Cancers

13 pages, 1204 KiB

Open AccessArticle

Clinical and Histopathological Features of Thyroid Cancer with TERT Promoter Molecular Alterations in Isolation Versus with Concurrent Molecular Alterations: A Multicenter Retrospective Study

by Emily Steinberg, Orr Dimitstein, Grégoire B. Morand, Véronique-Isabelle Forest, Sabrina D. da Silva, Marc Pusztaszeri, Sama Alohali and Richard J. Payne

Cancers 2024, 16(20), 3446; https://doi.org/10.3390/cancers16203446 (registering DOI) - 11 Oct 2024

Abstract

Background/Objectives: Molecular testing of thyroid nodules enables the detection of genetic alterations, which can help assess the risk of malignancy and tumor behavior. While telomerase reverse transcriptase (TERTp) mutations are known to be associated with aggressive disease, their exact prognostic significance [...] Read more.

Background/Objectives: Molecular testing of thyroid nodules enables the detection of genetic alterations, which can help assess the risk of malignancy and tumor behavior. While telomerase reverse transcriptase (TERTp) mutations are known to be associated with aggressive disease, their exact prognostic significance when occurring alone or with other molecular alterations remains underreported. Methods: This study examined patients with thyroid cancer treated at two tertiary care hospitals from 2017 to 2024. We compared tumor behavior in patients with TERTp molecular alterations occurring alone and with concurrent molecular alterations. Aggressive histologic subtypes were defined as tall-cell, hobnail, and columnar variants of papillary carcinoma, as well as poorly differentiated and anaplastic carcinoma. High-risk disease was defined according to the 2015 ATA guidelines as gross extrathyroidal extension, lymph node metastasis >3 cm, postoperative elevated serum thyroglobulin, distant metastases, and/or positive resection margins. Statistical analysis was performed to assess differences between groups. Results: 30 patients with TERTp-positive thyroid malignancies were included. TERTp/BRAF V600E was the most prevalent mutation combination (n = 13, 43.3%), followed by TERTp alone (n = 8, 26.7%) and TERTp/RAS (n = 7, 23.4%). TERTp/EIF1AX/GNAS and TERTp/EIF1AX/PIK3CA were the least common combinations (n = 1, 3.3% each). Nodules with TERTp and concurrent mutations were significantly more likely to be classified as high-risk (p = 0.006) and were more frequently associated with aggressive histologic subtypes (p = 0.003) compared to those with TERTp mutations alone, which tended to exhibit more benign behavior. Conclusions: Thyroid carcinomas harboring both TERTp and concurrent molecular alterations are associated with more aggressive features and a higher likelihood of being classified as high-risk. In contrast, TERTp mutations occurring alone do not confer an elevated risk. Full article

(This article belongs to the Section Cancer Pathophysiology)

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3 pages, 190 KiB

Open AccessEditorial

Comparison between N-803 and Erdafitinib in Bacillus Calmette-Guérin-Unresponsive Non-Muscle-Invasive Bladder Cancer

by Anusha Gupta, Shiv Verma and Sanjay Gupta

Cancers 2024, 16(20), 3445; https://doi.org/10.3390/cancers16203445 (registering DOI) - 11 Oct 2024

Abstract

Bladder cancer, the sixth most common cancer and the tenth leading cause of cancer-related death worldwide, remains a significant global health concern [...] Full article

(This article belongs to the Section Cancer Therapy)

2 pages, 1336 KiB

Open AccessCorrection

Correction: Mansoori et al. HMGA2 Supports Cancer Hallmarks in Triple-Negative Breast Cancer. Cancers 2021, 13, 5197

by Behzad Mansoori, Mikkel Green Terp, Ali Mohammadi, Christina Bøg Pedersen, Henrik Jørn Ditzel, Behzad Baradaran and Morten Frier Gjerstorff

