Journal of Oncology Medicine & Practice

Background: Cancer patients navigate through complex and dynamic health services/systems after diagnosis to receive high-quality and effective care. An understanding of a cancer patient’s journey will help in improving the quality of care. A survey was conducted on patients and medical oncologists across India with an objective to map various aspects of patient journey from diagnosis to treatment and follow-up for advanced Breast Cancer (BC) and Lung Cancer (LC).

Methods: A multidimensional survey was shared with adult patients diagnosed with advanced stage (stage III B and stage IV) breast or lung cancer who were undergoing therapy and medical oncologists who have more than 10-years of experience in treating breast or lung cancer.

Results: A total of 100 patients with a diagnosis of Stage III B/IV breast cancer (BC), 100 patients with Stage III B/IV Lung Cancer (LC), and 55 medical oncologists participated in the survey. It was noted that similar numbers of BC (49%) and LC (50%) patients were not aware about cancer symptoms and treatments while the surveyed medical oncologists believed only 11% and 20% patients were not aware of cancer symptoms and treatment, respectively. Selecting the right specialist was reported to be the primary challenge faced by patients. As per surveyed medical oncologists, only 5% of them discuss support from Patient Advocacy Groups (PAGs) with all their patients. The majority of medical oncologists (79%) reported that less than 30% of patients join PAGs. Most patients were expecting empathy and time for counselling from their medical oncologists.

Conclusion: Coordinated and comprehensive cancer care is essential for patients with advanced LC and BC. The survey results also highlight the importance of screening high risk populations, importance of educational material for patients, counseling on treatment plan, information about financial support programs, counseling on mental well-being, nutritional support, and information about PAGs.

Angiogenesis, the tumour microenvironment, and proteoglycans play pivotal roles in cancer biology. Angiogenesis, the formation of new blood vessels, is a critical process for tumour growth and metastasis. The tumor microenvironment, consisting of various cellular and non-cellular components, provides a supportive niche for cancer progression. Proteoglycans, a class of complex molecules, are involved in modulating both angiogenesis and the tumour microenvironment. Angiogenesis in cancer is driven by a delicate balance of pro-angiogenic and anti-angiogenic factors. Tumour cells release pro-antigenic factors, such as Vascular Endothelial Growth Factors (VEGFs), to stimulate the sprouting of new blood vessels from existing vasculature. The tumour microenvironment, including immune cells, fibroblasts, and extracellular matrix components, also contributes to angiogenesis through the secretion of angiogenic factors and remodelling of the surrounding vasculature. Disrupting angiogenesis has emerged as a promising therapeutic strategy in cancer treatment, with the development of anti-antigenic drugs targeting VEGF signalling.

A core of several tetraspanin proteins organizes other membrane proteins like growth factor receptors, integrins, and Human Leukocyte Antigen (HLA) antigens in these complexes. Albeit most tetraspanin proteins have been concentrated separately, tetraspanin proteins and their edifices can affect cell grip and motility, associations with stroma or influence announcing development factors, and for the greater part of them no ligand has been distinguished. Although they are found in all cell types, these proteins have primarily been studied functionally in lymphoid cells. Tetraspanins have been identified as metastasis suppressors in some tumors, but their significance is still unclear. Data are also available for these tumors. They are outlined, along with some of their implications for tumor biology and areas that require additional research. The biological properties of tumor cells, particularly those pertaining to tumor adhesion and dissemination, can be significantly affected by membrane proteins that are involved in cellular interactions with other cells or the stroma as well as signaling pathways. The tetraspanins, a brand-new class of membrane proteins, are beginning to gain importance in cell biology but have received very little attention in the context of cancer biology up until this point.

This study aims to compare the clinical efficacy of posaconazole and fluconazole as antifungal prophylaxis in the field of hematology. Antifungal prophylaxis plays a crucial role in preventing invasive fungal infections, which are a significant cause of morbidity and mortality in immunocompromised patients, particularly those undergoing Hematopoietic Stem Cell Transplantation (HSCT) or intensive chemotherapy. A comprehensive literature review was conducted to identify relevant studies comparing the clinical outcomes of posaconazole and fluconazole prophylaxis in hematology patients. The primary endpoints assessed were the incidence of IFIs, overall survival, and adverse events associated with each antifungal agent. The results of the reviewed studies demonstrated that posaconazole had superior efficacy compared to fluconazole in preventing IFIs in hematology patients. Posaconazole prophylaxis was associated with a significantly lower incidence of IFIs, including invasive aspergillosis and candidiasis, when compared to fluconazole. Additionally, posaconazole showed a favorable impact on overall survival, suggesting its potential as a more effective antifungal prophylactic agent in this patient population.

Heterochromatin Protein 1α (HP1α) is a critical player in chromatin organization and gene regulation, and its dysregulation has been implicated in various cellular processes, including cell proliferation and cancer development. This review focuses on the role of HP1α as a characteristic of cell proliferation that is pertinent to clinical oncology. Extensive research has demonstrated that HP1α plays a dual role in regulating cell proliferation. On one hand, it functions as a transcriptional repressor, modulating the expression of genes involved in cell cycle control and DNA replication. On the other hand, HP1α has also been found to interact with numerous signaling pathways and transcription factors, thereby promoting cell proliferation under certain conditions. Aberrant expression and localization of HP1α have been observed in various types of cancer, including breast, prostate, lung, and colorectal cancer. Furthermore, studies have shown that altered HP1α expression is associated with poor prognosis and resistance to conventional therapies in cancer patients. Understanding the molecular mechanisms underlying HP1α's involvement in cell proliferation is of significant interest in clinical oncology. Targeting HP1α and its associated pathways may offer promising therapeutic opportunities for cancer treatment. In addition, HP1α expression levels and subcellular localization can potentially serve as diagnostic and prognostic biomarkers in clinical practice.