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Cancers
Special Issues
Lifestyle Choices and Endocrine Dysfunction on Cancer Onset and Risk
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Lifestyle Choices and Endocrine Dysfunction on Cancer Onset and Risk

A special issue of Cancers (ISSN 2072-6694). This special issue belongs to the section "Tumor Microenvironment".

Deadline for manuscript submissions: 30 September 2024 | Viewed by 2430

Special Issue Editors

Dr. Ariane Zamoner

E-Mail Website
Guest Editor
Department of Biochemistry, Federal University of Santa Catarina, Florianopolis 88040-900, Brazil
Interests: endocrine dysfunction; cancer; toxicology; biochemistry; redox biology
Special Issues, Collections and Topics in MDPI journals
Dr. Marco G. Alves

E-Mail Website
Guest Editor
Institute of Biomedicine (iBiMED), Department of Medical Sciences, University of Aveiro, 3810-193 Aveiro, Portugal
Interests: metabolism; mitochondria; omics; andrology; oxidative stress
Special Issues, Collections and Topics in MDPI journals
Dr. Ana Paula S. Perez

E-Mail Website
Guest Editor
Academic Unit of Health Sciences, Medicine Course, Federal University of Jataí, BR 36, Km 195, Jataí, Goiás 75801-615, Brazil
Interests: endocrine disruptors; histopathology; reproductive biology; development; cancer

Special Issue Information

Dear Colleagues,

Cancer is a disease characterized by the uncontrollable proliferation and dissemination of abnormal cells. It ranks as one of the world's leading causes of mortality, hurling a profound shadow over individuals and their families. While the precise origins of cancer are multifaceted and diverse, they often involve an intricate interplay of genetic, environmental, and lifestyle factors. Understanding the influential and predictive roles of lifestyle variables and endocrine dysfunction holds the key to refining prediction models and identifying actionable, modifiable targets associated with cancer onset and risk. Unraveling the cellular and molecular pathways underlying cancer development and progression allows for the development of targeted therapeutic interventions to halt or treat the disease. The World Health Organization underscores the preventive power of adopting healthy lifestyles in averting numerous cancer cases. This Special Issue endeavors to provide the latest insights into how lifestyle choices and endocrine dysfunction intersect to impact cancer onset and risk, in addition to potential prophylactic and/or therapeutic interventions.

Dr. Ariane Zamoner
Dr. Marco G. Alves
Dr. Ana Paula S. Perez
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cancers is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2900 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • occupational exposure
  • obesity
  • nutrition
  • exercise
  • endocrine disruptors
  • reproduction
  • development
  • hormone

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Published Papers (2 papers)