Cancers 2024, 16(20), 3444; https://doi.org/10.3390/cancers16203444 (registering DOI) - 11 Oct 2024

Abstract

In the original publication [...] Full article

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19 pages, 2010 KiB

Open AccessReview

Immunotherapeutic Potential of Mutated NPM1 for the Treatment of Acute Myeloid Leukemia

by Jochen Greiner, Eithar Mohamed, Daniel M. Fletcher, Patrick J. Schuler, Hubert Schrezenmeier, Marlies Götz and Barbara-ann Guinn

Cancers 2024, 16(20), 3443; https://doi.org/10.3390/cancers16203443 (registering DOI) - 10 Oct 2024

Abstract

Acute myeloid leukemia (AML) is a malignant disease of the blood and bone marrow that is characterized by uncontrolled clonal proliferation of abnormal myeloid progenitor cells. Nucleophosmin 1 (NPM1) gene mutations are the most common genetic abnormality in AML, detectable in blast cells [...] Read more.

Acute myeloid leukemia (AML) is a malignant disease of the blood and bone marrow that is characterized by uncontrolled clonal proliferation of abnormal myeloid progenitor cells. Nucleophosmin 1 (NPM1) gene mutations are the most common genetic abnormality in AML, detectable in blast cells from about one-third of adults with AML. AML NPM1^mut is recognized as a separate entity in the World Health Organization classification of AML. Clinical and survival data suggest that patients with this form of AML often have a more favorable prognosis, which may be due to the immunogenicity created by the mutations in the NPM1 protein. Consequently, AML with NPM1^mut can be considered an immunogenic subtype of AML. However, the underlying mechanisms of this immunogenicity and associated favorable survival outcomes need to be further investigated. Immune checkpoint molecules, such as the programmed cell death-1 (PD-1) protein and its ligand, PD-L1, play important roles in leukemogenesis through their maintenance of an immunosuppressive tumor microenvironment. Preclinical trials have shown that the use of PD-1/PD-L1 checkpoint inhibitors in solid tumors and lymphoma work best in novel therapy combinations. Patients with AML NPM1^mut may be better suited to immunogenic strategies that are based on the inhibition of the PD-1 immune checkpoint pathway than patients without this mutation, suggesting the genetic landscape of patients may also inform best practice for the use of PD-1 inhibitors. Full article

(This article belongs to the Special Issue The Role of NPM1 Mutation in Acute Myeloid Leukemia)

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12 pages, 843 KiB

Open AccessArticle

Evaluating CDK4/6 Inhibitor Therapy in Elderly Patients with Metastatic Hormone Receptor-Positive, HER2-Negative Breast Cancer: A Retrospective Real-World Multicenter Study

by Palma Fedele, Matteo Landriscina, Lucia Moraca, Antonio Cusmai, Antonio Gnoni, Antonella Licchetta, Chiara Guarini, Laura Lanotte, Maria Nicla Pappagallo, Assunta Melaccio, Guido Giordano, Felicia Maria Maselli, Antonello Pinto, Francesco Giuliani, Vincenzo Chiuri, Francesco Giotta and Gennaro Gadaleta-Caldarola

Cancers 2024, 16(20), 3442; https://doi.org/10.3390/cancers16203442 - 10 Oct 2024

Abstract

Background: Metastatic HR+/HER2- breast cancer is commonly treated with CDK4/6 inhibitors in combination with endocrine therapy. However, the efficacy and safety of this approach in elderly patients (≥70 years) remain unclear, particularly in the context of real-world clinical practice. This study aims to [...] Read more.

