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Biomedicines
Special Issues
Targeted Therapies for Cancer
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Targeted Therapies for Cancer

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Cancer Biology and Oncology".

Deadline for manuscript submissions: closed (15 February 2022) | Viewed by 55729

Special Issue Editors

Dr. Chiara Brignole

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Guest Editor
Area Aggregazione Laboratori Ricerca, U.O.S.D. Laboratorio Terapie Sperimentali in Oncologia, IRCCS Istituto Giannina Gaslini, 16147 Genoa, Italy
Interests: neuroblastoma; targeted therapy; liposomes; precision medicine for cancer; tumor microenvironment; macrophages and cancer
Special Issues, Collections and Topics in MDPI journals
Dr. Fabio Pastorino

E-Mail Website
Guest Editor
Area Aggregazione Laboratori Ricerca, U.O.S.D. Laboratorio Terapie Sperimentali in Oncologia, IRCCS Istituto Giannina Gaslini, Genoa, Italy
Interests: neuroblastoma; precision medicine; PDXs; liposomes; targeted therapy
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Cancer is the second leading cause of death worldwide. Standard of care treatments are based on conventional chemotherapy, which is accompanied by severe and dose-limiting side effects as well as acquired drug resistance. This has prompted research efforts towards more tumor-selective treatment strategies.

Over the last two decades, new insights into the biology and the signaling pathways of tumor cells and cells of the tumor microenvironment involved in tumor growth and spread led to the development of so-called targeted therapies. Their cornerstone is represented by the identification of specific molecular and cellular targets, endowed with a pivotal role in cell growth and survival, useful for cancer diagnosis and actionable in anti-tumor strategies. To date, several targeted therapies have been developed and many of them have been recently approved by the Food and Drug Administration for treating different types of cancer. At present, the most commonly investigated targeted therapies are based on the use of small-molecule inhibitors, monoclonal antibodies and immunotoxins. In this context, nano-delivery systems can be also easily included among the cell-targeted therapies. Indeed, they exploit the presence of tumor-associated antigens on the surfaces of tumor cells and cells of the tumor microenvironment, to specifically deliver their payload (e.g., chemotherapeutics, small-molecule inhibitors, siRNA) to diseased tissues, while reducing healthy organs’ uptake.

This Special Issue aims to publish original and/or review articles covering the state of the art and future perspectives of targeted therapies in cancer treatment.

Dr. Chiara Brignole
Dr. Fabio Pastorino
Guest Editors

Manuscript Submission Information

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

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

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2600 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • cancer
  • targeted therapies
  • tumor-associated antigens
  • monoclonal antibodies
  • small molecule inhibitors
  • immunotoxins
  • targeted nano-delivery systems

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Published Papers (11 papers)

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Editorial

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4 pages, 198 KiB  
Editorial
Editorial of the Special Issue “Targeted Therapies for Cancer”
by Fabio Pastorino and Chiara Brignole
Biomedicines 2022, 10(5), 1114; https://doi.org/10.3390/biomedicines10051114 - 11 May 2022
Viewed by 1782
Abstract
Cancer, the second leading cause of death worldwide, continues to represent an impressive challenge for researchers and clinicians [...] Full article
(This article belongs to the Special Issue Targeted Therapies for Cancer)

