Cancer Translational Medicine

Review | Open Access

Vol.7 (2023) | Issue 1 | Page No: 12-19


The Role of IL-22 in the Prevention of Inflammatory Bowel Disease and Liver Injury

Xingli Qi1,2, Huaqing Lin2,3, Wen Rui2,3,4,5 and Hongyuan Chen1,2,3


1. Department of Pathogenic Biology and Immunology, School of Life Sciences and Biopharmaceuticals, Guangdong Pharmaceutical University, Guangzhou 510006, Guangdong Province, PR China.

2. Centrefor Novel Drug Research and Development, Guangdong Pharmaceutical University, Guangzhou 510006, Guangdong Province, PR China.

3. GDPU-HKU Zhongshan Biomedical Innovation Plaform, Zhongshan 528437, Guangdong Province, PR China.

4. Guangdong Engineering & Technology Research Center of Topical Precise Drug Delivery System, Guangdong Pharmaceutical University, Guangzhou 510006, Guangdong Province, PR China.

5. Key Laboratory of Digital Quality Evaluation of Chinese Materia Medica of State Administration of TCM, Guangzhou 510006, Guangdong Province, PR China. 6. Guangdong Cosmetics Engineering & Technology Research Center,Guangzhou 510006, Guangdong Province, PR China.

Address for correspondence

Dr. Wen Rui, Centre for Novel Drug Research and Development, Guangdong Pharmaceutical University, Guangzhou 510006, Guangdong Province, PR China. E-mail:

Important Dates  

Date of Submission:   11-Mar-2022

Date of Acceptance:   04-Apr-2023

Date of Publication:   15-Jul-2023


IL-22, produced by lymphocytes in the IL-10 cytokine family, is a pleiotropic cytokine involved in many aspects of immune regulation. By binding to a heterodimeric transmembrane receptor complex consisting of IL-22R1 and IL-10R2, it plays an important role in anti-infection, hepatoprotection, and the regulation of inflammatory diseases such as IBD, psoriasis, and rheumatoid arthritis. This review will focus on the role of IL-22 in inflammation and tissue protection, regeneration, and host defense in the development of IBD and liver injury, helping us strengthen the understanding of IL-22.

Keywords: IL-22; cytokines; IBD; liver injury; STAT3


Interleukin (IL)-22, which was found in the year 2000, is one of the most important members of the IL-10 cytokine family. As a cytokine with strong bioactivity, IL-22 is crucial for fighting infections, protecting the liver, and controlling inflammatory diseases.[1] The ligand of IL-22 is a heterodimer comprised of two transmembrane subunits: IL-22R1, and IL-10R2.[2] All types of cells express IL-10R2, while only non-hematopoietic cells express IL-22R1. As a result, the IL-22R1 expression determines the specific targeting of IL-22 to the innate cells.[2] IL-22-binding protein (IL-22BP), a coordinated binding protein for IL-22, is homologous to IL-22R1.[3] Since IL-22BP has a stronger affinity than the receptor, it prevents IL-22 from interacting with receptors attached to cell surfaces, reducing the ability of cells to govern signal transduction.[4] When the intestine is wounded, IL-22BP is mostly generated from Dendritic cells (DCs) and is expressed by DCs, eosinophils, and CD4+T cells at a steady state. Similarly, in a healthy liver, monocytes also express IL-22BP. When injured, however, liver DCs, monocytes, and T cells can all generate IL-22BP. In acute inflammation, DCs become active and mature and migrate out of the tissue. While in chronic inflammation, the regulation of DCs in the tissue is out of control. The expression change of IL-22BP is consistent with DCs during tissue inflammation. As a specific binding protein of IL-22, IL-22BP provides the possibility of fine-tuning IL-22 in vivo.

IL-22 is primarily generated by lymphocytes, including CD4+T, CD8+T, γδT, NKT, LTi, and newly described ILC3 cells.[1] In addition to lymphocytes, neutrophils have also been reported to generate IL-22. upon stimulation by serum amyloid A during DSS-induced colitis.[5] It was reported that macrophages were also observed to produce IL-22 in lung injury.[6] Unlike other cytokines, IL-22 does not control immune cell function due to its receptor expression. IL-22 works preferentially on various epithelial cells and is crucial for the development of the epithelial barrier and the healing of wounds. This effect is derived from its activation of the STAT3 signaling pathway. In general, when IL-22 binds to non-hematopoietic cells (epithelial cells or fibroblasts) expressing its receptor, both JAK 1 and TYK2 are phosphorylated, and the phosphorylation of the transcription factor STAT3, the main mediator of IL-22 signaling, is promoted.[7],[8] Moreover, other signaling pathways can also be activated, such as STAT1, STAT5, and MAPK (Figure 1). [7],[8]

[ArticleFigure 218]

As cytokines are usually produced at the site of inflammation, IL-22 is mainly generated by immune cells and can specifically act on various epithelial cells. It participates in the inflammation of many tissues (e.g., intestine, lung, liver, kidney, thymus, pancreas, skin), and has powerful biological and pathological functions. Interestingly, the location of inflammation and the level of other cytokines determine their protective and proinflammatory effects. Abundant evidence proves that the STAT3 signaling pathway can support epithelial cell survival and proliferation and take part in the healing of local tissue injury. IL-22, however, plays a critical role in elevated tissue inflammation, according to mounting data. Therefore, this dual function emphasizes the therapeutic potential of altering the cytokine network to control the inflammatory process. This article covers the most current developments of IL-22 in IBD and liver injury.