Background: Metastatic HR+/HER2- breast cancer is commonly treated with CDK4/6 inhibitors in combination with endocrine therapy. However, the efficacy and safety of this approach in elderly patients (≥70 years) remain unclear, particularly in the context of real-world clinical practice. This study aims to evaluate the clinical outcomes and tolerability of CDK4/6 inhibitor treatments in this fragile population, which is often under-represented in randomized clinical trials. Patients and methods: This retrospective multicenter study included elderly patients with metastatic HR+/HER2-negative breast cancer receiving first-line CDK4/6 inhibitors. The primary endpoint was progression-free survival (PFS). The secondary endpoints focused on the overall survival (OS), safety, and tolerability, considering variables such as tumor subtype, age, comorbidities, and treatment specifics. Results: The median PFS and OS were slightly lower than those reported in clinical trials, reflecting the inclusion of a more fragile population. The luminal B subtype was linked to a poorer PFS, while other factors like age, BMI, and ECOG status did not significantly affect the outcomes. A safety analysis indicated a higher incidence of grade 3 or higher toxicities, especially in frail patients, leading to dose reductions. Despite these challenges, CDK4/6 inhibitors were generally well-tolerated, allowing most patients to continue therapy. Conclusions: CDK4/6 inhibitors with endocrine therapy are effective in elderly patients with metastatic HR+/HER2- breast cancer, though careful management is crucial to balance efficacy and minimize adverse events. Full article

(This article belongs to the Special Issue New Perspectives in the Management of Breast Cancer)

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25 pages, 9863 KiB

Open AccessArticle

Targeting PARP-1 and DNA Damage Response Defects in Colorectal Cancer Chemotherapy with Established and Novel PARP Inhibitors

by Philipp Demuth, Lea Thibol, Anna Lemsch, Felix Potlitz, Lukas Schulig, Christoph Grathwol, Georg Manolikakes, Dennis Schade, Vassilis Roukos, Andreas Link and Jörg Fahrer

Cancers 2024, 16(20), 3441; https://doi.org/10.3390/cancers16203441 - 10 Oct 2024

Abstract

The DNA repair protein PARP-1 emerged as a valuable target in the treatment of tumor entities with deficiencies of BRCA1/2, such as breast cancer. More recently, the application of PARP inhibitors (PARPi) such as olaparib has been expanded to other cancer entities [...] Read more.

The DNA repair protein PARP-1 emerged as a valuable target in the treatment of tumor entities with deficiencies of BRCA1/2, such as breast cancer. More recently, the application of PARP inhibitors (PARPi) such as olaparib has been expanded to other cancer entities including colorectal cancer (CRC). We previously demonstrated that PARP-1 is overexpressed in human CRC and promotes CRC progression in a mouse model. However, acquired resistance to PARPi and cytotoxicity-mediated adverse effects limit their clinical applicability. Here, we detailed the role of PARP-1 as a therapeutic target in CRC and studied the efficacy of novel PARPi compounds in wildtype (WT) and DNA repair-deficient CRC cell lines together with the chemotherapeutics irinotecan (IT), 5-fluorouracil (5-FU), and oxaliplatin (OXA). Based on the ComPlat molecule archive, we identified novel PARPi candidates by molecular docking experiments in silico, which were then confirmed by in vitro PARP activity measurements. Two promising candidates (X17613 and X17618) also showed potent PARP-1 inhibition in a CRC cell-based assay. In contrast to olaparib, the PARPi candidates caused no PARP-1 trapping and, consistently, were not or only weakly cytotoxic in WT CRC cells and their BRCA2- or ATR-deficient counterparts. Importantly, both PARPi candidates did not affect the viability of nonmalignant human colonic epithelial cells. While both olaparib and veliparib increased the sensitivity of WT CRC cells towards IT, no synergism was observed for X17613 and X17618. Finally, we provided evidence that all PARPi (olaparib > veliparib > X17613 > X17618) synergize with chemotherapeutic drugs (IT > OXA) in a BRCA2-dependent manner in CRC cells, whereas ATR deficiency had only a minor impact. Collectively, our study identified novel lead structures with potent PARP-1 inhibitory activity in CRC cells but low cytotoxicity due to the lack of PARP-1 trapping, which synergized with IT in homologous recombination deficiency. Full article

