Open Access
Open access

Advances in Experimental Medicine and Biology

Springer Nature
Springer Nature
ISSN: 00652598, 22148019
SCImago
Q3
SJR
0.244
CiteScore
5.9
Categories
Biochemistry, Genetics and Molecular Biology (miscellaneous)
Medicine (miscellaneous)
Areas
Biochemistry, Genetics and Molecular Biology
Medicine
Years of issue
1971-2025
journal names
Advances in Experimental Medicine and Biology
Publications
40 554
Citations
447 368
h-index
154
Top-3 citing journals
Top-3 organizations
Harvard University
Harvard University (582 publications)
University of Pennsylvania
University of Pennsylvania (522 publications)
Johns Hopkins University
Johns Hopkins University (363 publications)
Top-3 countries
USA (16118 publications)
United Kingdom (3361 publications)
Germany (3194 publications)

Most cited in 5 years

Chan H., Samala R.K., Hadjiiski L.M., Zhou C.
Advances in Experimental Medicine and Biology Q3 Open Access
2020-02-06 citations by CoLab: 418 Abstract
Deep learning is the state-of-the-art machine learning approach. The success of deep learning in many pattern recognition applications has brought excitement and high expectations that deep learning, or artificial intelligence (AI), can bring revolutionary changes in health care. Early studies of deep learning applied to lesion detection or classification have reported superior performance compared to those by conventional techniques or even better than radiologists in some tasks. The potential of applying deep-learning-based medical image analysis to computer-aided diagnosis (CAD), thus providing decision support to clinicians and improving the accuracy and efficiency of various diagnostic and treatment processes, has spurred new research and development efforts in CAD. Despite the optimism in this new era of machine learning, the development and implementation of CAD or AI tools in clinical practice face many challenges. In this chapter, we will discuss some of these issues and efforts needed to develop robust deep-learning-based CAD tools and integrate these tools into the clinical workflow, thereby advancing towards the goal of providing reliable intelligent aids for patient care.
Zhang L., Lu Q., Chang C.
Advances in Experimental Medicine and Biology Q3 Open Access
2020-05-22 citations by CoLab: 400 Abstract
Epigenetic mechanisms, which include DNA methylation, histone modification, and microRNA (miRNA), can produce heritable phenotypic changes without a change in DNA sequence. Disruption of gene expression patterns which are governed by epigenetics can result in autoimmune diseases, cancers, and various other maladies. Mechanisms of epigenetics include DNA methylation (and demethylation), histone modifications, and non-coding RNAs such as microRNAs. Compared to numerous studies that have focused on the field of genetics, research on epigenetics is fairly recent. In contrast to genetic changes, which are difficult to reverse, epigenetic aberrations can be pharmaceutically reversible. The emerging tools of epigenetics can be used as preventive, diagnostic, and therapeutic markers. With the development of drugs that target the specific epigenetic mechanisms involved in the regulation of gene expression, development and utilization of epigenetic tools are an appropriate and effective approach that can be clinically applied to the treatment of various diseases.
Ai L., Xu A., Xu J.
Advances in Experimental Medicine and Biology Q3 Open Access
2020-03-17 citations by CoLab: 319 Abstract
Immunotherapies that target PD-1/PD-L1 axis have shown unprecedented success in a wide variety of human cancers. PD-1 is one of the key coinhibitory receptors expressed on T cells upon T cell activation. After engagement with its ligands, mainly PD-L1, PD-1 is activated and recruits the phosphatase SHP-2 in proximity to T cell receptor (TCR) and CD28 signaling. This event results in dephosphorylation and attenuation of key molecules in TCR and CD28 pathway, leading to inhibition of T cell proliferation, activation, cytokine production, altered metabolism and cytotoxic T lymphocytes (CTLs) killer functions, and eventual death of activated T cells. Bodies evolve coinhibitory pathways controlling T cell response magnitude and duration to limit tissue damage and maintain self-tolerance. However, tumor cells hijack these inhibitory pathways to escape host immune surveillance by overexpression of PD-L1. This provides the scientific rationale for clinical application of immune checkpoint inhibitors in oncology. The aberrantly high expression of PD-L1 in tumor microenvironment (TME) can be attributable to the “primary” activation of multiple oncogenic signaling and the “secondary” induction by inflammatory factors such as IFN-γ. Clinically, antibodies targeting PD-1/PD-L1 reinvigorate the “exhausted” T cells in TME and show remarkable objective response and durable remission with acceptable toxicity profile in large numbers of tumors such as melanoma, lymphoma, and mismatch-repair deficient tumors. Nevertheless, most patients are still refractory to anti-PD-1/PD-L1 therapy. Identifying the predictive biomarkers and design rational PD-1-based combination therapy become the priorities in cancer immunotherapy. PD-L1 expression, cytotoxic T lymphocytes infiltration, and tumor mutation burden (TMB) are generally considered as the most important factors affecting the effectiveness of PD-1/PD-L1 blockade. The revolution in cancer immunotherapy achieved by PD-1/PD-L1 blockade offers the paradigm for scientific translation from bench to bedside. The next decades will without doubt witness the renaissance of immunotherapy.