IBD is a chronic digestive disease associated with the autoimmune system and includes ulcerative colitis(UC) and Crohn disease(CD). The precise cause and pathogenesis of IBD are not fully elucidated. At present, the widespread consensus is that the aberrant intestinal mucosal immunity and intestinal epithelial barrier damage in IBD are caused by genetic susceptibility, environmental factors, and intestinal microbial disorders.[10]

Given its participation in various signaling pathways, IL-22 is connected to several bodily processes. IL-22 regulates congenital and adaptive immune responses by acting on liver cells, pancreatic cells, epithelial cells from diverse organs, and certain fibroblasts. In epithelial cells, IL-22 increases antimicrobial binding proteins, MMP1, MMP3, and granulocyte chemokines. IL-22 can increase the synthesis of MUC1 in the colon and respiratory tract to exert a protective effect. In addition, Immune cells in the resting or active states are unaffected by IL-22. Because of the wide involvement in tissue repair and disease development, IL-22 has emerged as a promising target in the clinical treatment strategy for IBD.

Additionally, IBD patients' intestinal and peripheral blood as well as various IBD animal models show increased IL-22 release. In a T cell transfer IBD model, exogenous administration of IL-22 improves symptoms, while giving neutralized anti-IL-22 antibodies or utilizing T cells of IL-22 deficient mice causes more extensive structural impairment to the intestine and severe colitis symptoms.[11],[12],[13] IBD may benefit from IL-22's protective effects, and a variety of immunomodulators related to the IL-22 pathway (e.g. Janus kinase inhibitor, anti-TNF, anti-IL-23) have been tested in clinical trials. Among them, anti-IL-23 demonstrates favorable therapeutic effects and lower infection and malignancy rates.[14]

Two disulfide-linked subunits of IL-23, p19, and p40, are participating in the production of TH17 and ILC3. The IL-23R protein is expressed by TH17, ILC3, T, and NKT cells, all of which are expected to generate IL-22 when stimulated in vitro with IL-23. IL-23R signaling promotes innate colitis via IL-22, and IL-22 treatment of IL-23R-deficient animals restores symptoms.[15] In a phase II clinical study, risankizumab selectively blocks IL-23 by inhibiting the p19 subunit, showing a good therapeutic effect on CD patients.[16] In another phase II clinical study in individuals with ineffective TNF antagonist intervention, human IL-23 blocking monoclonal antibody showed therapeutic effects, and the individual treatment effect was positively correlated with IL-22 level in serum.[17]


1.1 IL-22 and the intestinal epithelial barrier

IL-22 can directly work on epithelial cells expressing IL-22R1 to boost their proliferation and safeguard the integrity of the intestinal epithelial barrier.[18] The mucus layer in the intestine serves as a physiological barrier between the luminal contents and the mucosal epithelium, protecting intestinal epithelial cells and diminishing pathogen stimulation. Its primary component, mucin (MUC) 1, is membrane-bound mucin that is strongly O-glycosylated.

IL-22 signaling can significantly affect epithelial cells, induce the proliferation of intestinal epithelial cells and tissue repair, and promote the expressions of tight junction protein, Muc 1, and antimicrobial peptide. IL-22 signaling is also crucial for maintaining the intestinal epithelial barrier in studies using mouse models, intestinal organoids, and cell cultures.[19] By activating the SATA3 signaling pathway, IL-22 enhances intestinal stem cell-mediated epithelial regeneration and wound repair. In addition, lncRNA can regulate cell proliferation, differentiation, and migration, and IL-22 can boost intestinal epithelial growth and mucosal repair by causing intestinal epithelial cells to produce the lncRNA H19 via PKA.[20]

It is widely assumed that IL-22, via the STAT3 signaling pathway, can protect stem cells, promote epithelial cell proliferation and mucin expression, and produce antimicrobial peptides, thereby promoting tissue repair and regeneration and regulating epithelial homeostasis. Nevertheless, more research is needed.[21] There is substantial debate concerning IL-22's function. Despite increased IL-22 expression in CD patients, mucosal regeneration is problematic. In an ileal organoid model, high IL-22 levels restrict epithelial stem cell proliferation, resulting in decreased ileal organoid survival. All of these events suggest that IL-22 is not protective.