(This article belongs to the Special Issue Cancer Chemotherapy: Combination with Inhibitors (2nd Edition))

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14 pages, 279 KiB

Open AccessArticle

Characteristics and Management of Children with Appendiceal Neuroendocrine Neoplasms: A Single-Center Study

by Stefano Mastrangelo, Giorgio Attinà, Guido Rindi, Alberto Romano, Palma Maurizi and Antonio Ruggiero

Cancers 2024, 16(20), 3440; https://doi.org/10.3390/cancers16203440 - 10 Oct 2024

Abstract

Background/Objectives: Appendiceal neuroendocrine neoplasms (ANENs) are usually found incidentally during histology examination after appendectomy for appendicitis. Due to their rarity in pediatric populations, there is no consensus on treatment or follow-up. The analysis of patients with ANENs of our and other studies will [...] Read more.

Background/Objectives: Appendiceal neuroendocrine neoplasms (ANENs) are usually found incidentally during histology examination after appendectomy for appendicitis. Due to their rarity in pediatric populations, there is no consensus on treatment or follow-up. The analysis of patients with ANENs of our and other studies will increase the understanding of this tumor. Methods: Pediatric patients with ANENs were uniformly managed at our center between 1998 and 2023. Patients’ presenting symptoms, surgery, tumor histology, post-surgical work-up, follow-up and outcome were analyzed. Results: Our report describes 17 patients with a diagnosis of ANEN after appendectomy. The median age was 14 years (range of 4–17 years). Tumors were located at the tip of the appendix in 58.8% of cases and only one had a diameter >1 cm. All were well-differentiated tumors with free resection margins. The submucosa was invaded in five cases, muscularis propria in eight and subserosa in four. Post-appendectomy work-up included tumor marker measurement, abdominal ultrasound and computed tomography or magnetic resonance imaging, chest X-ray and octreotide scintigraphy. No residual tumors or metastases were detected. Additional surgery was not necessary. Follow-up was carried out for a median duration of 6 years (range of 1–10 years). Only one patient was lost to follow-up and all other patients are alive without tumor recurrence. Conclusions: The tumor characteristics of our patients confirmed data from the literature. With the lack of a sufficient number of large prospective trials, it is important to add more information to confirm the benign nature and excellent outcome of this tumor, even without additional surgery. Consensus guidelines are needed for ANENs in pediatric populations. Full article

(This article belongs to the Special Issue Rare Tumors in Children: Trends in Diagnosis, Treatment and Prevention (2nd Edition))

13 pages, 1417 KiB

Open AccessArticle

MUC16 Retention after Neoadjuvant Chemotherapy in Pancreatic Ductal Adenocarcinoma

by Kathryn M. Muilenburg, Evie G. Ehrhorn, Madeline T. Olson, Carly C. Isder, Kelsey A. Klute, Geoffrey A. Talmon, Mark A. Carlson, Quan P. Ly and Aaron M. Mohs

Cancers 2024, 16(20), 3439; https://doi.org/10.3390/cancers16203439 - 10 Oct 2024

Abstract

Background/Objectives: Pancreatic ductal adenocarcinoma (PDAC) has a poor prognosis. Currently, surgical resection is the only potentially curative treatment. Unfortunately, less than 20% of PDAC patients are eligible for surgical resection at diagnosis. In the past few decades, neoadjuvant chemotherapy treatment (NCT) has [...] Read more.

