Clinical staging systems use physical examination and blood count results to provide prognostic information. Various biological and genetic markers provide additional prognostic information. Short-arm deletions of chromosome 17 (del[17p]) and or mutations in the TP53 gene predict resistance to chemoimmunotherapy and shortened time to progression with most targeted therapies. The CLL International Prognostic Index integrates genetic, biological and clinical variables to identify different risk groups of CLL patients.

•  Cell diagnosis

•  Monoclonal antibodies

•  Immunophenotyping

•  Epigenome

Although classified as a grade I tumor by the World Health Organization, craniopharyngiomas are highly susceptible due to their close involvement and massive impact on surrounding vital structures, including the hypothalamus, pituitary gland and optic chiasm, and their propensity to Even after successful relapse, it can cause significant morbidity. treatment. Many extensive and detailed studies have been conducted on craniopharyngioma. However, due to benign histology, epidemiological rarity compared to malignant tumors, and absence of tumors, two major subtypes of craniopharyngioma (adamantinoma and squamous) have been identified in the last century. Research on the genetic and molecular basis of papillae) has been limited. Research platforms and technical conditions relevant to these lesions.

Esthetineuroblastoma presents with numerous chromosomal aberrations, deletions, and gains, but no consistent pattern. In one study, specific deletions of chromosome 11 and gains of chromosome 1p were associated with metastasis and poor prognosis [6]. Gains are more common than losses, and high-stage esthetic eurobratoma show more changes than low-stage tumors. Increases in 20q and 13q may be important for the progression of this neoplasm. These regions may harbor genes functionally related to esthesion eurobratoma. PTCH1, GL/1, and GL/2 were detected in 70%, 70%, and 65% of human esthesion euroblastoma specimens, respectively, implicating the SHH signaling pathway in the pathogenesis of this neoplasm. suggesting that it is possible.

Colorectal cancer needs better early detection and treatment options. Incidence is increasing in the young population. Circulating tumor DNA provides a way to select patients for adjuvant chemotherapy. Immunotherapy is an option for patients with mismatch repair protein deficiency. However, efficacy outside this patient population remains a challenge. Targeted therapies such as BRAF inhibitors are an option for poor prognosis patients for whom cytotoxic chemotherapy is not very effective.

Mathematical modeling can be used to study the pharmacokinetic and pharmacodynamic relationships of available anticancer agents to improve their treatment. Achieving the optimal balance between toxicity and efficacy has become an increasingly complex task as the number of drug-deliverable molecular targets and possible drug combinations continues to grow. As a result, standard empirical approaches for optimizing patient drug dosing and planning are currently of limited use. Mathematical modeling can greatly advance this practice by improving the rationalization of treatment strategies.

The rapid proliferation of liver cancer creates vulnerabilities in its energy production and cell aggregation processes that can be effectively exploited in new combination therapeutic strategies. Hepatocytes, the main type of primary liver cancer (HCC) alters its metabolism to make it vulnerable to disruption of the supply of the key molecule arginine. They found that this arginine vulnerability was present in all his HCC cancers, regardless of the specific genetic mutation that caused them.

Approximately 30% of patients with RCC have metastases at diagnosis and 30-70% of tumors can recur after surgery. Targeted therapies such as tyrosine kinase inhibitors (TKIs) and mTOR inhibitors, and VEGF monoclonal antibodies and immune checks to prolong progression-free survival (PFS) and overall survival (OS) in patients with advanced or metastatic disease Despite the promise of immunotherapies such as point inhibitors, RCC patients eventually succumb to inevitable drug resistance.

Many genetic mutations that are being studied as possible factors that increase the risk of prostate cancer are transmitted along the chromosome from both parents. Several recent studies have shown that certain types of mitochondrial DNA, inherited only from the mother, may increase the risk of prostate cancer in men. Some substances in tomatoes (lycopene) and soybeans (isoflavones) may help prevent prostate cancer.

