المؤلفون: Asghari, F.¹, Karimi, M. H.^2,3, Pourfathollah, A. A.¹ pourfa@modares.ac.ir

المصدر: Immunopharmacology & Immunotoxicology. Dec2023, Vol. 45 Issue 6, p719-729. 11p.

مصطلحات موضوعية: *T cells, *MTOR inhibitors, *OXIDATIVE stress, *GENE expression, *CELL proliferation, *CD28 antigen, *IMMUNOSENESCENCE

مستخلص: Background: Due to the increase of the elderly's population and related social and economic problems, it is very important to provide strategies on health. In this regard, induction of T lymphocytes responses, the most important cells of the immune system, may be a good approach. Among different agents considered as antiaging factors, mTORC1 pathway inhibitors are significant. So, the purpose of this study was to evaluate the effect of two mTORC1 inhibitors, Everolimus and Metformin, on age-related features of activated T cells. Materials and Methods: Optimum doses of drugs was determined with evaluating the effect of treatments on IL-2 gene expression. T cells isolated from old and young mice were treated with drugs and PHA. IL-2 production was evaluated by ELISA. Also, the expression of CD28, PD-1, and KLRG-1, proliferation, and intracellular oxidative stress were assessed by flow cytometry-based assays, phenotyping, CFSE, and DCF-DA assay respectively. Results: Both drugs increased IL-2 production in the T cells of old mice. Also, using drugs especially Metformin could improve age-related phenotypical markers and increase the proliferation of T cells of old mice significantly. In addition, Metformin and Everolimus reduced intracellular oxidative stress in aged cells. However, the effect of both drugs on the T cells of young mice wasn't significant or was in opposite to the results of old mice T cells. Discussion: In line with studies noting mTOR inhibitors as antiaging drugs, Metformin and Everolimus may improve T cells affected from aging in vitro, and a decrease in intracellular oxidative stress may be one of their mechanism of function. [ABSTRACT FROM AUTHOR]

المؤلفون: Wiese, Wojciech¹ (AUTHOR) wojciech.wiese@stud.umed.lodz.pl, Barczuk, Julia¹ (AUTHOR) julia.barczuk@stud.umed.lodz.pl, Racinska, Olga¹ (AUTHOR) olga.racinska@stud.umed.lodz.pl, Siwecka, Natalia¹ (AUTHOR) natalia.siwecka@stud.umed.lodz.pl, Rozpedek-Kaminska, Wioletta¹ (AUTHOR) wioletta.rozpedek@umed.lodz.pl, Slupianek, Artur² (AUTHOR) aslupian@temple.edu, Sierpinski, Radoslaw³ (AUTHOR) r.sierpinski@uksw.edu.pl, Majsterek, Ireneusz¹ (AUTHOR) ireneusz.majsterek@umed.lodz.pl

المصدر: Cancers. Nov2023, Vol. 15 Issue 21, p5297. 18p.

مصطلحات موضوعية: *PHOSPHOTRANSFERASES, *MTOR inhibitors, *LEUKEMIA, *CELLULAR signal transduction, *CELL cycle, *HEMATOLOGIC malignancies, *CELL proliferation

مستخلص: Simple Summary: The PI3K/Akt/mTOR pathway plays a crucial role in cancer, including leukemia. Abnormalities in this pathway drive carcinogenesis by inducing uncontrolled growth, increased survival, and treatment resistance. The abovementioned pathway is also disrupted in various types of leukemia, which makes it a potential therapeutic target for this disease. Current treatment approaches for leukemia are limited and fraught with numerous side effects. This review article aims to summarize recent research data on inhibitors of the PI3K/Akt/mTOR pathway. Inhibition of this pathway may potentially provide improved treatment outcomes for leukemia. Blood malignancies remain a therapeutic challenge despite the development of numerous treatment strategies. The phosphatidylinositol-3 kinase (PI3K)/protein kinase B/mammalian target of rapamycin (PI3K/Akt/mTOR) signaling pathway plays a central role in regulating many cellular functions, including cell cycle, proliferation, quiescence, and longevity. Therefore, dysregulation of this pathway is a characteristic feature of carcinogenesis. Increased activation of PI3K/Akt/mTOR signaling enhances proliferation, growth, and resistance to chemo- and immunotherapy in cancer cells. Overactivation of the pathway has been found in various types of cancer, including acute and chronic leukemia. Inhibitors of the PI3K/Akt/mTOR pathway have been used in leukemia treatment since 2014, and some of them have improved treatment outcomes in clinical trials. Recently, new inhibitors of PI3K/Akt/mTOR signaling have been developed and tested both in preclinical and clinical models. In this review, we outline the role of the PI3K/Akt/mTOR signaling pathway in blood malignancies' cells and gather information on the inhibitors of this pathway that might provide a novel therapeutic opportunity against leukemia. [ABSTRACT FROM AUTHOR]

