Immunological analysis of Interleukin-10 (IL-10),tumor necrosis factor-a (TNF-a),and Prostate-specific antigen (PSA) in benign and malignant prostate cancer

Abstract

INTRODUCTION:

Among the cancers that impacts men, prostate cancer considerably raises deaths for males around the world. Persons with tumours can have a localized or advanced form of the illness.

OBJECTIVE:

The present study aimed to determining the relationship between the level of cytokines (IL-10 and TNF-a) and PSA in the sera of patients and compared it with healthy.

MATERIALS AND METHODS:

A case control study consist of three group included was in this study. The first group involves 50 patients with PC were observation in Al-Amal Oncology Hospital in the period from April 2021 to April 2022 under the supervision of oncology specialists was included in this study. Second group consist of 30 patients. They have benign hyper plaisa (BHP), this group has been collected from urosergical department . Third group was include 20 healthy volunteers (non prostate cancer and non BHP). Prostate specific antigen (PSA) was measured by mini – VIDAS device using kit supplied by Biomerieux – France. IL-10 and TNF-a levels were measured by ELISA technique using kit supplied by CAUSABIO – China.

RESULTS:

Results of the present study showed the 60–69 years age group scored highest percentage in benign (56.7%), malignant (54.0%), compared to control (healthy) (50.0%), while $>$ 69 years scored least percentage in these groups (3.3%, 14.0%, and 25.0%) respectively with significant different ( $p<$ 0.05). Additionally, the IL-10 and PSA scored highest mean levels in the malignant group (1.22 $\pm$ 0.23 and 27.66 $\pm$ 6.31), while TNF-a scored highest mean levels in a benign group (0.30 $\pm$ 0.11). The least mean level of IL-10 was in healthy (0.42 $\pm$ 0.15), TNF-a in malignant (0.23 $\pm$ 0.03), and PSA in benign (6.73 $\pm$ 1.36). Finally, there is a significant difference among age groups and PSA, IL-10, and TNF-parameters.

CONCLUSIONS:

We concluded the PSA, TNF-a and IL-10 parameters are play important roles in pathogenesis patients with prostate cancer. PCa is high prevalence in elderly population.

Keywords

Prostate cancer PSA IL-10 TNF-a

1. Introduction

In addition to being one of the most often identified malignancies in men, type of cancer also ranks among the major sources of cancer mortality globally [1]. Beginning tumor frequently has no symptoms and progresses slowly, necessitating little or no therapy. The most major complaint, therefore, is discomfort urinating, increased frequency, and nocturia, all of which are prostatic hypertrophy-related indications [2].

Prostate cancer is thought to affect 1.6 million men annually, with 366,000 of them dying from it [3]. With 1,276,106 new cases and 358,989 fatalities (3.8% of all cancer-related mortality in men), prostate cancer was the foremost common malignancy in males globally after malignancy in 2018 [4]. Prostate cancer risk of death and morbidity are both correlated with aging globally, with a mean lifespan of 66 at detection. The incident rate is greater for African-American males than for White men, with 158.3 new cases diagnosed per 100,000 men, and their mortality is around twice as high [5]. Prostate cancer is the most commonly occurring infectious tumor in Swedish males and is roughly as common as breast cancer, with more than 10,000 cases reported detected in 2018 [6].

On the basis of elevated plasmatic levels of prostate-specific antigen (PSA $>$ 4 ng/mL), a glycoprotein usually expressed by prostate tumors, many cases of prostate cancer are discovered. However, a tissue biopsy is the standard of care to determine the existence of cancer because men without cancer have also been seen to have increased PSA levels [7]. Since its invention, PSA has dominated the field of biomarkers used for testing and treatment, illness monitoring (whether it has been treated or not), and lengthy fate prediction [8].