Research

Jump to: Editorial, Review, Other

20 pages, 3199 KiB  
Article
The Pyrazolo[3,4-d]Pyrimidine Derivative Si306 Encapsulated into Anti-GD2-Immunoliposomes as Therapeutic Treatment of Neuroblastoma
by Enrico Rango, Fabio Pastorino, Chiara Brignole, Arianna Mancini, Federica Poggialini, Salvatore Di Maria, Claudio Zamperini, Giulia Iovenitti, Anna Lucia Fallacara, Samantha Sabetta, Letizia Clementi, Massimo Valoti, Silvia Schenone, Adriano Angelucci, Mirco Ponzoni, Elena Dreassi and Maurizio Botta
Biomedicines 2022, 10(3), 659; https://doi.org/10.3390/biomedicines10030659 - 12 Mar 2022
Cited by 9 | Viewed by 3534
Abstract
Si306, a pyrazolo[3,4-d]pyrimidine derivative recently identified as promising anticancer agent, has shown favorable in vitro and in vivo activity profile against neuroblastoma (NB) models by acting as a competitive inhibitor of c-Src tyrosine kinase. Nevertheless, Si306 antitumor activity is associated with [...] Read more.
Si306, a pyrazolo[3,4-d]pyrimidine derivative recently identified as promising anticancer agent, has shown favorable in vitro and in vivo activity profile against neuroblastoma (NB) models by acting as a competitive inhibitor of c-Src tyrosine kinase. Nevertheless, Si306 antitumor activity is associated with sub-optimal aqueous solubility, which might hinder its further development. Drug delivery systems were here developed with the aim to overcome this limitation, obtaining suitable formulations for more efficacious in vivo use. Si306 was encapsulated in pegylated stealth liposomes, undecorated or decorated with a monoclonal antibody able to specifically recognize and bind to the disialoganglioside GD2 expressed by NB cells (LP[Si306] and GD2-LP[Si306], respectively). Both liposomes possessed excellent morphological and physio-chemical properties, maintained over a period of two weeks. Compared to LP[Si306], GD2-LP[Si306] showed in vitro specific cellular targeting and increased cytotoxic activity against NB cell lines. After intravenous injection in healthy mice, pharmacokinetic profiles showed increased plasma exposure of Si306 when delivered by both liposomal formulations, compared to that obtained when Si306 was administered as free form. In vivo tumor homing and cytotoxic effectiveness of both liposomal formulations were finally tested in an orthotopic animal model of NB. Si306 tumor uptake resulted significantly higher when encapsulated in GD2-LP, compared to Si306, either free or encapsulated into untargeted LP. This, in turn, led to a significant increase in survival of mice treated with GD2-LP[Si306]. These results demonstrate a promising antitumor efficacy of Si306 encapsulated into GD2-targeted liposomes, supporting further therapeutic developments in pre-clinical trials and in the clinic for NB. Full article
(This article belongs to the Special Issue Targeted Therapies for Cancer)
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15 pages, 3232 KiB  
Article
RICTOR Affects Melanoma Tumorigenesis and Its Resistance to Targeted Therapy
by Ahlem Jebali, Maxime Battistella, Céleste Lebbé and Nicolas Dumaz
Biomedicines 2021, 9(10), 1498; https://doi.org/10.3390/biomedicines9101498 - 19 Oct 2021
Cited by 15 | Viewed by 3073
Abstract
The network defined by phosphatidylinositol-3-kinase (PI3K), AKT, and mammalian target of rapamycin (mTOR) plays a major role in melanoma oncogenesis and has been implicated in BRAF inhibitor resistance. The central role of RICTOR (rapamycin-insensitive companion of mTOR) in this pathway has only recently [...] Read more.
The network defined by phosphatidylinositol-3-kinase (PI3K), AKT, and mammalian target of rapamycin (mTOR) plays a major role in melanoma oncogenesis and has been implicated in BRAF inhibitor resistance. The central role of RICTOR (rapamycin-insensitive companion of mTOR) in this pathway has only recently begun to be unraveled. In the present study, we assessed the role of mTORC2/RICTOR in BRAF-mutated melanomas and their resistance to BRAF inhibition. We showed that RICTOR was significantly overexpressed in melanoma and associated with bad prognoses. RICTOR overexpression stimulated melanoma-initiating cells (MICs) with ‘stemness’ properties. We also showed that RICTOR contributed to melanoma resistance to BRAF inhibitors and rendered the cells very sensitive to mTORC2 inhibition. We highlighted a connection between mTORC2/RICTOR and STAT3 in resistant cells and revealed an interaction between RAS and RICTOR in resistant melanoma, which, when disrupted, impeded the proliferation of resistant cells. Therefore, as a key signaling node, RICTOR contributes to BRAF-dependent melanoma development and resistance to therapy and, as such, is a valuable therapeutic target in melanoma. Full article
(This article belongs to the Special Issue Targeted Therapies for Cancer)
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16 pages, 1755 KiB  
Article
Role of Lamin A/C as Candidate Biomarker of Aggressiveness and Tumorigenicity in Glioblastoma Multiforme
by Giuliana Gatti, Laura Vilardo, Carla Musa, Chiara Di Pietro, Fabrizio Bonaventura, Ferdinando Scavizzi, Alessio Torcinaro, Barbara Bucci, Raffaele Saporito, Ivan Arisi, Francesca De Santa, Marcello Raspa, Loredana Guglielmi and Igea D’Agnano
Biomedicines 2021, 9(10), 1343; https://doi.org/10.3390/biomedicines9101343 - 28 Sep 2021
Cited by 10 | Viewed by 3361
Abstract
Nuclear lamina components have long been regarded as scaffolding proteins, forming a dense fibrillar structure necessary for the maintenance of the nucleus shape in all the animal kingdom. More recently, mutations, aberrant localisation and deregulation of these proteins have been linked to several [...] Read more.