المؤلفون: Campanelli, Gisella, Francois, Ekniel, Parupathi, Prashanth, Devarakonda, Lakshmi Sirisha, Yang, Ching, Kumar, Avinash, Levenson, Anait S.

المصدر: Cancers; Apr2024, Vol. 16 Issue 7, p1344, 15p

مصطلحات موضوعية: PHYTOTHERAPY, BIOLOGICAL models, PROTEINS, PROSTATE-specific antigen, RESEARCH funding, CELL proliferation, APOPTOSIS, PROSTATE tumors, CELLULAR signal transduction, DESCRIPTIVE statistics, PLANT extracts, MICE, MEDICINAL plants, DRUG efficacy, ANIMAL experimentation, MOLECULAR structure, MTOR inhibitors, POLYPHENOLS, EVALUATION

مستخلص: Simple Summary: Incidence and mortality rates for prostate cancer remain high due to advanced disease characterized by the heterogeneous activation of numerous molecular pathways. In the current study, utilizing a genetic mouse model of advanced prostate cancer with hyperactivated metastasis-associated protein 1/mammalian target of rapamycin (MTA1/mTOR) tumor-promoting pathway, we show for the first time that gnetin C, a natural compound from the melinjo plant, blocks the progression of prostate cancer by reducing cell proliferation and angiogenesis and promoting cell death through the efficient targeting of the MTA1/mTOR pathway. These data may provide a foundation from which to explore gnetin C as a monotherapy and/or combination therapy with approved drugs against advanced prostate cancer in patients with a loss of phosphatase and tensin homolog (PTEN) expression and activated MTA1/mTOR signaling. The metastasis-associated protein 1/protein kinase B (MTA1/AKT) signaling pathway has been shown to cooperate in promoting prostate tumor growth. Targeted interception strategies by plant-based polyphenols, specifically stilbenes, have shown great promise against MTA1-mediated prostate cancer progression. In this study, we employed a prostate-specific transgenic mouse model with MTA1 overexpression on the background of phosphatase and tensin homolog (Pten) null (R26^MTA1; Pten^f/f) and PC3M prostate cancer cells which recapitulate altered molecular pathways in advanced prostate cancer. Mechanistically, the MTA1 knockdown or pharmacological inhibition of MTA1 by gnetin C (dimer resveratrol) in cultured PC3M cells resulted in the marked inactivation of mammalian target of rapamycin (mTOR) signaling. In vivo, mice tolerated a daily intraperitoneal treatment of gnetin C (7 mg/kg bw) for 12 weeks without any sign of toxicity. Treatment with gnetin C markedly reduced cell proliferation and angiogenesis and promoted apoptosis in mice with advanced prostate cancer. Further, in addition to decreasing MTA1 levels in prostate epithelial cells, gnetin C significantly reduced mTOR signaling activity in prostate tissues, including the activity of mTOR-target proteins: p70 ribosomal protein S6 kinase (S6K) and eukaryotic translational initiation factor 4E (elF4E)-binding protein 1 (4EBP1). Collectively, these findings established gnetin C as a new natural compound with anticancer properties against MTA1/AKT/mTOR-activated prostate cancer, with potential as monotherapy and as a possible adjunct to clinically approved mTOR pathway inhibitors in the future. [ABSTRACT FROM AUTHOR]

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المؤلفون: Xavier, Alcides Euzebio Tavares, Veronez, Luciana Chain, Nagano, Luís Fernando Peinado, Correa, Carolina Alves Pereira, Baroni, Mirela, Ramos, Milena Silva, Queiroz, Rosane de Gomes de Paula, Fernandes Molina, Carlos Augusto, Yunes, José Andres, Brandalise, Silvia Regina, Antonini, Sonir Antonio Rauber, Tone, Luiz Gonzaga, Valera, Elvis Terci, Scrideli, Carlos Alberto