Background/Objectives: Pancreatic ductal adenocarcinoma (PDAC) has a poor prognosis. Currently, surgical resection is the only potentially curative treatment. Unfortunately, less than 20% of PDAC patients are eligible for surgical resection at diagnosis. In the past few decades, neoadjuvant chemotherapy treatment (NCT) has been investigated as a way to downstage PDAC tumors for surgical resection. Fluorescence-guided surgery (FGS) is a technique that can aid in increasing complete resection rates by enhancing the tumor through passive or active targeting of a contrast agent. In active targeting, a probe (e.g., antibody) binds a protein differentially upregulated in the tumor compared to normal tissue. Mucin 16 (MUC16), a transmembrane glycoprotein, has recently been explored as an FGS target in preclinical tumor models. However, the impact of chemotherapy on MUC16 expression is unknown. Methods: To investigate this issue, immunohistochemistry was performed on PDAC patient samples. Results: We found that MUC16 expression was retained after NCT in patient samples (mean expression = 5.7) with minimal change in expression between the matched diagnostic (mean expression = 3.66) and PDAC NCT patient samples (mean expression = 4.5). Conclusions: This study suggests that MUC16 is a promising target for FGS and other targeted therapies in PDAC patients treated with NCT. Full article

(This article belongs to the Special Issue Enhancing Cancer Treatments through Fluorescence-Guided Surgery)

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33 pages, 1547 KiB

Open AccessReview

Strategies to Target Chemoradiotherapy Resistance in Small Cell Lung Cancer

by Tony Yu and Benjamin H. Lok

Cancers 2024, 16(20), 3438; https://doi.org/10.3390/cancers16203438 - 10 Oct 2024

Abstract

Background: Small cell lung cancer (SCLC) is a lethal form of lung cancer with few treatment options and a high rate of relapse. While SCLC is initially sensitive to first-line DNA-damaging chemo- and radiotherapy, relapse disease is almost universally therapy-resistant. As a result, [...] Read more.

Background: Small cell lung cancer (SCLC) is a lethal form of lung cancer with few treatment options and a high rate of relapse. While SCLC is initially sensitive to first-line DNA-damaging chemo- and radiotherapy, relapse disease is almost universally therapy-resistant. As a result, there has been interest in understanding the mechanisms of therapeutic resistance in this disease. Conclusions: Progress has been made in elucidating these mechanisms, particularly as they relate to the DNA damage response and SCLC differentiation and transformation, leading to many clinical trials investigating new therapies and combinations. Yet there remain many gaps in our understanding, such as the effect of epigenetics or the tumor microenvironment on treatment response, and no single mechanism has been found to be ubiquitous, suggesting a significant heterogeneity in the mechanisms of acquired resistance. Nevertheless, the advancement of techniques in the laboratory and the clinic will improve our ability to study this disease, especially in patient populations, and identify methods to surmount therapeutic resistance. Full article

(This article belongs to the Special Issue New and Emerging Strategies for Targeting Genomic Instability and Overcoming Drug Resistance in Lung Cancer)

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16 pages, 1686 KiB

Open AccessArticle

Brain Metastases from Genito-Urinary Cancers in the Canton of Geneva (Switzerland): Study of Incidence, Management and Outcomes

by Philippe Gonnet, Eliana Marinari, Vérane Achard, Robin Schaffar, Isabelle Neyroud-Caspar, Adrien May, Cristina Goga, Pierre-Yves Dietrich, Karl Schaller and Anna Patrikidou

Cancers 2024, 16(20), 3437; https://doi.org/10.3390/cancers16203437 - 10 Oct 2024

Abstract

Background: Incidence of brain metastases is precisely unknown and there is no clear consensus on their management. We aimed to determine the incidence of brain metastases among patients with genito-urinary primaries, present patients’ characteristics and identify prognostic factors. Method: We identified 51 patients [...] Read more.