IL-10 appears to play an important role in both the emergence of human cancer and its immunological evasion. These have indicated that it might be used as a therapy aim or an indicator for disorders that are prognostic [9]. Greater IL10 serum concentrations have been linked to a poor prognosis in medical examinations, including those of prostate cancer patients, comment colon cancer patients, and those with breast cancer [10]. In a previous research, it was discovered that the IL-10 plasma strongly correlated with Gleason scores and was associated with the tumor growth and metastasis of PCa individuals’ tumors [11].

TNF serves as one of the immunological system’s main top player cytokines, and it has been linked to a number of malignant tumors, including breast, gastric, pancreatic, ovarian, endometrial, prostate, bladder, colorectal, oral, and liver cancers [12]. Additionally, it has been found in lymphomas and leukemias. Even yet, as the cytokine is elevated in many other disorders as well, there is currently debate about whether TNF activation should be considered an indicator. TNF-plays a critical role in the aggressive and symptom pathways in a number of cancer types, including oral, breast, and prostate cancer, according to epidemiology and genomic studies [13]. Interleukin-6 and sarcoma inflammatory major end product have been shown in prior studies to induce epithelial mesenchymal transition in PCa cells, enhance cell proliferation and metastasis, and offer a fresh route for further study [14]. The current study sought to compare PSA levels in patient serum to control subjects in order to determine the association among cytokine levels (IL-10 and TNF-a).

2. Materials and methods

2.1 Population studies

2.2 Determination of PSA, IL-10, and TNF-a parameters

Five ml of blood sample were collected from patients and healthy in gel tube and stay it for 10 minutes then separate by centrifugation 3000 pm for 5 minute to have serum. Prostate specific antigen (PSA) was measured by mini – VIDAS device using kit supplied by Biomerieux – France. IL-10 and TNF-a levels were measured by ELISA technique using kit supplied by CAUSABIO – China.

2.3 Statistical analysis

First, the normalcy of the PSA, IL-10, and TNF-a variables was assessed (Kolmogorov-Smirnov and Shapiro-Wilk test). The mean and standard error (SD) of the parameters that fit both tests (no substantial difference) were supplied, with the undergraduate $t$ test being used to compare two categories and the $F$ test being used to compare more than two groups. The parameters were shown as maximum and mean if they failed the normality tests (notable change), and Mann-Whitney analysis revealed a significant variation seen between medians (for comparison between two groups). The remaining characteristics (nominal scale) were presented as percentage frequencies, and Pearson Chi-Square tests or 2 different Fisher exact probabilities were used to determine whether there were any big variation between the frequencies ( $p$ ). To conduct these investigations, the statistical package SPSS version 25.0 and Graphpad Software version 6 were used.

Table 1
Distribution of study groups according to age groups

		Study groups
		Benign ( $n=$ 30)	Malignant ( $n=$ 50)	Healthy ( $n=$ 20)	Total	$P$ value
50–59	$n$	12	16	5	33	$P<$ 0.05 ${}^{*}$
	%	40.0%	32.0%	25.0%	31.0%
60–69	$n$	17	27	10	54	$P<$ 0.05 ${}^{*}$
	%	56.7%	54.0%	50.0%	47.0%
$>$ 69	$n$	1	7	5	13	$p>$ 0.05
	%	3.3%	14.0%	25.0%	10.0%
$P$ value		$P<$ 0.001 ${}^{***}$	$P<$ 0.001 ${}^{***}$	$p>$ 0.05	$P<$ 0.001 ${}^{***}$

3. Results and discussion

3.1 Distribution of study groups according to age groups

Results of the present study showed there is significant differences ( $p<$ 0.05) among age groups and among study groups, where the 60–69 years age group scored highest percentage in benign (56.7%), malignant (54.0%), compared to control (healthy) (50.0%), while $>$ 69 years scored least percentage in these groups (3.3%, 14.0%, and 25.0%) respectively (Table 1).