Epithelial polarity, which is derived from the cell program mediated by complex protein networks, is a crucial structure for the epithelial barrier to execute the function.  This program correctly locates the molecular components related to different polarities to the apical or basal lateral epithelial compartment and regulates the coordinated assembly of tight junctions and adhesion linkage structures between cells. By reprogramming a complicated biological program that induces intestinal epithelial activity, IL-22 compromises the integrity of the intestinal cell barrier. The ERK pathway, rather than STAT3 or AKT, promotes epithelial-mesenchymal transition (EMT), regulates the production of tight junction proteins and polar proteins, and causes the tight junction barrier to be compromised.[22]

Transit-amplifying cells (TACs) are a class of progenitors in between adult stem cells and their terminally differentiated daughter cells. They are multifunctional cells and can differentiate into secretory cells under normal conditions and into absorbing cells. Lgr5+ stem cells divide asymmetrically to self-renew, resulting in TA cells, which differentiate further to produce all cell types found in the intestinal epithelium. High doses of IL-22 in intestinal organoids can enhance TA cell proliferation while inhibiting organoid differentiation and causing defects in intestinal stem cell self-renewal. Another study also shows that IL-22 promotes TA cell proliferation, but decreases the survival of Lgr5+ stem cells by inhibiting Notch and Wnt signaling.[23] Therefore, IL-22 can either promote or hinder mucosal repair, possibly depending on whether the effect on TA cells is predominant.[24]

In addition to promoting epithelial cell death and inhibiting stem cell proliferation, IL-22 also reportedly promotes inflammation in animal IBD models. Intestinal pathology induced by Treg cell-depleted CD4 CD45RB+lo T cells is characterized by mucosal thickening and epithelial hyperplasia, which were not found in the same model of knockout IL-22 gene, suggesting that memory IL-22 generated by T cells may have a pro-inflammatory effect.[25] IL-23R-dependent IL-22 increased innate colitis, as demonstrated in mice models, where IL-22 neutralization protected mice from colitis and IL-22 reintroduction recovered the disease.[15] The use of an IL-12p40 antibody to suppress IL-22 signaling reduced colonic endoplasmic reticulum stress and alleviated colitis in CD patients. Moreover, inhibiting the upstream cytokine IL-23, which produces IL-22, with a monoclonal antibody had similar effects.[26]

As a result, the exact function of IL-22 in the intestine is unknown, and its significance in IBD can be double-edged. While promoting tissue healing, it may also inhibit intestinal epithelial cell development and expand inflammation.


1.2 IL-22 interacts with microorganisms

IL-22 can interact with intestinal microbes to maintain the dynamic balance among intestinal microbes, the epithelial barrier, and the mucosal immune system. It also promotes epithelial cell regeneration, produces antimicrobial peptides and mucins, and contributes significantly to intestinal inflammation. IL-22R–/– mice had lower antimicrobial peptide synthesis and a different microbial makeup.[27] The administration of anti-IL-22 antibody to germ-free mice altered the gut microbiota composition, indicating IL-22-mediated host glycosylation plays a role in gut microbe modulation.[28] Moreover, this alteration is thought to inhibit the onset of IBD. As reported, host N-glycosylation is reduced in UC patients.[29] The above results suggest that impaired IL-22-mediated host glycosylation in UC patients may lead to intestinal ecological disorders. IL-22–/– mice developed more severe colitis symptoms when stimulated by DSS, and their microorganisms were transmitted to normal mice in the same place, which in turn influenced antimicrobial peptide levels and colitis severity in these wild-type mice.[30] IL-22 can affect the composition of intestinal microorganisms, thereby affecting the development of IBD. Intestinal microorganisms can also in turn affect IL-22 expression.

Th17 and ILC3 are encouraged to produce IL-22 via the cytoplasmic transcription factor AhR. Indole-3-carbinol, an endogenous AhR-activating ligand, decreases microbial diseases and colitis-related inflammation through an IL-22-mediated mechanism. Tryptophan metabolites of intestinal flora, significant ligands of AhR, may inhibit enterocolitis by activating the IL-22/AhR pathway, and play an essential role in intestinal mucosal immunity.[31] The indole compound indigo, one main component of indigo naturalis (IN), is the proven ligand of AhR and can alleviate colitis in mice via AhR signaling and boosting the IL-22 level in lymphocytes. In AhR-deficient mice, this impact was abolished.[32] Furthermore, AhR expression was lower in the intestine of IBD patients, and several colitis model mice treated with AhR antagonists produced more pro-inflammatory cytokines with fewer IL-22, leading to severe colitis.[33]

Gut bacteria can also cause DC cells to secrete retinoic acid, and thereby raise IL-22 production by promoting the attachment of ILCs and γδT cells receptors to the IL-22 promoter.[34]

Through a variety of methods, IL-22 strengthens mucosal epithelial cells' antimicrobial defenses, such as maintaining the epithelial cell barrier to reduce inflammation and bacteria's ability to harm the epithelium, increasing the secretion of MUC, and producing a protective mucus layer.[9]


1.3 IL-22 and IBD susceptibility genes

The pathogenesis of IBD is largely determined by genetic predisposition and involves many genes that are found in the IL-22 and associated pathways.