Nuclear lamina components have long been regarded as scaffolding proteins, forming a dense fibrillar structure necessary for the maintenance of the nucleus shape in all the animal kingdom. More recently, mutations, aberrant localisation and deregulation of these proteins have been linked to several diseases, including cancer. Using publicly available data we found that the increased expression levels of the nuclear protein Lamin A/C correlate with a reduced overall survival in The Cancer Genome Atlas Research Network (TCGA) patients affected by glioblastoma multiforme (GBM). We show that the expression of the LMNA gene is linked to the enrichment of cancer-related pathways, particularly pathways related to cell adhesion and cell migration. Mimicking the modulation of LMNA in a GBM preclinical cancer model, we confirmed both in vitro and in vivo that the increased expression of LMNA is associated with an increased aggressiveness and tumorigenicity. In addition, delving into the possible mechanism behind LMNA-induced GBM aggressiveness and tumorigenicity, we found that the mTORC2 component, Rictor, plays a central role in mediating these effects. Full article
(This article belongs to the Special Issue Targeted Therapies for Cancer)
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14 pages, 3029 KiB  
Article
RIOK2 Inhibitor NSC139021 Exerts Anti-Tumor Effects on Glioblastoma via Inducing Skp2-Mediated Cell Cycle Arrest and Apoptosis
by Min Yu, Xiaoyan Hu, Jingyu Yan, Ying Wang, Fei Lu and Junlei Chang
Biomedicines 2021, 9(9), 1244; https://doi.org/10.3390/biomedicines9091244 - 17 Sep 2021
Cited by 8 | Viewed by 3785
Abstract
Up to now, the chemotherapy approaches for glioblastoma were limited. 1-[2-Thiazolylazo]-2-naphthol (named as NSC139021) was shown to significantly inhibit the proliferation of prostate cancer cells by targeting the atypical protein kinase RIOK2. It is documented that RIOK2 overexpressed in glioblastoma. However, whether NSC139021 [...] Read more.
Up to now, the chemotherapy approaches for glioblastoma were limited. 1-[2-Thiazolylazo]-2-naphthol (named as NSC139021) was shown to significantly inhibit the proliferation of prostate cancer cells by targeting the atypical protein kinase RIOK2. It is documented that RIOK2 overexpressed in glioblastoma. However, whether NSC139021 can inhibit the growth of glioblastoma cells and be a potential drug for glioblastoma treatment need to be clarified. In this study, we investigated the effects of NSC139021 on human U118MG, LN-18, and mouse GL261 glioblastoma cells and the mouse models of glioblastoma. We verified that NSC139021 effectively inhibited glioblastoma cells proliferation, but it is independent of RIOK2. Our data showed that NSC139021 induced cell cycle arrest at G0/G1 phase via the Skp2-p27/p21-Cyclin E/CDK2-pRb signaling pathway in G1/S checkpoint regulation. In addition, NSC139021 also increased the apoptosis of glioblastoma cells by activating the p53 signaling pathway and increasing the levels of Bax and cleaved caspase 3. Furthermore, intraperitoneal administration of 150 mg/kg NSC139021 significantly suppressed the growth of human and mouse glioblastoma in vivo. Our study suggests that NSC139021 may be a potential chemotherapy drug for the treatment of glioblastoma by targeting the Skp2-p27/p21-Cyclin E/CDK2-pRb signaling pathway. Full article
(This article belongs to the Special Issue Targeted Therapies for Cancer)
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28 pages, 14411 KiB  
Article
Targeted Inhibition of Anti-Inflammatory Regulator Nrf2 Results in Breast Cancer Retardation In Vitro and In Vivo
by Venugopal R. Bovilla, Mahadevaswamy G. Kuruburu, Vidya G. Bettada, Jayashree Krishnamurthy, Olga A. Sukocheva, Rajesh K. Thimmulappa, Nanjunda Swamy Shivananju, Janardhan P. Balakrishna and SubbaRao V. Madhunapantula
Biomedicines 2021, 9(9), 1119; https://doi.org/10.3390/biomedicines9091119 - 30 Aug 2021
Cited by 35 | Viewed by 5029
Abstract
Nuclear factor erythroid-2 related factor-2 (Nrf2) is an oxidative stress-response transcriptional activator that promotes carcinogenesis through metabolic reprogramming, tumor promoting inflammation, and therapeutic resistance. However, the extension of Nrf2 expression and its involvement in regulation of breast cancer (BC) responses to chemotherapy remain [...] Read more.
Nuclear factor erythroid-2 related factor-2 (Nrf2) is an oxidative stress-response transcriptional activator that promotes carcinogenesis through metabolic reprogramming, tumor promoting inflammation, and therapeutic resistance. However, the extension of Nrf2 expression and its involvement in regulation of breast cancer (BC) responses to chemotherapy remain largely unclear. This study determined the expression of Nrf2 in BC tissues (n = 46) and cell lines (MDA-MB-453, MCF-7, MDA-MB-231, MDA-MB-468) with diverse phenotypes. Immunohistochemical (IHC)analysis indicated lower Nrf2 expression in normal breast tissues, compared to BC samples, although the difference was not found to be significant. However, pharmacological inhibition and siRNA-induced downregulation of Nrf2 were marked by decreased activity of NADPH quinone oxidoreductase 1 (NQO1), a direct target of Nrf2. Silenced or inhibited Nrf2 signaling resulted in reduced BC proliferation and migration, cell cycle arrest, activation of apoptosis, and sensitization of BC cells to cisplatin in vitro. Ehrlich Ascites Carcinoma (EAC) cells demonstrated elevated levels of Nrf2 and were further tested in experimental mouse models in vivo. Intraperitoneal administration of pharmacological Nrf2 inhibitor brusatol slowed tumor cell growth. Brusatol increased lymphocyte trafficking towards engrafted tumor tissue in vivo, suggesting activation of anti-cancer effects in tumor microenvironment. Further large-scale BC testing is needed to confirm Nrf2 marker and therapeutic capacities for chemo sensitization in drug resistant and advanced tumors. Full article
(This article belongs to the Special Issue Targeted Therapies for Cancer)
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Graphical abstract