The present study showed a high occurrence of prostate cancer with age progression, where we found the highest percentage of these diseases appeared in elderly patients due to lifestyle, chronic diseases, organ dysfunction, immune system dysfunction, and genetic disorders. Prostate cancer risk has been rising across the globe, especially in Asia and Northern and Western Europe [15]. According to postmortem investigations, the prevalence of prostate cancer similarly rises with age, from an average 5% rate in males under 30 to 59% in those over 79 [16]. The Global Health Organization reports that the average male lifespan rose from 64.1 years in 2000 to 69.1 years in 2015 [17].

An older population is predicted to increase the prevalence of the disorder prostate cancer. Early findings indicated that the aging-adjusted incidence rates of prostate cancer in the Asian region and the growing Developed powers was already rising, but these levels had previously stopped growing and even declined over time in the major Advanced economies [18].

As people age, several systems lose cellular mass and lose their ability to regenerate. The prostate, on the other hand, keeps expanding in size. In actuality, the biggest risk factor for prostate cancer is age. Furthermore, the structure, shape, and biochemical factors of prostate epithelial progenitor cells – the cells that give rise to prostate cancer – are influenced by time of life variables [19].

Dominant males and non-Hispanic Black men have a higher risk of developing prostate cancer. It is uncommon in men under 40 and is identified in about 6 out of 10 men who are 65 or older. For men, the diagnostic age is often around 66 [20].

The previous research found that the cohort effect found important reducing patterns from the 1917–1921 to the 2002–2006 birth cohorts, but the external displayed sharp growing trends from 40 to 79 years, and the period effect showed both of them constantly rising with advancing time [21].

According to research conducted in Australia in 2021, less than one person per 100,000 men treated for prostate cancer within this age range survived. This is known as the time of life incidence and mortality (AMR). On the other hand, the predicted age-specific mortality rate for men with prostate cancer who are beyond 90 years old is above 314 per 100,000 people [22].

3.2 Relationship of immunological parameters with study groups

Table 2
Comparative levels of immunological parameters within study groups

Parameters	$N$	Mean	SD	Statistics
IL-10	Benign	30	0.45	0.13	$P<$ 0.001 ${}^{***}$
	Malignant	50	1.22	0.23	LSD $=$ 0.18
	Healthy	20	0.42	0.15
TNF-a	Benign	30	0.30	0.11	$P<$ 0.001 ${}^{***}$
	Malignant	50	0.23	0.03	LSD $=$ 0.03
	Healthy	20	0.25	0.01
PSA	Benign	30	6.73	1.36	$P<$ 0.001 ${}^{***}$
	Malignant	50	27.66	6.31	LSD $=$ 4.04
	Healthy	20	14.55	7.79

Figure 1.

Comparative mean levels of immunological parameters among study groups.

Results of the present study showed there are significant differences ( $p<$ 0.05) between IL-10, TNF-a, and PSA parameters and study groups, where it is found the IL-10 and PSA scored highest mean levels in the malignant group (1.22 $\pm$ 0.23 and 27.66 $\pm$ 6.31), while TNF-a scored highest mean levels in a benign group (0.30 $\pm$ 0.11). The least mean level of IL-10 was in healthy (0.42 $\pm$ 0.15), TNF-a in malignant (0.23 $\pm$ 0.03), and PSA in benign (6.73 $\pm$ 1.36) (Table 2 and Fig. 1). The conducted study showed increased levels of TNF-a in benign prostate cancer and decreased it in malignant compared to healthy. TNF has a wide range of uses and effects, including those on tumor cells. TNF has been said to have conflicting effects on practically all cancer types. TNF is capable of totally eradicate methylcolanthrene (MCA)-induced benign cysts in high quantities, as first discovered by Carswell, and about 28% of malignancies are responsive to sTNF [23].