The IL-22 gene, located on the 12q15 chromosome, is one of the high-risk loci linked to UC etiology.[35] STAT3, Jak2 and Tyk2 in the IL-22/STAT3 pathway are all well-defined CD susceptibility genes. The control of different IL-22-producing cells involves the connection between IL-23 and IL-23R. The presence of functional polymorphisms in IL-23R is negatively associated with IBD (Figure 2).[36],[37]


The liver is a key location for IL-22 to act biologically. Only hepatocytes, hepatic stem cells, and HSCs in the liver carry IL-22R1, which may take the IL-22 signal, exert anti-steatosis, anti-apoptosis, and anti-fibrosis effects and promote liver regeneration.

IL-22 has an ameliorating effect in practically all kinds of liver injury models. IL-22 substantially protects liver cells in mice liver injury models provoked by ConA, CCl4, D-galactosamine, and Gal/LPS, or APAP. Acute phase proteins, anti-apoptotic proteins, mitotic proteins, and regenerative and antibacterial proteins are all produced in hepatocytes as a result of IL-22.

Apoptosis, cell proliferation-related activities, and angiogenesis are all modulated by STAT3 signaling. IL-22 upregulates proliferation and anti-apoptotic genes, different mitochondrial DNA repair genes, and antioxidant genes by stimulating the production of downstream pathway proteins of STAT3 signaling. It also downregulates adipogenesis genes. By directly inhibiting hepatocyte mortality, the IL-22/STAT3 signaling pathway can protect the liver from several types of liver injury.[38],[39]

IL-22 treatment alleviated fatty liver and liver oxidative stress in mice with alcoholic liver injury.[40] Serum IL-22 levels are significantly up-regulated in HFD-induced hepatic steatosis mice. Moreover, exogenous administration of recombinant murine IL-22 can reduce the gene expressions of lipogenic factors and the triglyceride levels in the liver and cholesterol, and ameliorate HFD-induced increases in ALT and AST. The liver production of fatty acid synthase and TNF-α is decreased after long-term therapy with recombinant murine IL-22.[41] In a neutrophil-driven mouse model of nonalcoholic fatty liver disease, treatment with the IL-22Fc fusion protein significantly increased the hepatic antioxidant enzyme metallothionein and reduced the oxidative stress and inflammatory molecules, indicating IL-22Fc has potential for therapy in NASH treatment.[42]

IL-22 has long been considered to be a crucial element in tissue regeneration and healing of wounds, as it can boost the generation of liver stem cells and progenitor cells, and induces the production of cyclin D and anti-apoptotic proteins, both of which are beneficial for liver regeneration.[43]

IL-22 is expected to have a protective impact in acute liver injury but plays a dual role in chronic liver inflammation: levels of IL-22 and the fraction of T cells secreting IL-22 are high in pathogen-induced liver injury models. IL-22 produced by inflammatory cells can protect individuals with chronic HBV infection by promoting the proliferation of hepatocytes and tissue repair by STAT3.[43] However, by recruiting hepatic Th17 cells, IL-22 has an adverse function in developing chronic liver inflammation and fibrosis.[44] Similarly, in patients with HCV infection, IL-22 is positively connected with the severity of liver disease.[45]

Short-term therapy with recombinant IL-22 can reduce APAP-induced liver injury.[46],[47] Animals lacking IL-22BP are more vulnerable to liver injury caused by APAP.[48] Moreover, chronic persistent overexpression of IL-22 exacerbates APAP-induced liver injury by increasing the levels of Cyp2E1 and toxic APAP metabolites.[49]

IL-22 has environment-dependent protective and pathogenic effects in the liver, which emphasizes the necessity for endogenous mechanisms to tightly regulate IL-22 activity. The function of IL-22/IL-22BP in acute injury is essential for coordinating liver regeneration and restoring liver function. For example, administration of IL-22 has beneficial effects on liver ischemia-reperfusion injury (IRI), and rmIL-22 pretreatment in mice is protective in liver IRI. However, neutralizing IL-22 with antibodies does not change disease severity after liver IRI.[48] Moreover, IL-22 depletion is unaffected by the severity of illness or liver regeneration following IRI. IL-22BP deficiency will lead to increased cell death and DNA damage after acute liver injury, and uncontrolled expression of IL-22 induces hepatocytes to express CXCL10, resulting in increased migration of inflammatory monocytes to the liver. In IL-22BP-deficient animals, a high degree of infiltration aggravates liver injury, which can be restored by utilizing neutralizing antibodies to block the function of CXCL10.[49] Uncontrolled production of IL-22 may increase the CXCL10 expression, promoting tissue damage by recruiting pro-inflammatory immune subsets.