Background: Incidence of brain metastases is precisely unknown and there is no clear consensus on their management. We aimed to determine the incidence of brain metastases among patients with genito-urinary primaries, present patients’ characteristics and identify prognostic factors. Method: We identified 51 patients treated in Geneva University Hospitals between January 1992 and December 2019. We retrospectively correlated their overall survival with 23 variables. We repeated a multivariate analysis with significant variables. Results: Overall incidence of Brain Metastases (BMs) among Genito-Urinary (GU) patients is estimated to be 1.76% (range per primary GU tumour type: 0.00–6.65%). BMs originate from germ cell tumours in two cases (3.92%), from urothelial cell carcinoma in 15 cases (29.41%), from prostate cancer in 13 cases (25.49%), and from renal cell carcinoma in 21 cases (41.18%); there are no BMs from penile cancer in our cohort. The median age at BM diagnosis is 67 years old (range: 25–92). Most patients (54%) have a stage IV disease at initial diagnosis and 11 patients (22%) have BM at initial diagnosis. Only six patients (12%) are asymptomatic at BM diagnosis. The median Overall Survival (OS) from BM diagnosis is 3 months (range: 0–127). Five patients (10%) are long survivors (OS > 24 months). OS is significantly influenced by patient performance status and administration of systemic treatment. In the absence of meningeal carcinomatosis, OS is influenced by systemic treatment and stereotactic radiosurgery. We also apply the Graded Prognostic Assessment (GPA) score to our cohort and note significant differences between groups. Conclusion: Brain metastases from solid tumours is not a uniform disease, with a prognosis varying a lot among patients. The optimal management for patients with genito-urinary malignancies with brain metastases remain unclear and further research is needed. Full article

(This article belongs to the Section Cancer Therapy)

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12 pages, 1439 KiB

Open AccessArticle

Radiotherapy with 15 × 2.633 Gy vs. 20 × 2.0 Gy in Patients with Malignant Spinal Cord Compression and Favorable Survival Prognoses: A Secondary Analysis of the RAMSES-01 Trial

by Dirk Rades, Darejan Lomidze, Natalia Jankarashvili, Fernando Lopez Campos, Arturo Navarro-Martin, Barbara Segedin, Blaz Groselj, Christian Staackmann, Nathan Y. Yu and Jon Cacicedo

Cancers 2024, 16(20), 3436; https://doi.org/10.3390/cancers16203436 - 10 Oct 2024

Abstract

Many patients with malignant spinal cord compression (MSCC) who are not candidates for neurosurgery receive radiotherapy alone. This study compared 15 × 2.633 Gy over three weeks to 20 × 2.0 Gy over four weeks in patients with favorable survival prognoses. The outcomes [...] Read more.

Many patients with malignant spinal cord compression (MSCC) who are not candidates for neurosurgery receive radiotherapy alone. This study compared 15 × 2.633 Gy over three weeks to 20 × 2.0 Gy over four weeks in patients with favorable survival prognoses. The outcomes of 34 patients treated with 15 × 2.633 Gy (equivalent dose 41.6 Gy₁₀) in the RAMSES-01 trial were compared to 239 patients from an existing database receiving 20 × 2.0 Gy using propensity-score-adjusted Cox and logistic regression models. All patients had favorable survival prognoses. Endpoints included local progression-free survival (LPFS), improvement of motor function, post-treatment ambulatory status, and overall survival (OS). After propensity score adjustment, the 12-month rates of LPFS and OS were 98.1% (RAMSES-01 cohort) vs. 91.6% (p = 0.265) and 79.1% vs. 82.2% (p = 0.704), respectively. Regarding improvement of motor function, 15 × 2.633 Gy appeared superior (p = 0.073). No significant difference was observed regarding ambulatory status (p = 0.822). The three-week regimen for MSCC has similar outcomes and reduces treatment time when compared to a four-week regimen. Full article

(This article belongs to the Special Issue Bone and Spine Metastases)

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1 pages, 171 KiB

Open AccessCorrection

Correction: Marin et al. Clinical Correlations between Serological Markers and Endometrial Cancer. Cancers 2024, 16, 1935

by Alina-Gabriela Marin, Alexandru George Filipescu, Răzvan Cosmin Petca, Radu Vlădăreanu and Aida Petca