المصدر: Cancers; Mar2024, Vol. 16 Issue 6, p1094, 20p

مصطلحات موضوعية: PROTEINS, IN vitro studies, NF-kappa B, RESEARCH funding, CANCER relapse, SURVIVAL rate, CELL proliferation, TREATMENT effectiveness, TUMOR markers, AMP-activated protein kinases, MULTIVARIATE analysis, AGE distribution, CANCER patients, CELLULAR signal transduction, CYTOSKELETAL proteins, CELL motility, GENE expression, CELL lines, METASTASIS, MTOR inhibitors, ADRENAL tumors, POLYPHENOLS, WNT proteins, TUMOR necrosis factors, PHARMACODYNAMICS

مصطلحات جغرافية: BRAZIL

مستخلص: Simple Summary: Adrenocortical tumors are rare neoplasms with an uncertain prognosis. A greater understanding of the biology of these tumors will allow new therapeutic targets to be identified and the prognosis of these patients to be better understood, enabling more precise therapeutic targeting. Our study sought to evaluate the expression of the PRKAB2 gene as a prognostic biomarker in 63 cases of pediatric adrenocortical tumors and to analyze how efficient Rottlerin is in altering the tumorigenic profile of the NCI-H295R adrenocortical carcinoma (ACC) cell line. Pediatric adrenocortical tumors (ACTs) are rare, highly heterogeneous neoplasms with limited therapeutic options, making the investigation of new targets with potential therapeutic or prognostic purposes urgent. The PRKAB2 gene produces one of the subunits of the AMP-activated protein kinase (AMPK) complex and has been associated with cancer. However, little is known about the role AMPK plays in ACTs. We have evaluated how PRKAB2 is associated with clinical and biological characteristics in 63 pediatric patients with ACTs and conducted in vitro studies on the human NCI-H295R ACC cell line. An analysis of our cohort and the public ACC pediatric dataset GSE76019 showed that lower PRKAB2 expression was associated with relapse, death, metastasis, and lower event-free and overall survival rates. Multivariate analysis showed that PRKAB2 expression was an independent prognostic factor when associated with age, tumor weight and volume, and metastasis. In vitro tests on NCI-H295R cells demonstrated that Rottlerin, a drug that can activate AMPK, modulated several pathways in NCI-H295R cells, including AMPK/mTOR, Wnt/β-catenin, SKP2, HH, MAPK, NFKB, and TNF. Treatment with Rottlerin decreased cell proliferation and migration, clonogenic capacity, and steroid production. Together, these results suggest that PRKAB2 is a potential prognostic marker in pediatric ACTs, and that Rottlerin is promising for investigating drugs that can act against ACTs. [ABSTRACT FROM AUTHOR]

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المؤلفون: Zhang, Yue, Xiao, Yan-wei, Ma, Jing-xin, Wang, Ao-xue

المصدر: Chinese Journal of Integrative Medicine; Mar2024, Vol. 30 Issue 3, p213-221, 9p

مصطلحات موضوعية: WOUND healing, PROTEINS, REVERSE transcriptase polymerase chain reaction, IN vitro studies, RAPAMYCIN, EPIDERMAL growth factor receptors, ANIMAL experimentation, WESTERN immunoblotting, MTOR inhibitors, PLASMIDS, CELL motility, CELLULAR signal transduction, RATS, CELL proliferation, TRANSFERASES, MESSENGER RNA, CELL lines, PLANT extracts, KERATINOCYTES