18 pages, 3256 KiB  
Article
Targeting ErbB3 Receptor in Cancer with Inhibitory Antibodies from Llama
by Igor E. Eliseev, Valeria M. Ukrainskaya, Anna N. Yudenko, Anna D. Mikushina, Stanislav V. Shmakov, Anastasiya I. Afremova, Viktoria M. Ekimova, Anna A. Vronskaia, Nickolay A. Knyazev and Olga V. Shamova
Biomedicines 2021, 9(9), 1106; https://doi.org/10.3390/biomedicines9091106 - 28 Aug 2021
Cited by 6 | Viewed by 3707
Abstract
The human ErbB3 receptor confers resistance to the pharmacological inhibition of EGFR and HER2 receptor tyrosine kinases in cancer, which makes it an important therapeutic target. Several anti-ErbB3 monoclonal antibodies that are currently being developed are all classical immunoglobulins. We took a different [...] Read more.
The human ErbB3 receptor confers resistance to the pharmacological inhibition of EGFR and HER2 receptor tyrosine kinases in cancer, which makes it an important therapeutic target. Several anti-ErbB3 monoclonal antibodies that are currently being developed are all classical immunoglobulins. We took a different approach and discovered a group of novel heavy-chain antibodies targeting the extracellular domain of ErbB3 via a phage display of an antibody library from immunized llamas. We first produced three selected single-domain antibodies, named BCD090-P1, BCD090-M2, and BCD090-M456, in E. coli, as SUMO fusions that yielded up to 180 mg of recombinant protein per liter of culture. Then, we studied folding, aggregation, and disulfide bond formation, and showed their ultimate stability with half-denaturation of the strongest candidate, BCD090-P1, occurring in 8 M of urea. In surface plasmon resonance experiments, two most potent antibodies, BCD090-P1 and BCD090-M2, bound the extracellular domain of ErbB3 with 1.6 nM and 15 nM affinities for the monovalent interaction, respectively. The receptor binding was demonstrated by immunofluorescent confocal microscopy on four different ErbB3+ cancer cell lines. We observed that BCD090-P1 and BCD090-M2 bind noncompetitively to two distinct epitopes on the receptor. Both antibodies inhibited the ErbB3-driven proliferation of MCF-7 breast adenocarcinoma cells and HER2-overexpressing SK-BR-3 cells, with the EC50 in the range of 0.1–25 μg/mL. BCD090-M2 directly blocks ligand binding, whereas BCD090-P1 does not compete with the ligand and presumably acts through a distinct allosteric mechanism. We anticipate that these llama antibodies can be used to engineer new biparatopic anti-ErbB3 or bispecific anti-ErbB2/3 antibodies. Full article
(This article belongs to the Special Issue Targeted Therapies for Cancer)
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Review