Tumor lysis syndrome (TLS) is characterized by hyperuricemia, hyperkalemia, hypocalcemia, and hyperphosphatemia released after extensive cell death due to malignant tumors, and is associated with normal homeostasis of the body. These electrolyte and metabolic disturbances can lead to toxic effects clinically, including renal failure, cardiac arrhythmias, stroke, and death. TLS occurs when tumor cells release their contents into the bloodstream. TLS is most common after systemic treatment of advanced hematologic malignancies, but is rare in solid tumors and there are only a few case reports in the literature.

A total of 150 patients with a mean age of 10.3 [0.2-21.0] were included. Patients treated for high-risk neuroblastoma and localized Ewing sarcoma with both high-dose cyclophosphamide and doxorubicin required the most platelet transfusions during the course of treatment, with an average of 13 and 13 transfusions, respectively. he was 9 times. Partly due to CIT, it was greatest in patients treated for high- and intermediate-risk rhabdomyosarcoma. Fifty-six percent of high-risk patients had an RDI decrease in the last two treatment cycles, and 69% of intermediate-risk patients had an RDI decrease in the last four treatment cycles.

The pathophysiology of radiotherapy, chemotherapy, or radiotherapy and chemotherapy-induced oral mucositis is thought to result from a complex process beginning with tissue damage in a five-step model proposed by Sonis. The five stages of RT- and chemotherapy-induced OM occur sequentially, including initiation, signaling, amplification, ulceration, and healing. First, radiation or chemotherapy causes tissue damage leading to death of basal epithelial cells and generation of reactive oxygen species.

 The increasing prevalence of cancer and cachexia, especially due to the growing geriatric population, is driving the demand for advanced treatments and pharmaceuticals, which primarily drives the market growth. This is further supported by growing consumer awareness of the availability of new therapeutic agents to treat cancer cachexia.

In addition, changes in patient propensity towards pharmacological, non-pharmacologic treatments and combination therapies to improve lean Body Mass (LBM) through clinical trials serve as another growth-promoting factor. Therefore, widespread use of several appetite stimulants such as megestrol acetate, dexamethasone and methylprednisolone to improve digestion also contributes to the market growth.

Currently approved treatments for MDS include those aimed at reducing the transfusion burden and improving anemia in low-risk disease (recombinant erythropoietin, lenalidomide, and laspatercept) and those for prolonging survival in high-risk MDS. hypomethylating agent (HMA). However, these are not curative treatments, so allogeneic stem cell transplantation remains the only possible treatment. Patients eligible for clinical trials may benefit from investigational drugs. Treatment should be aimed at maintaining or improving health-related quality of life. This special issue outlines the unmet needs of patients with MDS and is designed to provide readers with a broader understanding of emerging biological insights integrated into current and future treatment options and their outcomes.

Over the decades, advances in diagnosis, imaging, interventions, surgery, transplantation, and anticancer therapy have improved survival for patients with hepatocellular carcinoma. However, the overall long-term prognosis for hepatocellular carcinoma patients remains poor. Therefore, there is an urgent need to understand the biology of carcinogenesis, progression, metastasis, recurrence, and resistance to cancer therapies in order to develop new preventive/therapeutic approaches for hepatocellular carcinoma. Recently, in addition to curative treatments such as transplantation, resection, and ablation, tyrosine kinase inhibitors, PD-1 inhibitors, and their combinations have improved progression-free survival and overall survival in patients with unresectable advanced hepatocellular carcinoma. The period has been extended. In addition, antifibrotic, antiviral, and anti-inflammatory agents have been shown to reduce the risk of fibrosis progression and, accordingly, the risk of developing hepatocellular carcinoma.

In new developments and significant advances have been made in the treatment of GBM. However, despite progress, recurrence is often inevitable and patient survival remains low. A variety of factors, including tumor complexity, presence of the blood-brain barrier (BBB), and presence of GBM cancer stem cells, complicate the identification of effective treatment options and require existing therapeutic approaches to be improved. And the research will yield new therapies to improve treatment strategies for GBM.