Zhang Y., Sun Z., Jia J., Du T., Zhang N., Tang Y., Fang Y., Fang D.
Advances in Experimental Medicine and Biology Q3 Open Access
2020-11-07 citations by CoLab: 281 Abstract
Epigenetics is the epi-information beyond the DNA sequence that can be inherited from parents to offspring. From years of studies, people have found that histone modifications, DNA methylation, and RNA-based mechanism are the main means of epigenetic control. In this chapter, we will focus on the general introductions of epigenetics, which is important in the regulation of chromatin structure and gene expression. With the development and expansion of high-throughput sequencing, various mutations of epigenetic regulators have been identified and proven to be the drivers of tumorigenesis. Epigenetic alterations are used to diagnose individual patients more accurately and specifically. Several drugs, which are targeting epigenetic changes, have been developed to treat patients regarding the awareness of precision medicine. Emerging researches are connecting the epigenetics and cancers together in the molecular mechanism exploration and the development of druggable targets.
Leiter U., Keim U., Garbe C.
Advances in Experimental Medicine and Biology Q3 Open Access
2020-09-11 citations by CoLab: 251 Abstract
Melanoma and keratinocyte skin cancer (KSC) are the most common types of cancer in White-skinned populations. Both tumor entities showed increasing incidence rates worldwide but stable or decreasing mortality rates. Rising incidence rates of cutaneous melanoma (CM) and KSC are largely attributed to increasing exposure to ultraviolet (UV) radiation, the main causal risk factor for skin cancer. Incidence rates of KSC, comprising of basal cell carcinoma (BCC) and squamous cell carcinoma (SCC), are much higher than that of melanoma. BCC development is mainly the cause of an intensive UV exposure in childhood and adolescence, while SCC development is related to chronic, cumulative UV exposure over decades. Although mortality is relatively low, KSC is an increasing problem for health care services causing significant morbidity. Cutaneous melanoma is rapidly increasing in White populations, with an estimated annual increase of around 3–7% over the past decades. In contrast to SCC, melanoma risk is associated with intermittent and chronic exposure to sunlight. The frequency of its occurrence is closely associated with the constitutive color of the skin and the geographical zone. Changes in outdoor activities and exposure to sunlight during the past 70 years are an important factor for the increasing incidence of melanoma. Mortality rates of melanoma show stabilization in the USA, Australia, and in European countries. In the USA even dropping numbers of death cases were recently reported, probably reflecting efficacy of the new systemic treatments. Among younger cohorts in some populations (e.g., Australia and New Zealand,), stabilizing or declining incidence rates of CM are observed, potentially caused by primary prevention campaigns aimed at reducing UV exposure. In contrast, incidence rates of CM are still rising in most European countries and in the USA. Ongoing trends towards thinner melanoma are largely ascribed to earlier detection.
Zhang Y., Zheng J.