TNF has a variety of antitumor mechanisms, some of which are as follows: thorough overview of inducing cell damage [24]; stimulating cytokines and preventing monocyte maturation to inhibitory morphologies, driving neutrophils and monocytes to tumor locations, disrupting tumorigenesis, and directing tumor-associated macrophages (TAMs) to the M1 profile (antitumoral phenotype) [24]. Given the foregoing, TNF expression at low levels has been shown to have a widely documented top player effect [25].

TNF serves as one of the immunological system’s primary pro-inflammatory cytokines, and it has been linked to a number of human malignancies, including breast, gastric, pancreatic, ovarian, uterine, prostate, bladder, colorectal, oral, and liver cancers [12]. Additionally, it has been found in malignancies and myeloma. Even yet, as the cytokine is elevated in many other disorders as well, there is currently debate about whether TNF production should be considered a diagnostic.

The clinical significance of TNF to promoting or impeding the efficacy of immunotherapy has not yet been thoroughly clarified, according to a new study. Furthermore, in actuality, the use of anti-TNF medications to avoid the adverse events (irAEs) brought on by immune checkpoint inhibitors and adoptive cell treatment (ACT) has yielded intriguing findings, demonstrating that blocking particular cytokine may have anticancer effects. Then again, the significance of TNF blocking in prostate, renal, and cytogenetic cancers has been shown in numerous clinical trials because it increases mortality risk (OS). Additionally, there is a ton of experimental evidence demonstrating TNF’s capacity to promote immunotherapy resistance. For instance, TNF can cause the upregulation of PD-L1 in many different types of cancers, resulting in an immunological TME, compromising the suppression of immunological gatekeepers, and causing sensitivity to therapeutic strategies [26]. Furthermore, all of the aforementioned evidence points to the use of Monotherapy as a novel approach to treating cancer, especially when combined with the gold standard therapy for each individual cancer [12]. Earlier studies shown that Interleukin-6 and tumor necrosis factor can inhibit the endothelium changeover in PCa cells, enhance cell proliferation and metastasis, and offer a fresh approach for further study [14].

The performed investigation revealed that both benign and tumorous prostate cancer had higher levels of IL-10 than normal prostate tissue. IL-10 appears to play an important role in both the emergence of human cancer and its immunological evasion. These have suggested that it might be used as a target for therapy or a diagnostic for malignant illnesses. High amounts of this cytokine in the system and specific genes should both be taken into account First investigations to measure serum IL-10 levels in cancer patients observed an increase than in normal subjects, which is concerning given their potential significance in the formation and growth of tumor tissue [9].

Cytokines are signaling proteins with crucial roles in biological longevity that are mostly produced by lymphocytes. IL-10 promotes anti-inflammatory responses and prevents the production of key pro-inflammatory proinflammatory cytokines. The researchers concentrate on the impact of IL-10, IL-4, and TGF- on different types of cancer as well as the possibility for these three cytokines to act as brand-new indicators that can help individuals with cancer receive successful treatments [11].

By working on lymphocytes to inhibit the antitumor response, IL10 is best studied as an anti-inflammatory, immune suppressive cytokine that promotes to encouraging cancer malignancy. IL10 serum concentrations in cancer patients are positively correlated with Gleason scores and are associated with a worse survival in bc patients [27]. IL10 may be created by the tumor cells themselves or by the induction of immune lymphocytes that produce IL10 and infiltrate the tumor [10]. The antitumor allergic reaction is inhibited by IL10 in a way that also affects myeloid (macrophage and dendritic cell) and T effector cell activity. Additionally, PDL1 (CD274) activation on activated macrophages is upregulated by IL10. When PDL1 binds to the inhibitory receptor PD1 on T cells, the T cell is rendered inactive and the host T cell antitumor antibody reaction is suppressed [28].

