CD30, also known as TNFRSF8 (tumor necrosis factor receptor superfamily member 8), is a protein receptor that is heavily glycosylated inside the Golgi apparatus, as well as a tumor marker that is found on the surface of specific cells in the body, including certain immune cells and cancer ones. This review aims to shed light on the critical importance of CD30, from its emergence in the cell to its position in diagnosing various diseases, including Hodgkin lymphoma, where it is expressed on Hodgkin and Reed–Sternberg cells, as well as embryonal carcinoma, anaplastic large cell lymphoma (ALCL), and cutaneous T-cell lymphoma (CTCL). In addition to its role in positive diagnosis, targeting CD30 has been a promising approach treating CD30-positive lymphomas, and there is ongoing research into the potential use of CD30-targeted therapies for autoimmune disorders. We aim to elaborate on CD30’s roles as a tumor marker, supporting thus the hypothesis that this receptor might be the aim of cytostatic treatment.

Breast cancer (BC) remains the most prevalent cancer among women and the leading cause of cancer-related mortality worldwide. The heterogeneity of BC in terms of histopathological features, genetic polymorphisms, and response to therapies necessitates a personalized approach to treatment. This review focuses on the impact of molecular profiling on therapy management in breast cancer, emphasizing recent advancements in next-generation sequencing (NGS) and liquid biopsies. These technologies enable the identification of specific molecular subtypes and the detection of blood-based biomarkers such as circulating tumor cells (CTCs), circulating tumor DNA (ctDNA), and tumor-educated platelets (TEPs). The integration of molecular profiling with traditional clinical and pathological data allows for more tailored and effective treatment strategies, improving patient outcomes. This review also discusses the current challenges and prospects of implementing personalized cancer therapy, highlighting the potential of molecular profiling to revolutionize BC management through more precise prognostic and therapeutic interventions.

Aggressive thyroid carcinomas are rare malignancies characterized by a high impact on patient’s lives and poor prognosis. The available literature is scarce presenting divergent data concerning the clinical outcomes, prognostic factors and variable mutational signature studies. We aim to collect data from the literature and assemble a systematic review. The literature from 2007 until May 2025 was searched using PubMed. Studies bearing data concerning clinical aspects, prognostic outcomes, or molecular characteristics of differentiated high-grade (DHGTC), poorly differentiated (PDTC), and anaplastic thyroid carcinomas (ATC) were retrieved. Original articles in English, ethically conducted on human patients, were selected. From 688 articles, 39 were included. DHGTC has a good 5-year survival rate (5YSR) of 76%, 23.18% metastasis rate, 42.23%, lymph node involvement (LNI), 61.44% extrathyroidal extension (ETE), majority being diagnosed in stage III. PDTC has an intermediate 5YSR of 65.71%, 21.17% distant metastasis, 32.22% LNI, and 55.19% ETE, majority diagnosed in stage III. ATC has a grim 2-year survival rate of 11.15%, 42.15% metastasis, 44.14%, LNI, and 58.51% ETE, majority presented in stage IV-B. Mutational profiling shows that each carcinoma has its unique set of molecular alterations. Most positive prognostic comes for DHGTC, then PDTC, and finally, ATC.

A rare entity of non-hiatal type transdiaphragmatic hernias, which must be clearly differentiated from paraoesophageal hernias, are the phrenic defects that bear the generic name of congenital hernias—Bochdalek hernia and Larey-Morgagni hernia, respectively. The etiological substrate is relatively simple: the presence of preformed anatomical openings, which either do or do not enable transit from the thoracic region to the abdominal region or, most often, vice versa, from the abdomen to the thorax, of various visceral elements (spleen, liver, stomach, colon, pancreas, etc.). Apart from the congenital origin, a somewhat rarer group is described, representing about 1–7% of the total: an acquired variant of the traumatic type, frequently through a contusive type mechanism, which produces diaphragmatic strains/ruptures. Apparently, the symptomatology is heterogeneous, being dependent on the location of the hernia, the dimensions of the defect, which abdominal viscera is involved through the hernial opening, its degree of migration, and whether there are volvulation/ischemia/obstruction phenomena. Often, its clinical appearance is modest, mainly incidental discoveries, the majority being digestive manifestations. Severe digestive complications such as strangulation, volvus, and perforation are rare and are accompanied by severe shock, suddenly appearing after several non-specific digestive prodromes. Diagnosis combines imaging evaluations (plain radiology, contrast, CT) with endoscopic ones. Surgical treatment is recommended regardless of the side on which the diaphragmatic defect is located or the secondary symptoms due to potential complications. The approach options are thoracic, abdominal or combined thoracoabdominal approach, and classic or minimally invasive. Most often, selection of the type of approach should be made taking into account two elements: the size of the defect, assessed by CT, and the presence of major complications. Any hiatal defect that is larger than 5 cm² (the hiatal hernia surface (HSA)) has a formal recommendation of mesh reinforcement. The recurrence rate is not negligible, and statistical data show that the period of the first postoperative year is prime for recurrence, being directly proportional to the size of the defect. As a result, in patients who were required to use mesh, the recurrence rate is somewhere between 27 and 41% (!), while for cases with primary suture, i.e., with a modest diaphragmatic defect, this is approx. 4%.

(1) Background: Cutaneous melanoma (CM) originates from melanocytes and causes 90% of skin cancer deaths; therefore, the comparison of different soluble and tissue markers could be valuable in the detection of melanoma progression and therapy monitoring. The present study is focused on the potential correlations between soluble S100B and MIA protein levels in different melanoma stages or with tissue expression of S100, gp100 (HMB45), and MelanA biomarkers. (2) Methods: Soluble S100B and MIA levels were evaluated by means of immunoassay methods in blood samples from 176 patients with CM, while tissue expressions of S100, MelanA, and gp100 (HMB45) were detected by means of immunohistochemistry in 76 melanomas. (3) Results: Soluble S100B correlated with MIA in stages III (r = 0.677, p < 0.001) and IV (r = 0.662, p < 0.001) but not in stages I and II; however, 22.22% and 31.98% of stage I and II patients, respectively, had high values for at least one of the two soluble markers. S100 tissue expression correlated with both MelanA (r = 0.610, p < 0.001) and HMB45 (r = 0.476, p < 0.01), while HMB45 and MelanA also significantly positively correlated (r = 0.623, p < 0.001). (4) Conclusions: Blood levels of S100B and MIA corroborated with melanoma tissue markers expression could help to improve the stratification process for patients with a high risk of tumor progression.