Oncolytic viruses (OVs) are emerging as potential treatment options for cancer. Natural and genetically engineered viruses exhibit various antitumor mechanisms. OVs act by direct cytolysis, the potentiation of the immune system through antigen release, and the activation of inflammatory responses or indirectly by interference with different types of elements in the tumor microenvironment, modification of energy metabolism in tumor cells, and antiangiogenic action. The action of OVs is pleiotropic, and they show varied interactions with the host and tumor cells. An important impediment in oncolytic virotherapy is the journey of the virus into the tumor cells and the possibility of its binding to different biological and nonbiological vectors. OVs have been demonstrated to eliminate cancer cells that are resistant to standard treatments in many clinical trials for various cancers (melanoma, lung, and hepatic); however, there are several elements of resistance to the action of viruses per se. Therefore, it is necessary to evaluate the combination of OVs with other standard treatment modalities, such as chemotherapy, immunotherapy, targeted therapies, and cellular therapies, to increase the response rate. This review provides a comprehensive update on OVs, their use in oncolytic virotherapy, and the future prospects of this therapy alongside the standard therapies currently used in cancer treatment.

Melanoma is a common and aggressive tumor originating from melanocytes. The increasing incidence of cutaneous melanoma in recent last decades highlights the need for predictive biomarkers studies. Melanoma development is a complex process, involving the interplay of genetic, epigenetic, and environmental factors. Genetic aberrations include BRAF, NRAS, NF1, MAP2K1/MAP2K2, KIT, GNAQ, GNA11, CDKN2A, TERT mutations, and translocations of kinases. Epigenetic alterations involve microRNAs, non-coding RNAs, histones modifications, and abnormal DNA methylations. Genetic aberrations and epigenetic marks are important as biomarkers for the diagnosis, prognosis, and prediction of disease recurrence, and for therapeutic targets. This review summarizes our current knowledge of the genomic and epigenetic changes in melanoma and discusses the latest scientific information.

Background: Alteration of the expression of human epidermal growth factor receptor-2 gene as an oncogenic pathway in breast cancer was first explored in the 1980'. Since then, tremendous progress has been made in treating HER2-positive breast cancer. Methods: We performed a narrative type review of the existing literature using as a starting point the PubMed database, investigated by keywords, later the search being refined and the articles that we considered relevant were selected. The approach to the topic under discussion being variable in the various studies identified convinced us of the inappropriateness of a meta-analysis. As a secondary method of analysis, we evaluated the bibliography of each of the selected studies and from this we identified other publications of interest. Results: At present, there are three major classes of FDA-approved anti-HER2 agents: monoclonal antibodies (Trastuzumab, Pertuzumab and Margetuximab), TKIs (Lapatinib, Neratinib and Tucatinib) and antibody-drug conjugates (T-DM1 and T-DXd). The treatment of HER2+ breast cancer suffered some changes in the last few years. If in 2018, after progression under first-line treatment with taxane-trastuzumab/pertuzumab and second line with T-DM1 was a big challenge, being up to the oncologist to choose from lapatinib-capecitabine, trastuzumab-lapatinib or different chemotherapeutic agents, depending on toxicities and therapies available in the country, nowadays we have a new third- and fourth-line FDA approved standard, which consists of tucatinib-trastuzumab-capecitabine and trastuzumab-deruxtecan. Conclusion: Times are very exciting for HER2-positive disease. What differentiates novel therapies and if we do it better is both the question that we tried to give an answer to in this review of literature, but it remains at the same time a topic of discussion and a directive for analysis in the future, because we are only getting closer to an optimal version of treatment for HER2+ breast cancer, hoping that the introduction of new drugs and the establishment of new indications for old drugs will allow us to standardize the treatment of these patients.

Colorectal cancer is a major cause of cancer-related death worldwide and is correlated with genetic and epigenetic alterations in the colonic epithelium. Genetic changes play a major role in the pathophysiology of colorectal cancer through the development of gene mutations, but recent research has shown an important role for epigenetic alterations. In this review, we try to describe the current knowledge about epigenetic alterations, including DNA methylation and histone modifications, as well as the role of non-coding RNAs as epigenetic regulators and the prognostic and predictive biomarkers in metastatic colorectal disease that can allow increases in the effectiveness of treatments. Additionally, the intestinal microbiota’s composition can be an important biomarker for the response to strategies based on the immunotherapy of CRC. The identification of biomarkers in mCRC can be enhanced by developing artificial intelligence programs. We present the actual models that implement AI technology as a bridge connecting ncRNAs with tumors and conducted some experiments to improve the quality of the model used as well as the speed of the model that provides answers to users. In order to carry out this task, we implemented six algorithms: the naive Bayes classifier, the random forest classifier, the decision tree classifier, gradient boosted trees, logistic regression and SVM.