مستخلص: Objective: To investigate the effect and possible mechanism of hydroxysafflor yellow A (HSYA) on human immortalized keratinocyte cell proliferation and migration. Methods: HaCaT cells were treated with HSYA. Cell proliferation was detected by the cell counting kit-8 assay, and cell migration was measured using wound healing assay and Transwell migration assay. The mRNA and protein expression levels of heparin-binding epidermal growth factor (EGF)-like growth factor (HBEGF), EGF receptor (EGFR), phosphatidylinositol 3-kinase (PI3K), protein kinase B (AKT), mammalian target of rapamycin (mTOR), and hypoxia-inducible factor-1α (HIF-1α) were detected by quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot, respectively. Circ_0084443-overexpressing HaCaT cells and empty plasmid HaCaT cells were constructed using the lentiviral stable transfection and treated with HSYA. The expression of circ_0084443 was detected by qRT-PCR. Results: HSYA (800 µmol/L) significantly promoted HaCaT cell proliferation and migration (P<0.05 or P<0.01). It also increased the mRNA and protein expression levels of HBEGF, EGFR, PI3K, AKT, mTOR and HIF-1α, and increased the phosphorylation levels of PI3K and AKT (P<0.05 or P<0.01). Furthermore, HSYA promoted HaCaT cell proliferation and migration via the HBEGF/EGFR and PI3K/AKT/mTOR signaling pathways (P<0.01). Circ_0084443 attenuated the mRNA expression levels of HBEGF, EGFR, PI3K, AKT, mTOR and HIF-1α (P<0.05). HSYA inhibited the circ_0084443 expression, further antagonized the inhibition of circ_0084443 on HBEGF, EGFR, PI3K, AKT, mTOR and HIF-1α, and promoted the proliferation of circ_0084443-overexpressing HaCaT cells (P<0.05 or P<0.01). However, HSYA could not influence the inhibitory effect of circ_0084443 on HaCaT cell migration (P>0.05). Conclusion: HSYA played an accelerative role in HaCaT cell proliferation and migration, which may be attributable to activating HBEGF/EGFR and PI3K/AKT signaling pathways, and had a particular inhibitory effect on the keratinocyte negative regulator circ_0084443. [ABSTRACT FROM AUTHOR]

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المؤلفون: Bouyahya, Abdelhakim¹ (AUTHOR) bouyahya@um5r.ac.ma, El Allam, Aicha² (AUTHOR), Aboulaghras, Sara³ (AUTHOR), Bakrim, Saad⁴ (AUTHOR), El Menyiy, Naoual⁵ (AUTHOR), Alshahrani, Mohammed Merae⁶ (AUTHOR), Al Awadh, Ahmed Abdullah⁶ (AUTHOR), Benali, Taoufiq⁷ (AUTHOR), Lee, Learn-Han⁸ (AUTHOR), El Omari, Nasreddine⁹ (AUTHOR), Goh, Khang Wen¹⁰ (AUTHOR), Ming, Long Chiau¹¹ (AUTHOR) bouyahya@um5r.ac.ma, Mubarak, Mohammad S.¹² (AUTHOR)

المصدر: Cancers. Nov2022, Vol. 14 Issue 22, p5520. 41p.

مصطلحات موضوعية: *AUTOPHAGY, *MTOR inhibitors, *ORGANIC compounds, *APOPTOSIS, *CELLULAR signal transduction, *MESSENGER RNA, *CELL proliferation, *TUMORS, *IMMUNOTHERAPY, *MEDICAL research

مستخلص: The mammalian target of rapamycin (mTOR) is a highly conserved serine/threonine-protein kinase, which regulates many biological processes related to metabolism, cancer, immune function, and aging. It is an essential protein kinase that belongs to the phosphoinositide-3-kinase (PI3K) family and has two known signaling complexes, mTOR complex 1 (mTORC1) and mTOR complex 2 (mTORC2). Even though mTOR signaling plays a critical role in promoting mitochondria-related protein synthesis, suppressing the catabolic process of autophagy, contributing to lipid metabolism, engaging in ribosome formation, and acting as a critical regulator of mRNA translation, it remains one of the significant signaling systems involved in the tumor process, particularly in apoptosis, cell cycle, and cancer cell proliferation. Therefore, the mTOR signaling system could be suggested as a cancer biomarker, and its targeting is important in anti-tumor therapy research. Indeed, its dysregulation is involved in different types of cancers such as colon, neck, cervical, head, lung, breast, reproductive, and bone cancers, as well as nasopharyngeal carcinoma. Moreover, recent investigations showed that targeting mTOR could be considered as cancer therapy. Accordingly, this review presents an overview of recent developments associated with the mTOR signaling pathway and its molecular involvement in various human cancer types. It also summarizes the research progress of different mTOR inhibitors, including natural and synthetised compounds and their main mechanisms, as well as the rational combinations with immunotherapies. [ABSTRACT FROM AUTHOR]