Another of the most common acute malignancies in males worldwide is prostate cancer, and fatality rates have been rising [29]. It may be possible to employ tumor tissue-infiltrating cytokines as a favorable predictive marker for cancer. An examination of 50 catheter – based prostate samples with high-grade PC revealed that the percentage of CD20 $+$ B lymphocytes physically identified in the PC was much greater than in the treatment group [30]. That research likely suggests that B lymphocytes may play a significant part in the mechanism of cancer progression and tumor creation. Additional study found that castration-resistant prostate cancer (CRPC) patients’ malignant cells can stimulate transcription factors by producing cytokines like lymphotoxin, which is produced by B cells [31]. According to Shimabukuro-Vornhagen et al. (2014), immunological escape may be represented by a decline in B cells in colorectal cancer and an increase in the fraction of Organs or tissue that aid in spreading [32].

Carcinoma B cells can function as Bregs that, in a number of investigations on diverse lymphoid malignancy in patients, inhibit anti-tumor inflammatory cells by binding to suppressive ligands [33]. Overall, these B cell investigations suggest that these cells have regulatory abilities and directly influence the development of cancer [34]. Roya et al. (2020) showed that PC patients had considerably more CD19 $+$ IL-10 $+$ B cells than patients with benign prostatic disease, and these findings were consistent with the current results [35]. The PC environment is crucial for the maturation or invasion of CD19 $+$ IL-10 $+$ B cells, and experiments using breast cancer cells show that even these cells can cause Bregsactivation in mouse splenocytes [36].

Researchers discovered that in vitro stimulation with IL10 or anastrozole of prostate cancer cell lines resulted in indicators of regional development and decreased androgen receptor reporter function. Both also increased the levels of programmed death-ligand 1 (PD-L1), which by inhibiting antitumor immunity by interacting with the innate immune regulatory target PD1 may boost tumor growth in vivo. These results imply that IL10’s direct impact on prostate cancer cells may promote the spread of the disease without IL10’s inhibition of innate immunity cells [28].

Table 3

Comparative mean levels of immunological parameters among patients (benign and malignancy) according to age groups

Age groups (years)		Mean	SD	Mean	SD	Statistics
		Benign tumor		Malignancy tumor
IL10	50–59	0.38	0.10	1.26	0.24	$P<$ 0.001 ${}^{***}$
	60–69	0.49	0.14	1.20	0.22	LSD $=$ 0.16
	$>$ 69	0.56	0.00	1.17	0.30
TNF-a	50–59	0.33	0.11	0.23	0.02	$P<$ 0.05 ${}^{*}$
	60–69	0.28	0.12	0.24	0.03	LSD $=$ 0.4
	$>$ 69	0.23	0.00	0.23	0.01
PSA	50–59	6.75	1.42	26.94	6.74	$P<$ 0.001 ${}^{***}$
	60–69	6.71	1.40	27.56	6.41	LSD $=$ 5.06
	$>$ 69	7.00	0.00	29.71	5.28

Along with s, o Prostate-specific antigen (PSA) is a serine protease that is primarily responsible for liquifying seminal bringing together different. It is generated by squamous prostatic cells. Since it was the first cancer biomarker recognized by the FDA, PSA is currently used as an indicator for the diagnosis and detection of prostate cancer. Male PSA levels and serum proteins enable the distinction between prostate cancer and benign autoimmune illness. At first, it was believed that PSA was only made by the prostate and that men were the only ones who displayed this molecule. Moreover, according to a number of writers, PSA is a protein that is expressed by a wide range of tissues besides the prostate in both men and women. Additionally, some writers claim that there is a strong correlation between the expression of this protein and breast and colon cancer in women. Consequently, it may serve as an indicator for the rapid recognition, prognosis, and detection of malignant malignancies in female patients. This research will concentrate on the biomolecules of the PSA, its recent treatment significance, the expression of this protein in tissues other than the prostate, and its association with cancer, particularly in women [37]. The widely used blood test for cancer antigen (PSA) detects the return of tumors. Although its diagnostic accuracy is debatable, serum PSA levels are correlated with tumor growth. As a result, tremendous advancement was made in creating modified PSA tests such the STHLM3 test, Prostate Healthy Index, PSA density, PSA glycoprofiling, and PSA rate. PSA, The epithelial cells of the prostate release a serine protease. Because PSA is active in prostate tumors and plays a key role in prostate cancer transcription factors such as proliferation, invasion, metastasis, angiogenesis, apoptosis, immune response, and tumor microenvironment modulation, it has been proposed as a biomolecule for prostate immunotherapy [8].