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Research

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15 pages, 1813 KiB  
Article
Clinical Correlations between Serological Markers and Endometrial Cancer
by Alina-Gabriela Marin, Alexandru George Filipescu, Răzvan Cosmin Petca, Radu Vlădăreanu and Aida Petca
Cancers 2024, 16(10), 1935; https://doi.org/10.3390/cancers16101935 - 20 May 2024
Viewed by 980
Abstract
Background: Endometrial cancer is associated with changes in blood cell counts and with high levels of inflammatory markers, thus reflecting the tumor’s impact on various biological processes and suggesting their potential as biomarkers for endometrial cancer diagnosis, prognosis, and treatment response. The neutrophil-to-lymphocyte [...] Read more.
Background: Endometrial cancer is associated with changes in blood cell counts and with high levels of inflammatory markers, thus reflecting the tumor’s impact on various biological processes and suggesting their potential as biomarkers for endometrial cancer diagnosis, prognosis, and treatment response. The neutrophil-to-lymphocyte ratio, platelet-to-lymphocyte ratio, and monocyte-to-lymphocyte ratio in peripheral blood sampled preoperatively from patients have been reported to be independently associated with the prognosis of different types of malignancies. Objectives: This study aimed to compare several blood markers—red blood cells, white blood cells, platelet parameters, neutrophil-to-lymphocyte ratio, platelet-to-lymphocyte ratio, monocyte-to-lymphocyte ratio, C-reactive protein, and fibrinogen—in patients with benign or malignant endometrial tumors. Material and methods: Our retrospective study included 670 patients (192 diagnosed with endometrial cancer and 478 with endometrial hyperplasia), and we compared the serological parameters discussed above with those sampled the day before surgery. Results: Analysis of complete blood count indices revealed no significant differences in red blood cell or total white blood cell parameters between the endometrial cancer group and the endometrial hyperplasia group. However, a distinct pattern emerged in the white blood cell differential. The endometrial cancer group showed a statistically significant decrease in lymphocyte count compared with the endometrial hyperplasia group. In contrast, the endometrial cancer group showed significantly higher mean platelet counts and increased mean platelet volume compared with controls. Furthermore, the endometrial cancer group demonstrated a marked inflammatory response, as evidenced by significantly elevated levels of C-reactive protein, fibrinogen, neutrophil-to-lymphocyte ratio, platelet-to-lymphocyte ratio, and monocyte-to-lymphocyte ratio compared with the endometrial hyperplasia group. Conclusions: The current research revealed statistically significant differences in multiple serological biomarkers between the two groups. These findings support the initial hypothesis regarding the potential utility of these biomarkers in endometrial cancer diagnosis, prognosis, and treatment response, highlighting the existence of biomarkers affordable for analysis under any health system, regardless of the country’s level of development. Full article
(This article belongs to the Special Issue Lifestyle Choices and Endocrine Dysfunction on Cancer Onset and Risk)
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Figure 1

Figure 1
<p>Neutrophile–lymphocyte ratio: box plot comparing NLR between the EC and EH groups. The median NLR was significantly higher in the EC group (4.191) compared with the EH group (2.396, <span class="html-italic">p</span>-value = 0.004). The interquartile range (IQR) for the EC group (2.128–5.063) was larger than for the EH group (1.786–3.421), suggesting greater variability in NLR within the EC group.</p> Full article ">Figure 2
<p>Platelet–lymphocyte ratio: box plot comparing PLR between the EC and EH groups. The median PLR was significantly higher in the EC group (161.204) compared with the other group (136.878, <span class="html-italic">p</span>-value &lt; 0.0001). The IQR for the EC group (123.986–234.329) was more significant than for the EH group (105.089–174.808), suggesting greater variability in PLR within the EC group.</p> Full article ">Figure 3
<p>Monocyte–lymphocyte ratio: box plot comparing MLR between the EC and EH groups. The median MLR was significantly higher in the EC group (0.298) compared with the other group (0.262, <span class="html-italic">p</span>-value &lt; 0.0001). The IQR for EC group (0.243–0.480) was larger than the control group (0.208–0.337), suggesting greater variability in MLR within the EC group.</p> Full article ">Figure 4
<p>ROC curve for statistically significant markers.</p> Full article ">Figure 5
<p>ROC curve analysis for all serological markers tested.</p> Full article ">Figure 6
<p>ROC curve analysis for all serological markers and selected baseline characteristics.</p> Full article ">