Advances in Experimental Medicine and Biology Q3 Open Access
2020-03-17 citations by CoLab: 170 Abstract
Immune checkpoint molecules, including inhibitory and stimulatory immune checkpoint molecules, are defined as ligand–receptor pairs that exert inhibitory or stimulatory effects on immune responses. Most of the immune checkpoint molecules that have been described so far are expressed on cells of the adaptive immune system, particularly on T cells, and of the innate immune system. They are crucial for maintaining the self-tolerance and modulating the length and magnitude of immune responses of effectors in different tissues to minimize the tissue damage. More and more evidences have shown that inhibitory or stimulatory immune checkpoint molecules are expressed on a sizeable fraction of tumor types. Although the main function of tumor cell-associated immune checkpoint molecules is considered to mediate the immune evasion, it has been reported that the immune checkpoint molecules expressed on tumor cells also play important roles in the maintenance of many malignant behaviors, including self-renewal, epithelial–mesenchymal transition, metastasis, drug resistance, anti-apoptosis, angiogenesis, or enhanced energy metabolisms. In this section, we mainly focus on delineating the roles of the tumor cell-associated immune checkpoint molecules beyond immune evasion, such as PD-L1, PD-1, B7-H3, B7-H4, LILRB1, LILRB2, TIM3, CD47, CD137, and CD70.
Dysthe M., Parihar R.
Advances in Experimental Medicine and Biology Q3 Open Access
2020-02-08 citations by CoLab: 170 Abstract
Myeloid-derived suppressor cells (MDSCs) represent a heterogenous population of immature myeloid cells capable of modulating immune responses. In the context of cancer, MDSCs are abnormally produced and recruited to the tumor microenvironment (TME) to aid in the establishment of an immunosuppressive TME that facilitates tumor escape. Additionally, MDSCs contribute to non-immunologic aspects of tumor biology, including tumor angiogenesis and metastasis. The clinical significance of MDSCs has recently been appreciated as numerous studies have suggested a correlation between circulating and intratumoral MDSC frequencies and tumor stage, progression, and treatment resistance. In this chapter, we review MDSC characterization, development, expansion, and mechanisms that facilitate immunosuppression and tumor progression. Furthermore, we highlight studies demonstrating the clinical significance of MDSCs in various disease states in addition to strategies that modulate various aspects of MDSC biology for therapeutic gain.
Shao C., Wang J., Tian J., Tang Y.
Advances in Experimental Medicine and Biology Q3 Open Access
2020-04-03 citations by CoLab: 136 Abstract
In most developed countries, coronary artery disease (CAD), mostly caused by atherosclerosis of coronary arteries, is one of the primary causes of death. From 1990s to 2000s, mortality caused by acute MI declined up to 50%. The incidence of CAD is related with age, gender, economic, etc. Atherosclerosis contains some highly correlative processes such as lipid disturbances, thrombosis, inflammation, vascular smooth cell activation, remodeling, platelet activation, endothelial dysfunction, oxidative stress, altered matrix metabolism, and genetic factors. Risk factors of CAD exist among many individuals of the general population, which includes hypertension, lipids and lipoproteins metabolism disturbances, diabetes mellitus, chronic kidney disease, age, genders, lifestyle, cigarette smoking, diet, obesity, and family history. Angina pectoris is caused by myocardial ischemia in the main expression of pain in the chest or adjoining area, which is usually a result of exertion and related to myocardial function disorder. Typical angina pectoris would last for minutes with gradual exacerbation. Rest, sit, or stop walking are the usual preference for patients with angina, and reaching the maximum intensity in seconds is uncommon. Rest or nitroglycerin usage can relieve typical angina pectoris within minutes. So far, a widely accepted angina pectoris severity grading system included CCS (Canadian Cardiovascular Society) classification, Califf score, and Goldman scale. Patients with ST-segment elevated myocardial infarction (STEMI) may have different symptoms and signs of both severe angina pectoris and various complications. The combination of rising usage of sensitive MI biomarkers and precise imaging techniques, including electrocardiograph (ECG), computed tomography, and cardiac magnetic resonance imaging, made the new MI criteria necessary. Complications of acute myocardial infarction include left ventricular dysfunction, cardiogenic shock, structural complications, arrhythmia, recurrent chest discomfort, recurrent ischemia and infarction, pericardial effusion, pericarditis, post-myocardial infarction syndrome, venous thrombosis pulmonary embolism, left ventricular aneurysm, left ventricular thrombus, and arterial embolism.
