशी संबंधित भिन्न हिस्टोपॅथॉलॉजिकल आणि आण्विक उपप्रकार, महामारीशास्त्र आणि जोखीम घटक, हिस्टोपॅथॉलॉजिकल आणि आण्विक प्रगतीचे नमुने, केंद्रकीय आणि मायटोकॉन्ड्रियल अनुवांशिक बदल, एपिजेनेटिक बदल, रोगप्रतिकार प्रणालीतील बिघाड आणि मायक्रोबायोममधील असंतुलन देखील सादर केले आहेत.
Roadmap of lung cancer Biology (Introduction)
Int J Mol Sci. 2025 Apr 17;26(8):3818. doi: 10.3390/ijms26083818
The Current Roadmap of Lung Cancer Biology, Genomics and Racial Disparity
Enas S Alsatari 1,2, Kelly R Smith 1,2, Sapthala P Loku Galappaththi 1,2, Elba A Turbat-Herrera 1,2, Santanu Dasgupta 1,2,3,*
Editor: Robert Arthur Kratzke
Introduction
Lung cancer ranks as the second most prevalent malignancy, with an 11.4% incidence rate [1].
Over 230,000 new cases were detected in the United States in 2018, leading to more fatalities than all other cancers including breast, colon, and prostate cancer combined [2].
According to GLOBOCAN 2020 data, approximately 2.3 million new cases (11.4%) and almost 1.8 million deaths from lung cancer were recorded in 2020 [3].
Lung cancer is uncommon before the fifth decade of life, but its incidence rises with age [3].
In the U.S., lung cancer incidence among males continues to decline, while females showed an initial increase followed by a decline.
It is particularly marked among younger women who have recently demonstrated higher incidence rates than males, notably for non-Hispanic Whites and Asians/Pacific Islanders [4].
Similarly, a study by Nolen et al. reported higher rates of lung cancer in the United States in young women than men of similar age, extending to those aged 50–54 [5].
A very recent study showed reductions in lung cancer mortality rates that have exceeded reductions in incidence, particularly among men (5.0% vs. 2.6% annually) and women (4.3% vs. 1.1% annually) [6].
On the other hand, the disparity in lung cancer incidence still exists among various racial and ethnic groups.
The highest incidence rates and the slowest decline were seen in Native Americans, with various States, including Mississippi and Kentucky, continuing to experience mortality rates two to three times higher than most Western States due to historic smoking prevalence [6].
In addition, Cuban males show higher incidence rates among other Hispanic groups, whereas U.S.-born Black males show higher incidence rates than Caribbean-born Blacks [7].
Among females, US-born Blacks exhibit the highest incidence rates [7].
Nevertheless, lung cancer is the most common cause of cancer-related death in all parts of the world [8].
In 2020, lung cancer was responsible for around 1.8 million deaths, accounting for 18% of all cancer deaths.
The age-standardized mortality rate (ASMR) was 18.0 per 100,000 (25.9 in men and 11.2 in women) [9,10].
Mortality exhibits substantial regional variation. The highest rates are seen in countries with high Human Development Index (HDI) scores, primarily from Europe and North America, while the lowest rates are noted among those mainly located in Sub-Saharan Africa [9].
In this review article, we summarize the current knowledge of lung cancer and racial disparities, focusing on various aspects, including genomics, biology, and microbial landscapes.
We also presented divergent histopathological and molecular subtypes, epidemiology and risk factors, histopathological and molecular progression patterns, nuclear and mitochondrial genetic alterations, epigenetic alteration, immune system dysfunction, and microbiome dysbiosis associated with lung tumorigenesis.
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