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Jump to: Research

12 pages, 6598 KiB  
Hypothesis
Role of Oncostatin M in Exercise-Induced Breast Cancer Prevention
by Kara A. Negrini, Dan Lin, Dhruvil Shah, Hongke Wu, Katherine M. Wehrung, Henry J. Thompson, Tiffany Whitcomb and Kathleen M. Sturgeon
Cancers 2024, 16(15), 2716; https://doi.org/10.3390/cancers16152716 - 31 Jul 2024
Viewed by 436
Abstract
Moderate-to-vigorous-intensity physical activity decreases the risk of breast cancer. The muscle-derived cytokine (myokine), oncostatin M (OSM), has been shown to decrease breast cancer cell proliferation. We hypothesized that OSM is involved in physical activity-induced breast cancer prevention, and that OSM antibody (Anti-OSM) administration [...] Read more.
Moderate-to-vigorous-intensity physical activity decreases the risk of breast cancer. The muscle-derived cytokine (myokine), oncostatin M (OSM), has been shown to decrease breast cancer cell proliferation. We hypothesized that OSM is involved in physical activity-induced breast cancer prevention, and that OSM antibody (Anti-OSM) administration would mitigate the effect of physical activity in a rat model of mammary carcinoma. Female Sprague Dawley rats were injected with 50 mg/kg N-methyl-N-nitrosourea to induce mammary carcinogenesis. During the 20-week study, rats were exercise trained (EX) or remained sedentary (SED). Additional groups were treated with Anti-OSM antibody (SED + Anti-OSM and EX + Anti-OSM) to explore the impact of OSM blockade on tumor latency. Exercise training consisted of treadmill acclimation and progressive increases in session duration, speed, and grade, until reaching 30 min/day, 20 m/min at 15% incline. Experimentally naïve, age-matched, female rats also completed an acute exercise test (AET) with time course blood draws to evaluate OSM plasma concentrations. Relative tumor-free survival time was significantly longer in EX animals (1.36 ± 0.39) compared to SED animals (1.00 ± 0.17; p = 0.009), SED + Anti-OSM animals (0.90 ± 0.23; p = 0.019), and EX + Anti-OSM animals (0.93 ± 0.74; p = 0.004). There were no significant differences in relative tumor latency between SED, SED + Anti-OSM, or EX + Anti-OSM animals. Following the AET, OSM plasma levels trended higher compared to baseline OSM levels (p = 0.080). In conclusion, we observed that exercise-induced delay of mammary tumor development was mitigated through Anti-OSM administration. Thus, future studies of the OSM mechanism are required to lay the groundwork for developing novel chemo-prevention strategies in women who are unable or unwilling to exercise. Full article
(This article belongs to the Special Issue Lifestyle Choices and Endocrine Dysfunction on Cancer Onset and Risk)
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Figure 1

Figure 1
<p>Schematic of the experimental timeline. All rats were acclimated to the treadmill prior to randomization into experimental groups. After treadmill ramp up, exercised rats continued training 5 days per week for the duration of this study (week 3–20). MNU = n-methyl-n-nitrosourea. Anti-OSM = Mouse anti-oncostatin M.</p> Full article ">Figure 2
<p>(<b>A</b>) Rat body weight growth curve over 20 weeks. Week 0 = pre-MNU injection weight. All SED + Anti-OSM rats were euthanized by week 14 due to tumor burden reaching 4 cm<sup>3</sup>. The drop in average SED weights during weeks 19 and 20 was due to a decrease in animal numbers from tumor burden reaching 4 cm<sup>3</sup> (SED <span class="html-italic">n</span> = 2 at week 19). No statistical significance. (<b>B</b>) Average heart weight to carcass weight ratio. SED <span class="html-italic">n</span> = 15, EX <span class="html-italic">n</span> = 14, SED + Anti-OSM <span class="html-italic">n</span> = 5, EX + Anti-OSM <span class="html-italic">n</span> = 12. No statistical significance. x = group mean.</p> Full article ">Figure 3
<p>Representative photos of malignant tumors from each group. (<b>A</b>) SED. (<b>B</b>) EX. (<b>C</b>) SED + Anti-OSM. (<b>D</b>) EX + Anti-OSM. All scale bars represent 1 cm.</p> Full article ">Figure 4
<p>Average normalized tumor latency across groups (SED <span class="html-italic">n</span> = 14, EX <span class="html-italic">n</span> = 14, SED + Anti-OSM <span class="html-italic">n</span> = 5, EX + Anti-OSM <span class="html-italic">n</span> = 10). * <span class="html-italic">p</span> &lt; 0.05, † <span class="html-italic">p</span> &lt; 0.01. x = group mean.</p> Full article ">Figure 5
<p>Plasma OSM concentrations after 1 h of exercise on motorized treadmill. OSM was measured from plasma samples isolated from blood collected at three different timepoints (before, immediately after, and 2 h after) from experimentally naïve rats (<span class="html-italic">n</span> = 7). **: <span class="html-italic">p</span> = 0.080.</p> Full article ">
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