Hazard PSA testing includes a baseline, widely accessible, and reasonably priced PSA test that dictates the next course of action. The next step, if this baseline PSA level suggests that diagnostic testing is required, is not to immediately proceed with MRI and/or prostate biopsy but rather to start reflex testing to lower the rate of false-positive PSA tests so that if there is one [38].

According to prior research, the PSA level before to recovery therapy (SRT) may serve as a characteristics of the respondents for the effectiveness of antiresorptive therapy when combined with salvage radiation (SRT). Hormone treatment was linked to better outcomes in patients getting late SRT (PSA $>$ 0.6 ng/mL). Long-term antiresorptive therapy was not linked to better survival rates in men receiving early SRT (PSA 0.6 ng/mL) (OS) [39].

New studies shown that in specimens from radical hysterectomy procedures involving small and large prostates, the PSA density (PSA-D) is related to the discovery of medically unimportant PCa (CS-PCa). The International Society of Urological Pathology’s (ISUP) PCa grade group and PSA-D level are directly related. Furthermore, PSA-D is an advantageous, accessible, and reasonably priced tool for individuals with small and medium-sized prostate who are thinking about getting therapy for prostate cancer (PCa) [40]. The Prostate-specific antigen may guide biopsy choices and protect some men from the morbidity of a prostate biopsy and a low-grade prostate cancer scare [41].

Prostate preventative care, at best, results in a modest decline in disease-specific mortality over a ten-year period but has no impact on overall lifespan. Clinicians and patients who are investigating PSA-based monitoring must assess these advantages against the various short- and long-term risks of screening, such as the dangers of misdiagnosis and early treatment as well as problems from biopsies and subsequent treatment [42].

3.3 Relationship of immunological parameters with age groups of tumor patients

Results of present study showed there is significant differences ( $p<$ 0.05) between IL-10, TNF-a, and PSA parameters and age groups of tumor groups, where it is found the IL-10 scored highest mean levels at $>$ 69 years in benign group (0.56 $\pm$ 0.00), and at 50–59 years in malignant groups (1.26 $\pm$ 0.24). While the IL-10 scored least mean levels at 50–59 years in benign group (0.38 $\pm$ 0.10), and at $>$ 69 years in malignant groups (1.17 $\pm$ 0.30). TNF-a scored highest mean levels at 50–59 years in benign group (0.33 $\pm$ 0.11), and at 60–69 years in malignant groups (0.24 $\pm$ 0.03). While the TNF-a scored least mean levels at $>$ 69 years in benign group (0.23 $\pm$ 0.00), and at $>$ 69 years in malignant groups (0.23 $\pm$ 0.01). PSA scored highest mean levels at $>$ 69 years in benign group (7.00 $\pm$ 0.00), and malignant groups (29.71 $\pm$ 5.28). While the PSA scored least mean levels at 60–69 years in benign group (6.71 $\pm$ 1.40), and at 50–59 years in malignant groups (26.94 $\pm$ 6.74) (Table 3).

The present study showed increase levels of IL-10 with age progression benign and decrease it in malignant patients. Thomas et al. (2022) showed the circulating IL-10 is associated with reduced risk of prostate cancer in a prospective cohort of elderly men, and these results compatible to present study [11].