The numerous bioactivities of IL-22 make it an essential cytokine that cannot be ignored in various diseases and a good therapeutic tool to modulate disease by interfering with its production or modulating its signaling. Particularly in IBD, IL-23 and TNF-α, key inducers of IL-22 production, were successfully made into relevant biologics in the clinic. However, long-term use of such therapies can reduce their efficacy and may lead to side effects, such as higher rates of infection and malignancy.[14] Other inducers that regulate IL-22 production (e.g. AhR) can also be acted upon by their specific modulators to alter IL-22 activity in tissues.[33] In addition to controlling the production of IL-22, IL-22 can be neutralized by exogenous antibodies or endogenous inhibitors of IL-22BP.[48],[50] Conduction of the IL-22 signaling pathway can be inhibited by blocking IL-22R1, or by inhibiting downstream kinases and transcription factors (JAK and STAT3).[14] These options have legitimate uses in a variety of specific situations, but targeted regulation of IL22R1 seems the best option under permissive conditions. Because IL22R1 is only expressed in a limited population of non-haematopoietic cells in vivo, targeting IL-22/IL-22R in the treatment of liver injury and IBD does not cause unnecessary immune system disruption, and therapeutic approaches that block IL-22R1 also avoid the binding of IL-20 and IL-24 to IL22R1.[51] In some diseases, IL-22 causes chemokine production and exacerbates the inflammatory response, which can be inhibited by using chemokine neutralizing antibodies that block immune cell infiltration into the epithelial tissue.[48]

Notably, the extent of IL-22 activation in the tissues depends on the location and extent of the damage. When specific circumstances such as the duration of treatment are considered, choosing the suitable treatment regimen will be a top priority. Particularly, IL-22 is not fully protective in IBD and liver injury. Therefore, more research is needed to figure out how to minimize its side effects while maximizing the benefits of IL-22.


IL-22 has the functions of anti-infection and tissue cell repair promotion and has a positive effect on the body. However, Chemokine synthesis will be stimulated and chemotactic immune cells will arrive in the region by IL-22. IL-22 also participates in inflammatory reactions such as psoriasis, and aggravating inflammatory pathology. With further research, it may have promising applications in liver protection, inflammatory diseases, GVHD, and anti-infection.


Author contributions

Xingli Qi and Huaqing Lin wrote original draft preparation. Wen Rui and Hongyuan Cheng edited the manuscript, all authors read and approved the final manuscript.

Conflicts of interest

The author confirms that there are no potential conflicts of interest.

Financial support and sponsorship

This work was supported by the National Natural Science Foundation of China (NSFC) (no.82074017; 81573607; 81202917) and The Special Fund for Science and Technology Development in 2017 Guangdong Province of South China (no. 2017A030311031).



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I‑Kappa‑B Kinase‑epsilon Activates Nuclear Factor‑kappa B and STAT5B and Supports Glioblastoma Growth but Amlexanox Shows Little Therapeutic Potential in These Tumors

Nadège Dubois1, Sharon Berendsen2, Aurélie Henry1,2, Minh Nguyen1, Vincent Bours1,
Pierre Alain Robe1,2

Suppressive Effect of Mesenchymal Stromal Cells on Interferon‑g‑Producing Capability of Spleen Cells was Specifically Enhanced through Humoral Mediator(s) from Mouse Oral Squamous Cell Carcinoma Sq‑1979 Cells In Vitro

Toshihiro Inagaki1,2, Masako Mizuno‑Kamiya3, Eiji Takayama1, Harumi Kawaki1, Eiichi Chihara4, Yasunori Muramatsu5, Shinichiro Sumitomo5, Nobuo Kondoh1

An Interplay Between MicroRNA and SOX4 in the Regulation of Epithelial–Mesenchymal Transition and Cancer Progression

Anjali Geethadevi1, Ansul Sharma2, Manish Kumar Sharma3, Deepak Parashar1

MicroRNAs Differentially Expressed in Prostate Cancer of African‑American and European‑American Men

Ernest K. Amankwah

The Role of Reactive Oxygen Species in Screening Anticancer Agents

Xiaohui Xu1, Zilong Dang2, Taoli Sun3, Shengping Zhang1, Hongyan Zhang1

Panobinostat and Its Combination with 3‑Deazaneplanocin‑A Induce Apoptosis and Inhibit In vitro Tumorigenesis and Metastasis in GOS‑3 Glioblastoma Cell Lines

Javier de la Rosa*, Alejandro Urdiciain*, Juan Jesús Aznar‑Morales, Bárbara Meléndez1,
Juan A. Rey2, Miguel A. Idoate3, Javier S. Castresana

Cancer Stem‑Like Cells Have Cisplatin Resistance and miR‑93 Regulate p21 Expression in Breast Cancer

Akiko Sasaki1, Yuko Tsunoda2, Kanji Furuya3, Hideto Oyamada1, Mayumi Tsuji1, Yuko Udaka1, Masahiro Hosonuma1, Haruna Shirako1, Nana Ichimura1, Yuji Kiuchi1