Cancers 2024, 16(20), 3435; https://doi.org/10.3390/cancers16203435 - 10 Oct 2024

Abstract

Additional Affiliations [...] Full article

(This article belongs to the Special Issue Lifestyle Choices and Endocrine Dysfunction on Cancer Onset and Risk)

14 pages, 991 KiB

Open AccessReview

Advances in Targeted Therapy: Addressing Resistance to BTK Inhibition in B-Cell Lymphoid Malignancies

by Andres Bravo-Gonzalez, Maryam Alasfour, Deborah Soong, Jose Noy and Georgios Pongas

Cancers 2024, 16(20), 3434; https://doi.org/10.3390/cancers16203434 - 10 Oct 2024

Abstract

B-cell lymphoid malignancies are a heterogeneous group of hematologic cancers, where Bruton’s tyrosine kinase (BTK) inhibitors have received FDA approval for several subtypes. The first-in-class covalent BTK inhibitor, Ibrutinib, binds to the C481 amino acid residue to block the BTK enzyme and prevent [...] Read more.

B-cell lymphoid malignancies are a heterogeneous group of hematologic cancers, where Bruton’s tyrosine kinase (BTK) inhibitors have received FDA approval for several subtypes. The first-in-class covalent BTK inhibitor, Ibrutinib, binds to the C481 amino acid residue to block the BTK enzyme and prevent the downstream signaling. Resistance to covalent BTK inhibitors (BTKi) can occur through mutations at the BTK binding site (C481S) but also other BTK sites and the phospholipase C gamma 2 (PLCγ2) resulting in downstream signaling. To bypass the C481S mutation, non-covalent BTKi, such as Pirtobrutinib, were developed and are active against both wild-type and the C481S mutation. In this review, we discuss the molecular and genetic mechanisms which contribute to acquisition of resistance to covalent and non-covalent BTKi. In addition, we discuss the new emerging class of BTK degraders, which utilize the evolution of proteolysis-targeting chimeras (PROTACs) to degrade the BTK protein and constitute an important avenue of overcoming resistance. The moving landscape of resistance to BTKi and the development of new therapeutic strategies highlight the ongoing advances being made towards the pursuit of a cure for B-cell lymphoid malignancies. Full article

(This article belongs to the Special Issue Molecular Insights into Drug Resistance in Cancer)

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13 pages, 1119 KiB

Open AccessReview

Disparities in Testicular Cancer: A Review of the Literature

by Domenique Escobar and Siamak Daneshmand

Cancers 2024, 16(20), 3433; https://doi.org/10.3390/cancers16203433 - 10 Oct 2024

Abstract

Background: Testicular cancer is the most common malignancy diagnosed in adolescents and young adults, and evidence has emerged regarding disparities that affect different groups of patients. Methods: In this article, we conducted a thorough review of this area and summarized the [...] Read more.

Background: Testicular cancer is the most common malignancy diagnosed in adolescents and young adults, and evidence has emerged regarding disparities that affect different groups of patients. Methods: In this article, we conducted a thorough review of this area and summarized the existing literature. Results: Some of the pertinent findings from our review include poorer outcomes for various groups including the native Māori population of New Zealand, those who live in the United States–Mexico border region, those who live in Eastern Europe, those who are uninsured and those with poorer socioeconomic status, amongst others. In the United States specifically, there is significant evidence showing that racial/ethnic minorities, compared to white patients, tend to fare worse with later presentation at higher stages and worse survival rates. Hispanic patients in particular appear to have the potential for more aggressive tumor biology than other groups and are projected to have the highest incidence rates in the US by 2026. Conclusions: Overall, disparities exist in many aspects of testicular cancer and are striking in some instances, and further research is needed in this arena and in potential solutions. Full article

(This article belongs to the Special Issue The Evaluation of Cancer Treatment Patterns and Quality of Care across the World)

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Cancers, Volume 16, Issue 20 (October-2 2024) – 14 articles

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