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10 pages, 1186 KiB  
Review
Targeted Osmotic Lysis: A Novel Approach to Targeted Cancer Therapies
by Harry J. Gould III and Dennis Paul
Biomedicines 2022, 10(4), 838; https://doi.org/10.3390/biomedicines10040838 - 2 Apr 2022
Cited by 8 | Viewed by 3252
Abstract
The conventional treatment of cancer has been based on the delivery of non-selective toxins and/or ionizing energy that affect both the cancer and normal tissues in the hope of destroying the offending disease before killing the patient. Unfortunately, resistance often develops to these [...] Read more.
The conventional treatment of cancer has been based on the delivery of non-selective toxins and/or ionizing energy that affect both the cancer and normal tissues in the hope of destroying the offending disease before killing the patient. Unfortunately, resistance often develops to these treatments and patients experience severe, dose-limiting adverse effects that reduce treatment efficacy and compromise quality of life. Recent advances in our knowledge of the biology of tumor cells and their microenvironment, the recognition of surface proteins that are unique to specific cancers and essential to cell growth and survival and signaling pathways associate with invasion and metastasis have led to the development of targeted therapies that are able to identify specific cellular markers and more selectively deliver lethal treatment to the invading cancer thus improving efficacy and limiting adverse effects. In the context of targeted approaches to cancer therapy, we present targeted osmotic lysis as a novel and fundamentally different approach for treating advanced-stage carcinoma that exploits the conserved relationship between voltage-gated sodium channels and Na+, K+-ATPase and has the potential to increase survival without compromising quality of life in a broad spectrum of highly malignant forms of cancer. Full article
(This article belongs to the Special Issue Targeted Therapies for Cancer)
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18 pages, 1251 KiB  
Review
Targeted Toxins for the Treatment of Prostate Cancer
by Philipp Wolf
Biomedicines 2021, 9(8), 986; https://doi.org/10.3390/biomedicines9080986 - 9 Aug 2021
Cited by 7 | Viewed by 3083
Abstract
Prostate cancer is the second most common cancer and the fifth leading cause of cancer deaths worldwide. Despite improvements in diagnosis and treatment, new treatment options are urgently needed for advanced stages of the disease. Targeted toxins are chemical conjugates or fully recombinant [...] Read more.
Prostate cancer is the second most common cancer and the fifth leading cause of cancer deaths worldwide. Despite improvements in diagnosis and treatment, new treatment options are urgently needed for advanced stages of the disease. Targeted toxins are chemical conjugates or fully recombinant proteins consisting of a binding domain directed against a target antigen on the surface of cancer cells and a toxin domain, which is transported into the cell for the induction of apoptosis. In the last decades, targeted toxins against prostate cancer have been developed. Several challenges, however, became apparent that prevented their direct clinical use. They comprise immunogenicity, low target antigen binding, endosomal entrapment, and lysosomal/proteasomal degradation of the targeted toxins. Moreover, their efficacy is impaired by prostate tumors, which are marked by a dense microenvironment, low target antigen expression, and apoptosis resistance. In this review, current findings in the development of targeted toxins against prostate cancer in view of effective targeting, reduction of immunogenicity, improvement of intracellular trafficking, and overcoming apoptosis resistance are discussed. There are promising approaches that should lead to the clinical use of targeted toxins as therapeutic alternatives for advanced prostate cancer in the future. Full article
(This article belongs to the Special Issue Targeted Therapies for Cancer)
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25 pages, 986 KiB  
Review
Advances and Limitations of Antibody Drug Conjugates for Cancer
by Candice Maria Mckertish and Veysel Kayser
Biomedicines 2021, 9(8), 872; https://doi.org/10.3390/biomedicines9080872 - 23 Jul 2021
Cited by 101 | Viewed by 16589
Abstract
The popularity of antibody drug conjugates (ADCs) has increased in recent years, mainly due to their unrivalled efficacy and specificity over chemotherapy agents. The success of the ADC is partly based on the stability and successful cleavage of selective linkers for the delivery [...] Read more.
The popularity of antibody drug conjugates (ADCs) has increased in recent years, mainly due to their unrivalled efficacy and specificity over chemotherapy agents. The success of the ADC is partly based on the stability and successful cleavage of selective linkers for the delivery of the payload. The current research focuses on overcoming intrinsic shortcomings that impact the successful development of ADCs. This review summarizes marketed and recently approved ADCs, compares the features of various linker designs and payloads commonly used for ADC conjugation, and outlines cancer specific ADCs that are currently in late-stage clinical trials for the treatment of cancer. In addition, it addresses the issues surrounding drug resistance and strategies to overcome resistance, the impact of a narrow therapeutic index on treatment outcomes, the impact of drug–antibody ratio (DAR) and hydrophobicity on ADC clearance and protein aggregation. Full article
(This article belongs to the Special Issue Targeted Therapies for Cancer)
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Other