المؤلفون: Zhang, Yuanqin, Fang, Xiangwei, Wang, Jiuhui, Nie, Daotai

المصدر: Cancers; Dec2023, Vol. 15 Issue 23, p5691, 24p

مصطلحات موضوعية: PROTEIN metabolism, DISEASE progression, CELL receptors, MTOR inhibitors, CELLULAR signal transduction, CELL proliferation, TRANSFERASES, TAMOXIFEN, BREAST tumors, PROGESTERONE receptors

مستخلص: Simple Summary: Selective estrogen receptor modulators are a major treatment modality for estrogen receptor-positive breast cancers, but the emergence of resistance or a lack of initial responsiveness is a major cause of treatment failures. This study describes TMEM97, also known as sigma 2 receptor, as a novel regulator of estrogen receptor activation. High expression of TMEM97 is found in breast tumor tissues with estrogen receptor positivity. Depletion of TMEM97 expression reduces estrogen receptor activities and breast cancer cell growth. Increased expression of TMEM97 in breast cancer cells stimulates estrogen receptor activities and growth. Further, TMEM97 increases the resistance of breast cancer cells to tamoxifen through elaborating the mTOR/S6K1 signaling. The results suggest an important role for TMEM97 in estrogen receptor activation and resistance to tamoxifen in breast cancer cells. Aberrant estrogen receptor (ER) signaling is a major driver of breast tumor growth and progression. Sigma 2 receptor has long been implicated in breast carcinogenesis based on pharmacological studies, but its molecular identity had been elusive until TMEM97 was identified as the receptor. Herein, we report that the TMEM97/sigma 2 receptor is highly expressed in ER-positive breast tumors and its expression is strongly correlated with ERs and progesterone receptors (PRs) but not with HER2 status. High expression levels of TMEM97 are associated with reduced overall survival of patients. Breast cancer cells with increased expression of TMEM97 had a growth advantage over the control cells under both nutrition-limiting and sufficient conditions, while the knockdown of TMEM97 expression reduced tumor cell proliferations. When compared to their vector control cells, MCF7 and T47D cells with increased TMEM97 expression presented increased resistance to tamoxifen treatment and also grew better under estrogen-depleted conditions. The TMEM97/sigma 2 receptor enhanced the ERα transcriptional activities and increased the expression of genes responsive to estrogen treatment. Increased TMEM97 also stimulated the mTOR/S6K1 signaling pathways in the MCF7 and T47D cells. The increased level of active, phosphorylated ERα, and the enhanced resistance to tamoxifen treatment with increased TMEM97, could be blocked by an mTOR inhibitor. The knockdown of TMEM97 expression reduced the ERα and mTOR/S6K1 signaling activities, rendering the cells with an increased sensitivity to tamoxifen. The observations suggest that the TMEM97/sigma 2 receptor is a novel regulator of ERα activities in breast tumor cell growth. [ABSTRACT FROM AUTHOR]

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المؤلفون: Zhang, Minghui, Ma, Zonghua, Qi, Hao, Cui, Xu, Li, Rui, Gao, Xuejun

المصدر: British Journal of Nutrition; 11/28/2023, Vol. 130 Issue 10, p1665-1677, 13p

مصطلحات موضوعية: METHIONINE metabolism, BIOLOGICAL models, LACTATION, PROTEINS, SEQUENCE analysis, ANIMAL experimentation, CELL receptors, PUBERTY, MTOR inhibitors, MILK proteins, GENE expression profiling, BREAST, TISSUES, CELL proliferation, DESCRIPTIVE statistics, RESEARCH funding, POLYMERASE chain reaction, EPITHELIAL cells, CELL lines, FATTY acids, MICE, PHOSPHORYLATION