The Contribution of Hexokinase 2 in Glioma

Hui Liu1, Hongwei Yang2, Xin Wang3, Yanyang Tu1

The Mechanism of BMI1 in Regulating Cancer Stemness Maintenance, Metastasis, Chemo‑ and Radiation Resistance

Xiaoshan Xu, Zhen Wang, Nan Liu, Pengxing Zhang, Hui Liu, Jing Qi, Yanyang Tu

A Multisource Adaptive Magnetic Resonance Image Fusion Technique for Versatile Contrast Magnetic Resonance Imaging

Lei Zhang1,2, Fang‑Fang Yin1,2,3, Brittany Moore1,2, Silu Han1,2, Jing Cai1,2,4

Senescence and Cancer

Sulin Zeng1,2, Wen H. Shen2, Li Liu1

The “Wild”‑type Gastrointestinal Stromal Tumors: Heterogeneity on Molecule Characteristics and Clinical Features

Yanhua Mou1, Quan Wang1, Bin Li1,2

Retreatment with Cabazitaxel in a Long‑Surviving Patient with Castration‑Resistant Prostate Cancer and Visceral Metastasis

Raquel Luque Caro, Carmen Sánchez Toro, Lucia Ochoa Vallejo

Therapy‑Induced Histopathological Changes in Breast Cancers: The Changing Role of Pathology in Breast Cancer Diagnosis and Treatment

Shazima Sheereen1, Flora D. Lobo1, Waseemoddin Patel2, Shamama Sheereen3,
Abhishek Singh Nayyar4, Mubeen Khan5

Glioma Research in the Era of Medical Big Data

Feiyifan Wang1, Christopher J. Pirozzi2, Xuejun Li1

Transarterial Embolization for Hepatocellular Adenomas: Case Report and Literature Review

Jian‑Hong Zhong1,2, Kang Chen1, Bhavesh K. Ahir3, Qi Huang4, Ye Wu4, Cheng‑Cheng Liao1, Rong‑Rong Jia1, Bang‑De Xiang1,2, Le‑Qun Li1,2

Nicotinamide Phosphoribosyltransferase: Biology, Role in Cancer, and Novel Drug Target

Antonio Lucena‑Cacace1,2,3, Amancio Carnero1,2

Enhanced Anticancer Effect by Combination of Proteoglucan and Vitamin K3 on Bladder Cancer Cells

Michael Zhang, Kelvin Zheng, Muhammad Choudhury, John Phillips, Sensuke Konno

Molecular Insights Turning Game for Management of Ependymoma: A Review of Literature

Ajay Sasidharan, Rahul Krishnatry

IDH Gene Mutation in Glioma

Leping Liu1, Xuejun Li1,2

Challenges and Advances in the Management of Pediatric Intracranial Germ Cell Tumors: A Case Report and Literature Review

Gerard Cathal Millen1, Karen A. Manias1,2, Andrew C. Peet1,2, Jenny K. Adamski1

Assessing the Feasibility of Using Deformable Registration for Onboard Multimodality‑Based Target Localization in Radiation Therapy

Ge Ren1,2,3, Yawei Zhang1,2, Lei Ren1,2

Research Advancement in the Tumor Biomarker of Hepatocellular Carcinoma

Qing Du1, Xiaoying Ji2, Guangjing Yin3, Dengxian Wei3, Pengcheng Lin1, Yongchang Lu1,
Yugui Li3, Qiaohong Yang4, Shizhu Liu5, Jinliang Ku5, Wenbin Guan6, Yuanzhi Lu7

Novel Insights into the Role of Bacterial Gut Microbiota in Hepatocellular Carcinoma

Lei Zhang1, Guoyu Qiu2, Xiaohui Xu2, Yufeng Zhou3, Ruiming Chang4

Central Odontogenic Fibroma with Unusual Presenting Symptoms

Aanchal Tandon, Bharadwaj Bordoloi, Safia Siddiqui, Rohit Jaiswal

The Prognostic Role of Lactate in Patients Who Achieved Return of Spontaneous Circulation after Cardiac Arrest: A Systematic Review and Meta‑analysis

Dongni Ren1, Xin Wang2, Yanyang Tu1,2

Inhibitory Effect of Hyaluronidase‑4 in a Rat Spinal Cord Hemisection Model

Xipeng Wang1,2, Mitsuteru Yokoyama2, Ping Liu3

Research and Development of Anticancer Agents under the Guidance of Biomarkers

Xiaohui Xu1, Guoyu Qiu1, Lupeng Ji2, Ruiping Ma3, Zilong Dang4, Ruling Jia1, Bo Zhao1

Idiopathic Hypereosinophilic Syndrome and Disseminated Intravascular Coagulation

Mansoor C. Abdulla

Phosphorylation of BRCA1‑Associated Protein 1 as an Important Mechanism in the Evasion of Tumorigenesis: A Perspective