We present the case of a patient with breast neoplasm which presented a particular evolution with pronounced mo­le­cu­lar intratumoral heterogeneity proven at mul­ti­ple biopsies. If in the first instance, at the primary tu­mor it was discovered a negative molecular HER2 lu­mi­nal B pat­tern, in the end stage, after treatment with neo­ad­ju­vant chemotherapy, the residual tumor from the mas­tec­to­my tissue presented a luminal B profile with HER2 am­pli­fi­cation. Under targeted anti-HER2 treatment, there was cutaneous and pleural progression, lesions that were sub­jec­ted to biopsy and which revealed the presence of se­con­da­ry masses with triple negative molecular pattern.

Cancer immunotherapy has shifted the paradigm in cancer treatment in recent years. Immune checkpoint blockage (ICB), the active cancer vaccination and chimeric antigen receptor (CAR) for T-cell-based adoptive cell transfer represent the main developments, achieving a surprising increased survival in patients included in clinical trials. In spite of these results, the current state-of-the-art immunotherapy has its limitations in efficacy. The existence of an interdisciplinary interface involving current knowledge in biology, immunology, bioengineering and materials science represents important progress in increasing the effectiveness of immunotherapy in cancer. Cutaneous melanoma remains a difficult cancer to treat, in which immunotherapy is a major therapeutic option. In fact, enhancing immunotherapy is possible using sophisticated biomedical nanotechnology platforms of organic or inorganic materials or engineering various immune cells to enhance the immune system. In addition, biological devices have developed, changing the approach to and treatment results in melanoma. In this review, we present different modalities to modulate the immune system, as well as opportunities and challenges in melanoma treatment.

We are presenting the case of a young woman with asso­cia­ted renal carcinoma, bilateral breast cancer, metastatic co­lo­rec­tal cancer and benign tumor of the ovary. The pa­tient’s family history includes ovarian clear cell carcinoma, co­lo­rec­tal cancer, prostate carcinoma, breast cancer, me­la­no­ma and pulmonary carcinoma. First, she had surgery at the age of 28 years old for the ovarian mass, followed by the diagnosis of renal clear cell carcinoma at 42 years old, breast cancer at 47, colorectal cancer and renal cell car­ci­no­ma recurrence at 49 years old, and a new breast can­cer at 50 years old. We tried to analyze the history and to include the patient in one of the most common familial can­cer syndromes, taking into account that she has also a personal and a familial history of multiple neoplasms.

Noncoding RNAs (ncRNAs) include a diverse range of RNA species, including microRNAs (miRNAs) and long noncoding RNAs (lncRNAs). MiRNAs, ncRNAs of approximately 19–25 nucleotides in length, are involved in gene expression regulation either via degradation or silencing of the messenger RNAs (mRNAs) and have roles in multiple biological processes, including cell proliferation, differentiation, migration, angiogenesis, and apoptosis. LncRNAs, which are longer than 200 nucleotides, comprise one of the largest and most heterogeneous RNA families. LncRNAs can activate or repress gene expression through various mechanisms, acting alone or in combination with miRNAs and other molecules as part of various pathways. Until recently, most research has focused on individual lncRNA and miRNA functions as regulators, and there is limited available data on ncRNA interactions relating to the tumor growth, metastasis, and therapy of cancer, acting either on mRNA alone or as competing endogenous RNA (ceRNA) networks. Triple-negative breast cancer (TNBC) represents approximately 10%–20% of all breast cancers (BCs) and is highly heterogenous and more aggressive than other types of BC, for which current targeted treatment options include hormonotherapy, PARP inhibitors, and immunotherapy; however, no targeted therapies for TNBC are available, partly because of a lack of predictive biomarkers. With advances in proteomics, new evidence has emerged demonstrating the implications of dysregulation of ncRNAs in TNBC etiology. Here, we review the roles of lncRNAs and miRNAs implicated in TNBC, including their interactions and regulatory networks. Our synthesis provides insight into the mechanisms involved in TNBC progression and has potential to aid the discovery of new diagnostic and therapeutic strategies.

Campomelic dysplasia (CD) is a very rare, sporadic, autosomal dominant syndrome. CD is characterized by an association of skeletal (bowed long bones, pelvis and chest abnormalities, eleven rib pairs) and extraskeletal abnormalities (facial dysmorphism, sex-reversal in boy and visceral malformations). We report a case of a 3 days old male diagnosed by CD. At birth, the boy displayed severe asphyxia and therefore needed intensive care. Physical examination revealed short stature, a craniofacial dysmorphism, cleft palate, muscle hypotonia, skeletal anomalies (chest hypoplasia, curved short upper and lower limbs, talipes equinovarus ) cardiac malformations, normal male genitalia. The X-ray examination showed bell-shaped, narrow thoracic cage, hypoplastic scapulae, reduced cranial, pelvic, tibial and fibular ossification, absence of nasal and sternal ossification, cervical kyphosis, 11 pairs of ribs, flat and short vertebral bodies, short humerus with widened distal epiphysis, anterolateral femoral and tibial bowing and ankle valgus deformity. Dextrocardia was identified on X-ray examination and on echocardiography. Karyotype was 46,XY. The particularities of cases are campomelic dysplasia with dextrocardia, but without sex-reversal.