مستخلص: The G protein-coupled receptors (GPCR) sensing nutritional signals (amino acids, fatty acids, glucose, etc.) are not fully understood. In this research, we used transcriptome sequencing to analyse differentially expressed genes (DEG) in mouse mammary gland tissues at puberty, lactation and involution stages, in which eight GPCR were selected out and verified by qRT-PCR assay. It was further identified the role of GPR110-mediating nutrients including palmitic acid (PA) and methionine (Met) to improve milk synthesis using mouse mammary epithelial cell line HC11. PA but not Met affected GPR110 expression in a dose-dependent manner. GPR110 knockdown decreased milk protein and fat synthesis and cell proliferation and blocked the stimulation of PA on mechanistic target of rapamycin (mTOR) phosphorylation and sterol-regulatory element binding protein 1c (SREBP-1c) expression. In summary, these experimental results disclose DEG related to lactation and reveal that GPR110 mediates PA to activate the mTOR and SREBP-1c pathways to promote milk protein and fat synthesis. [ABSTRACT FROM AUTHOR]

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المؤلفون: Ali, Eunus S.^1,2,3 (AUTHOR), Mitra, Kangkana⁴ (AUTHOR), Akter, Shamima⁵ (AUTHOR), Ramproshad, Sarker⁶ (AUTHOR), Mondal, Banani⁶ (AUTHOR), Khan, Ishaq N.⁷ (AUTHOR), Islam, Muhammad Torequl⁸ (AUTHOR), Sharifi-Rad, Javad⁹ (AUTHOR) javad.sharifirad@gmail.com, Calina, Daniela¹⁰ (AUTHOR) calinadaniela@gmail.com, Cho, William C.¹¹ (AUTHOR) chocs@ha.org.hk

المصدر: Cancer Cell International. 9/15/2022, Vol. 22 Issue 1, p1-16. 16p.

مصطلحات موضوعية: *RAPAMYCIN, *MTOR inhibitors, *IMMUNOSUPPRESSIVE agents, *CELL transformation, *CANCER treatment, *CELL proliferation

مستخلص: The PI3K-Akt-mechanistic (formerly mammalian) target of the rapamycin (mTOR) signaling pathway is important in a variety of biological activities, including cellular proliferation, survival, metabolism, autophagy, and immunity. Abnormal PI3K-Akt-mTOR signalling activation can promote transformation by creating a cellular environment conducive to it. Deregulation of such a system in terms of genetic mutations and amplification has been related to several human cancers. Consequently, mTOR has been recognized as a key target for the treatment of cancer, especially for treating cancers with elevated mTOR signaling due to genetic or metabolic disorders. In vitro and in vivo, rapamycin which is an immunosuppressant agent actively suppresses the activity of mTOR and reduces cancer cell growth. As a result, various sirolimus-derived compounds have now been established as therapies for cancer, and now these medications are being investigated in clinical studies. In this updated review, we discuss the usage of sirolimus-derived compounds and other drugs in several preclinical or clinical studies as well as explain some of the challenges involved in targeting mTOR for treating various human cancers. [ABSTRACT FROM AUTHOR]

المؤلفون: Kapur, Payal, Brugarolas, James, Trpkov, Kiril

المصدر: Cancers; Aug2023, Vol. 15 Issue 16, p4043, 17p

مصطلحات موضوعية: RENAL cell carcinoma, CELL migration, IMMUNOHISTOCHEMISTRY, MICROBIOLOGICAL assay, MTOR inhibitors, SIGNAL peptides, CELLULAR signal transduction, KIDNEY tumors, CELL proliferation, TUBEROUS sclerosis

مستخلص: Simple Summary: In the past decade, several novel renal neoplasms characterized by mutations in the tuberous sclerosis complex (TSC) or mechanistic target of rapamycin (mTOR) pathway genes in both the sporadic and germline settings have been described. Herein, we review these entities, highlighting their clinical and molecular characteristics. A spectrum of renal tumors associated with frequent TSC/mTOR (tuberous sclerosis complex/mechanistic target of rapamycin) pathway gene alterations (in both the germline and sporadic settings) have recently been described. These include renal cell carcinoma with fibromyomatous stroma (RCC FMS), eosinophilic solid and cystic renal cell carcinoma (ESC RCC), eosinophilic vacuolated tumor (EVT), and low-grade oncocytic tumor (LOT). Most of these entities have characteristic morphologic and immunohistochemical features that enable their recognition without the need for molecular studies. In this report, we summarize recent advances and discuss their evolving complexity. [ABSTRACT FROM AUTHOR]

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