Guru Prasad Sharma1, Anjali Geethadevi2, Jyotsna Mishra3, G. Anupa4, Kapilesh Jadhav5,
K. S. Vikramdeo6, Deepak Parashar2

Progress in Diagnosis and Treatment of Mixed Adenoneuroendocrine Carcinoma of Biliary‑Pancreatic System

Ge Zengzheng1, Huang-Sheng Ling2, Ming-Feng Li2, Xu Xiaoyan1, Yao Kai1, Xu Tongzhen3,
Ge Zengyu4, Li Zhou5

Surface-Enhanced Raman Spectroscopy to Study the Biological Activity of Anticancer Agent

Guoyu Qiu1, Xiaohui Xu1, Lupeng Ji2, Ruiping Ma3, Zilong Dang4, Huan Yang5

Alzheimer’s Disease Susceptibility Genes in Malignant Breast Tumors

Steven Lehrer1, Peter H. Rheinstein2

OSMCC: An Online Survival Analysis Tool for Merkel Cell Carcinoma

Umair Ali Khan Saddozai1, Qiang Wang1, Xiaoxiao Sun1, Yifang Dang1, JiaJia Lv1,2, Junfang Xin1, Wan Zhu3, Yongqiang Li1, Xinying Ji1, Xiangqian Guo1

Protective Activity of Selenium against 5‑Fluorouracil‑Induced Nephrotoxicity in Rats

Elias Adikwu, Nelson Clemente Ebinyo, Beauty Tokoni Amgbare

Advances on the Components of Fibrinolytic System in Malignant Tumors

Zengzheng Ge1, Xiaoyan Xu1, Zengyu Ge2, Shaopeng Zhou3, Xiulin Li1, Kai Yao1, Lan Deng4

A Patient with Persistent Foot Swelling after Ankle Sprain: B‑Cell Lymphoblastic Lymphoma Mimicking Soft‑tissue Sarcoma

Crystal R. Montgomery‑Goecker1, Andrew A. Martin2, Charles F. Timmons3, Dinesh Rakheja3, Veena Rajaram3, Hung S. Luu3

Coenzyme Q10 and Resveratrol Abrogate Paclitaxel‑Induced Hepatotoxicity in Rats

Elias Adikwu, Nelson Clemente Ebinyo, Loritta Wasini Harris

Progress in Clinical Follow‑up Study of Dendritic Cells Combined with Cytokine‑Induced Killer for Stomach Cancer

Ling Wang1,2, Run Wan1,2, Cong Chen1,2, Ruiliang Su1,2, Yumin Li1,2

Supraclavicular Lymphadenopathy as the Initial Manifestation in Carcinoma of Cervix

Priyanka Priyaarshini1, Tapan Kumar Sahoo2

ABO Typing Error Resolution and Transfusion Support in a Case of an Acute Leukemia Patient Showing Loss of Antigen Expression

Debasish Mishra1, Gopal Krushna Ray1, Smita Mahapatra2, Pankaj Parida2

Protein Disulfide Isomerase A3: A Potential Regulatory Factor of Colon Epithelial Cells

Yang Li1, Zhenfan Huang2, Haiping Jiang3

Clinicopathological Association of p16 and its Impact on Outcome of Chemoradiation in Head‑and‑Neck Squamous Cell Cancer Patients in North‑East India

Srigopal Mohanty1, Yumkhaibam Sobita Devi2, Nithin Raj Daniel3, Dulasi Raman Ponna4,
Ph. Madhubala Devi5, Laishram Jaichand Singh2

Potential Inhibitor for 2019‑Novel Coronaviruses in Drug Development

Xiaohui Xu1, Zilong Dang2, Lei Zhang3, Lingxue Zhuang4, Wutang Jing5, Lupeng Ji6, Guoyu Qiu1

Best‑Match Blood Transfusion in Pediatric Patients with Mixed Autoantibodies

Debasish Mishra1, Dibyajyoti Sahoo1, Smita Mahapatra2, Ashutosh Panigrahi3

Characteristics and Outcome of Patients with Pheochromocytoma

Nadeema Rafiq1, Tauseef Nabi2, Sajad Ahmad Dar3, Shahnawaz Rasool4

Comparison of Histopathological Grading and Staging of Breast Cancer with p53‑Positive and Transforming Growth Factor‑Beta Receptor 2‑Negative Immunohistochemical Marker Expression Cases

Palash Kumar Mandal1, Anindya Adhikari2, Subir Biswas3, Amita Giri4, Arnab Gupta5,
Arindam Bhattacharya6

Chemical Compositions and Antiproliferative Effect of Essential Oil of Asafoetida on MCF7 Human Breast Cancer Cell Line and Female Wistar Rats

Seyyed Majid Bagheri1,2, Davood Javidmehr3, Mohammad Ghaffari1, Ehsan Ghoderti‑Shatori4

Cyclooxygenase‑2 Contributes to Mutant Epidermal Growth Factor Receptor Lung Tumorigenesis by Promoting an Immunosuppressive Environment