27 pages, 1800 KiB  
Perspective
Approaching Sites of Action of Temozolomide for Pharmacological and Clinical Studies in Glioblastoma
by Margaux Fresnais, Sevin Turcan, Dirk Theile, Johannes Ungermann, Yasmin Abou Zeed, Joshua Raoul Lindner, Marius Breitkopf, Jürgen Burhenne, Walter E. Haefeli and Rémi Longuespée
Biomedicines 2022, 10(1), 1; https://doi.org/10.3390/biomedicines10010001 - 21 Dec 2021
Cited by 10 | Viewed by 5158
Abstract
Temozolomide (TMZ), together with bulk resection and focal radiotherapy, is currently a standard of care for glioblastoma. Absorption, distribution, metabolism, and excretion (ADME) parameters, together with the mode of action of TMZ, make its biochemical and biological action difficult to understand. Accurate understanding [...] Read more.
Temozolomide (TMZ), together with bulk resection and focal radiotherapy, is currently a standard of care for glioblastoma. Absorption, distribution, metabolism, and excretion (ADME) parameters, together with the mode of action of TMZ, make its biochemical and biological action difficult to understand. Accurate understanding of the mode of action of TMZ and the monitoring of TMZ at its anatomical, cellular, and molecular sites of action (SOAs) would greatly benefit precision medicine and the development of novel therapeutic approaches in combination with TMZ. In the present perspective article, we summarize the known ADME parameters and modes of action of TMZ, and we review the possible methodological options to monitor TMZ at its SOAs. We focus our descriptions of methodologies on mass spectrometry-based approaches, and all related considerations are taken into account regarding the avoidance of artifacts in mass spectrometric analysis during sampling, sample preparation, and the evaluation of results. Finally, we provide an overview of potential applications for precision medicine and drug development. Full article
(This article belongs to the Special Issue Targeted Therapies for Cancer)
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