Santana-Codina N., Gikandi A., Mancias J.D.
Advances in Experimental Medicine and Biology Q3 Open Access
2021-08-09 citations by CoLab: 135 Abstract
Nuclear receptor coactivator 4 (NCOA4) is a selective cargo receptor that mediates the autophagic degradation of ferritin, the cytosolic iron storage complex, in a process known as ferritinophagy. NCOA4-mediated ferritinophagy is required to maintain intracellular and systemic iron homeostasis and thereby iron-dependent physiologic processes such as erythropoiesis. Given this role of ferritinophagy in regulating iron homeostasis, modulating NCOA4-mediated ferritinophagic flux alters sensitivity to ferroptosis, a non-apoptotic iron-dependent form of cell death triggered by peroxidation of polyunsaturated fatty acids (PUFAs). A role for ferroptosis has been established in the pathophysiology of cancer and neurodegeneration; however, the importance of ferritinophagy in these pathologies remains largely unknown. Here, we review the available evidence on biochemical regulation of NCOA4-mediated ferritinophagy and its role in modulating sensitivity to innate and induced ferroptosis in neurodegenerative diseases and cancer. Finally, we evaluate the potential of modulating ferritinophagy in combination with ferroptosis inducers as a therapeutic strategy.
Van Coillie S., Wiernicki B., Xu J.
Advances in Experimental Medicine and Biology Q3 Open Access
2020-03-17 citations by CoLab: 133 Abstract
Cytotoxic T-lymphocyte-associated protein 4 (CTLA-4) is an inhibitory receptor belonging to the CD28 immunoglobulin subfamily, expressed primarily by T-cells. Its ligands, CD80 and CD86, are typically found on the surface of antigen-presenting cells and can either bind CD28 or CTLA-4, resulting in a costimulatory or a co-inhibitory response, respectively. Because of its dampening effect, CTLA-4 is a crucial regulator of T-cell homeostasis and self-tolerance. The mechanisms by which CTLA-4 exerts its inhibitory function can be categorized as either cell-intrinsic (affects the CTLA-4 expressing T-cell) or cell-extrinsic (affects secondary cells). Research from the last decade has shown that CTLA-4 mainly acts in a cell-extrinsic manner via its competition with CD28, CTLA-4-mediated trans-endocytosis of CD80 and CD86, and its direct tolerogenic effects on the interacting cell. Nonetheless, intrinsic CTLA-4 signaling has been implicated in T-cell motility and the regulation of CTLA-4 its subcellular localization amongst others. CTLA-4 is well recognized as a key immune checkpoint and has gained significant momentum as a therapeutic target in the field of autoimmunity and cancer. In this chapter, we describe the role of costimulation in immune response induction as well as the main mechanisms by which CTLA-4 can inhibit this process.
from 3 chars
Publications found: 40554
Bone Tissue Engineering: From Biomaterials to Clinical Trials
Jagadale S., Damle M., Joshi M.G.
Q3
Springer Nature
Advances in Experimental Medicine and Biology 2025 citations by CoLab: 0
Open Access
Open access
Bioengineering Approaches for Male Infertility: From Microenvironmental Regeneration to in vitro Fertilization
Önen S., Gizer M., Çolak İ.Ö., Korkusuz P.
Q3
Springer Nature
Advances in Experimental Medicine and Biology 2025 citations by CoLab: 0
Open Access
Open access
The Role of Mesenchymal Stem Cell-Derived Exosomes in Skin Regeneration, Tissue Repair, and the Regulation of Hair Follicle Growth
Karimi N., Dinçsoy A.B.
Q3
Springer Nature
Advances in Experimental Medicine and Biology 2025 citations by CoLab: 0
Open Access
Open access
Contact Lenses in Therapeutic Care: A Comprehensive Review of Past Innovations, Present Applications, and Future Directions
Shuaibu A., Topah E.K., Suleman A., D’Esposito F., Tognetto D., Gagliano C., Zeppieri M., Musa M.
Q3
Springer Nature
Advances in Experimental Medicine and Biology 2025 citations by CoLab: 0
Open Access
Open access
Peptide Nanofibers and Skin Regeneration
Tekinay S.H., Tekinay A.B.