Mun Kyoung Kim1, Aidin Iravani2, Matthew K. Topham2,3

Potential role of CircMET as A Novel Diagnostic Biomarker of Papillary Thyroid Cancer

Yan Liu1,2,3,4#, Chen Cui1,2,3,4#, Jidong Liu1,2,3,4, Peng Lin1,2,3,4,Kai Liang1,2,3,4, Peng Su5, Xinguo Hou1,2,3,4, Chuan Wang1,2,3,4, Jinbo Liu1,2,3,4, Bo Chen6, Hong Lai1,2,3,4, Yujing Sun1,2,3,4* and Li Chen 1,2,3,4*

Cuproptosis-related Genes in Glioblastoma as Potential Therapeutic Targets

Zhiyu Xia1,2, Haotian Tian1, Lei Shu1,2, Guozhang Tang3, Zhenyu Han4, Yangchun Hu1*, Xingliang Dai1*

Cancer Diagnosis and Treatments by Porous Inorganic Nanocarriers

Jianfeng Xu1,2, Hanwen Zhang1,2, Xiaohui Song1,2, Yangong Zheng3, Qingning Li1,2,4*

Delayed (20 Years) post-surgical Esophageal Metastasis of Breast Cancer - A Case Report

Bowen Hu1#, Lingyu Du2#, Hongya Xie1, Jun Ma1, Yong Yang1*, Jie Tan2*

Subtyping of Undifferentiated Pleomorphic Sarcoma and Its Clinical Meaning

Umair Ali Khan Saddozai, Zhendong Lu, Fengling Wang, Muhammad Usman Akbar, Saadullah Khattak, Muhammad Badar, Nazeer Hussain Khan, Longxiang Xie, Yongqiang Li, Xinying Ji, Xiangqian Guo

Construction of Glioma Prognosis Model and Exploration of Related Regulatory Mechanism of Model Gene

Suxia Hu, Abdusemer Reyimu, Wubi Zhou, Xiang Wang, Ying Zheng, Xia Chen, Weiqiang Li, Jingjing Dai

ESRP2 as a Non-independent Potential Biomarker-Current Progress in Tumors

Yuting Chen, Yuzhen Rao, Zhiyu Zeng, Jiajie Luo, Chengkuan Zhao, Shuyao Zhang

Resection of Bladder Tumors at the Ureteral Orifice Using a Hook Plasma Electrode: A Case Report

Jun Li, Ziyong Wang, Qilin Wang

Structural Characterization and Bioactivity for Lycium Barbarum Polysaccharides

Jinghua Qi1,2,  Hangping Chen3,Huaqing Lin2,4,Hongyuan Chen1,2,5* and Wen Rui2,3,5,6*

RBM15 and YTHDF3 as Positive Prognostic Predictors in ESCC: A Bioinformatic Analysis Based on The Cancer Genome Atlas (TCGA)

Yulou Luo1, Lan Chen2, Ximing Qu3, Na Yi3, Jihua Ran4, Yan Chen3,5*

Mining and Analysis of Adverse Drug Reaction Signals Induced by Anaplastic Lymphoma Kinase-Tyrosine Kinase Inhibitors Based on the FAERS Database

Xiumin Zhang1,2#, Xinyue Lin1,3#, Siman Su1,3#, Wei He3, Yuying Huang4, Chengkuan Zhao3, Xiaoshan Chen3, Jialin Zhong3, Chong Liu3, Wang Chen3, Chengcheng Xu3, Ping Yang5, Man Zhang5, Yanli Lei5*, Shuyao Zhang1,3*

Advancements in Immunotherapy for Advanced Gastric Cancer

Min Jiang1#, Rui Zheng1#, Ling Shao1, Ning Yao2, Zhengmao Lu1*

Tumor Regression after COVID-19 Infection in Metastatic Adrenocortical Carcinoma Treated with Immune Checkpoint Blockade: A Case Report

Qiaoxin Lin1, Bin Liang1, Yangyang Li2, Ling Tian3*, Dianna Gu1*

Mining and Analysis of Adverse Events of BRAF Inhibitors Based on FDA Reporting System

Silan Peng1,2#, Danling Zheng1,3#, Yanli Lei4#, Wang Chen3, Chengkuan Zhao3, Xinyue Lin1, Xiaoshan Chen3, Wei He3, Li Li3, Qiuzhen Zhang5*, Shuyao Zhang1,3*

Malignant Phyllodes Tumor with Fever, Anemia, Hypoproteinemia: A Rare and Strange Case Report and Literature Review

Zhenghang Li1, Yuxian Wei1*

Construction of Cuproptosis-Related LncRNA Signature as a Prognostic Model Associated with Immune Microenvironment for Clear-Cell Renal Cell Carcinoma

Jiyao Yu1#, Shukai Zhang2#, Qingwen Ran3, Xuemei Li4,5,6*

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