Elderly causes severe immunological malfunction, which contributes to the loss in vaccine response that was traditionally explained to immunological flaws that are irreparable. In contrast to elevated interleukin-6 (IL-6), researchers discovered that old mice also have elevated levels of systemic IL-10, which only occurs in FoxP3-negative (FoxP3), not FoxP3 $+$ , CD4 $+$ T cells. We refer to the majority of IL-10-producing cells as Tfh10 cells since they exhibited a T functional helper (Tfh) morphology and needed the Tfh cytokines IL-6 and IL-21 for their accrual. To keep IL-6 and IL-10 levels in the serum at average levels, IL-21 was also necessary. Strikingly, Aged mice were immunized, and allergen Tfh10 cells developed. Neutralizing IL-10 receptor signaling greatly restored Tfh-dependent antibody responses, whereas depleting FoxP3 $+$ control and functional regulation cells showed not. Thus, these findings show that immune suppression with aging is recoverable and suggest that the fascinating relationship between “agents” and weakened innate immunity with maturing is mediated by Tfh10 cells [43].

The present study showed decrease levels of TNF-a with age progression of patients with PCa due to chronic diseases, organ dysfunction, microbial infection, radical therapy, malnutrition, and impaired immune response.

The present study showed increase levels of PSA with age progression of patients, and these results compatible to results Reza et al. (2021). This same results of this investigation showed a significant correlation between age and the subjects’ serum PSA content [44]. Other comparable investigations conducted in China (Lin et al., 2010) [45] and Shiraz also shown a favorable association (Iran) [44].

Finally, the increased levels of PSA and IL-10 with age progression in patients with PCa due to increasing severity of inflammation in elderly patients because of impaired immune status, chronic diseases, drugs, microbial infection, and malnutrition.

4. Conclusions

Current study present study showed increase levels of IL-10 with age progression benign and decrease it in malignant patients, where it is found the IL-10 and PSA highest mean levels in the malignant group, also PCa is high prevalence in elderly population. So increase levels of TNF-a in benign prostate cancer and decreased it in malignant.

Ethical consideration

Before beginning this study, ethical approval was obtained from the College of Science at the University of Al-Mustansiriyah and the Iraqi Ministry of Health in Baghdad. Every study participant provided their written informed consent.

Author contributions

Conceptualization: A.S.H.N and S.S.H.

Methodology: A.S.H.N, S.S.H and N.K.T.

Software: A.S.H.N.

Validation: A.S.H.N, S.S.H and N.K.T.

Formal analysis: A.S.H.N and S.S.H.

Investigation: A.S.H.N.

Resources: A.S.H.N.

Data curation: A.S.H.N.

Original draft preparation: A.S.H.N.

Review and editing: A.S.H.N, S.S.H and N.K.T.

Supervision: S.S.H and N.K.T.

All authors have read and agreed to the published version of the manuscript.

Footnotes

Acknowledgments

The first author (PhD Student) sincerely thanked to Prof. Dr. Suzan Saadi Hussian, Assist Prof. Dr. Nihad Khalawe Tektook for their insightful comments and suggestions that helped signifi-cantly improve this research work.

Conflict of interest

The authors declare that they have no conflict of interest.

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Immunological analysis of Interleukin-10 (IL-10),tumor necrosis factor-a (TNF-a),and Prostate-specific antigen (PSA) in benign and malignant prostate cancer

Abstract

INTRODUCTION:

OBJECTIVE:

MATERIALS AND METHODS:

RESULTS:

CONCLUSIONS:

Keywords

1. Introduction

2. Materials and methods

2.1 Population studies

2.2 Determination of PSA, IL-10, and TNF-a parameters

2.3 Statistical analysis

Table 1 Distribution of study groups according to age groups

3.1 Distribution of study groups according to age groups

3.2 Relationship of immunological parameters with study groups

Table 2 Comparative levels of immunological parameters within study groups

4. Conclusions

Ethical consideration

Author contributions

Footnotes

Acknowledgments

Conflict of interest

References

Table 1
Distribution of study groups according to age groups

Table 2
Comparative levels of immunological parameters within study groups