Q3
Springer Nature
Advances in Experimental Medicine and Biology 2025 citations by CoLab: 0
Open Access
Open access
Exploring Epigenetic Complexity in Regulation of Hematopoietic Stem Cells Niche: A Mechanistic Journey from Normal to Malignant Hematopoiesis
Yusoff N.A., Abd Hamid Z., Taib I.S., Abdul Razak S.R., Budin S.B.
Q3
Springer Nature
Advances in Experimental Medicine and Biology 2025 citations by CoLab: 0
Open Access
Open access
Cancer and Secretomes: HLA-G and Cancer Puzzle
Sel F.A., Oğuz F.S.
Q3
Springer Nature
Advances in Experimental Medicine and Biology 2025 citations by CoLab: 0
Open Access
Open access
Astrocytes in Primary Familial Brain Calcification (PFBC): Emphasis on the Importance of Induced Pluripotent Stem Cell-Derived Human Astrocyte Models
Kavakli E., Gul N., Begentas O.C., Kiris E.
Q3
Springer Nature
Advances in Experimental Medicine and Biology 2025 citations by CoLab: 0
Open Access
Open access
Hormone Signaling in Breast Development and Cancer
Agnoletto A., Brisken C.
Q3
Springer Nature
Advances in Experimental Medicine and Biology 2025 citations by CoLab: 0
Open Access
Open access
Models for Studying Ductal Carcinoma In Situ Progression
Nair I., Behbod F.
Q3
Springer Nature
Advances in Experimental Medicine and Biology 2025 citations by CoLab: 0
Open Access
Open access
Clinical Implications of Breast Cancer Intrinsic Subtypes
Rios-Hoyo A., Shan N., Karn P.L., Pusztai L.
Q3
Springer Nature
Advances in Experimental Medicine and Biology 2025 citations by CoLab: 0
Open Access
Open access
Immune Microenvironment in Breast Cancer Metastasis
Qian B., Ma R.
Q3
Springer Nature
Advances in Experimental Medicine and Biology 2025 citations by CoLab: 0
Open Access
Open access
RANK/RANKL Signaling Pathway in Breast Development and Cancer
Pérez-Chacón G., Santamaría P.G., Redondo-Pedraza J., González-Suárez E.
Q3
Springer Nature
Advances in Experimental Medicine and Biology 2025 citations by CoLab: 0
Open Access
Open access
The Microenvironment in DCIS and Its Role in Disease Progression
Roozitalab M.R., Prekete N., Allen M., Grose R.P., Louise Jones J.
Q3
Springer Nature
Advances in Experimental Medicine and Biology 2025 citations by CoLab: 0
Open Access
Open access
Metabolic Reprogramming and Adaption in Breast Cancer Progression and Metastasis
Zuo Q., Kang Y.
Q3
Springer Nature
Advances in Experimental Medicine and Biology 2025 citations by CoLab: 0
Open Access
Open access

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United Kingdom, 3361, 8.29%
Germany, 3194, 7.88%
Japan, 2748, 6.78%
Italy, 1899, 4.68%
Canada, 1702, 4.2%
China, 1591, 3.92%
France, 1477, 3.64%
Netherlands, 1223, 3.02%
Poland, 949, 2.34%
Australia, 919, 2.27%
Spain, 786, 1.94%
Sweden, 774, 1.91%
Switzerland, 741, 1.83%
Belgium, 535, 1.32%
Israel, 527, 1.3%
Greece, 504, 1.24%
Brazil, 447, 1.1%
Republic of Korea, 439, 1.08%
India, 408, 1.01%
Denmark, 329, 0.81%
Austria, 314, 0.77%
Iran, 287, 0.71%
Russia, 281, 0.69%
Turkey, 258, 0.64%
Finland, 249, 0.61%
Portugal, 247, 0.61%
Ireland, 210, 0.52%
Norway, 193, 0.48%
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Hungary, 161, 0.4%
Chile, 155, 0.38%
Czech Republic, 136, 0.34%
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Argentina, 104, 0.26%
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Romania, 77, 0.19%
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Serbia, 42, 0.1%
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