Oncology Reviews最新文献

Immune disorders and cancer share a common pathway involving NF-κb signaling. Through involvement with GM-CSF, NF-κB can contribute to proliferation and activation of T- and B- cells as well as immune cell migration to sites of inflammation. In breast cancer, this signaling pathway has been linked to resistance with endocrine and chemotherapies. Similarly, in ovarian cancer, NF-κB influences angiogenesis and inflammation pathways. Further, BRCA1 signaling common to both breast and ovarian cancer also has the capability to induce NF-κB activity. Immunotherapy involving NF-κB can also be implemented to combat chemoresistance. The complex signaling pathways of NF-κB can be harnessed for developing cancer therapeutics to promote immunotherapy for improving patient outcomes.

Due to their electrostatic nature, radon decay products can attach to solid particles and aerosols in the air. Inhalation and ingestion are therefore the two main routes through which people are exposed to radon and its decay products. During the inhalation of these radioactive aerosols, deposition takes place in different regions of the human respiratory tract. The deposited aerosols carrying radon and its progeny undergo a continuous radioactive transformation and expose the lung to ionizing alpha radiation, which can destroy the sensitive cells in the lung, causing a mutation that turns cancerous. Radon which is a colorless, odorless, and tasteless radioactive noble gas is a major health concern and is the second leading cause of lung cancer. To address this, an indoor radon survey was conducted in many countries internationally, with results showing that indoor radon concentration has a seasonal variation. This is due to the fluctuation of environmental parameters and the geological nature of buildings. Its concentration was found to be maximum in the cool (winter) season and a minimum concentration was recorded in the warm (summer) season of the year.

Breast cancer is the most commonly diagnosed cancer in women and is one of the leading causes of death from cancer in women worldwide. Despite the significant benefits of using conventional chemotherapy in the treatment of breast cancer, one of its subtypes, the triple-negative breast cancer, is still a challenge in clinical practice. Recent studies have been investigating the role of the immune system in breast cancer and the development of immunotherapy. Although recently the use of atezolizumab, an anti-PD-L1 monoclonal antibody, combined with chemotherapy was approved, an important step in the treatment of patients with triple-negative metastatic breast cancer, the use of immunotherapy to treat breast tumors remains a major challenge. In this systematic literature review, following PRISMA guidelines, we searched for clinical trials using immunotherapy in the treatment of metastatic triple-negative breast cancer published until March 2020 in the databases EMBASE, PubMed and Cochrane Central Register of Controlled Trials (CENTRAL), with no language restrictions. We did not contact the authors of the clinical trials to obtain additional information. Two researchers independently collected the data and assessed the quality of this study. The literature shows that immunotherapy with anti-PD-1/PD-L1 agents is emerging as a new treatment option in breast cancer. On the other hand, when compared to other types of cancer in which several agents have already been approved, the research is still in its infancy. The use of anti-PD-1/PD-L1 agents as monotherapy revealed encouraging results in the metastatic setting, especially when administered in the early course of the disease, although combination strategies with chemotherapy appear to increase its efficacy. The main limitation of this study is the approach of cancer only in advanced stages.

Imatinib and nilotinib are first-line treatments for chronic myeloid leukemia (CML) patients, which act specifically against target cells. However, these drugs may cause side effects, such as electrolyte disturbances. This literature review aimed to provide a comparison of the effects of imatinib and nilotinib on blood potassium and calcium levels. It also summarized their hypothetical mechanism. A comprehensive electronic search of the different databases was conducted using 'chronic myeloid leukemia', 'tyrosine kinase inhibitors', 'imatinib', 'nilotinib', 'potassium', 'calcium', 'electrolytes' as keywords. This review used PubMed- MEDLINE, Cochrane Library, and Google Scholar as the source databases. Sixteen articles published from 2006 to 2020 were reviewed. Changes in blood potassium levels range from increased to decreased levels, while changes in blood calcium levels range from the lower normal values to below normal values (hypocalcemia). Tyrosine kinase inhibitors (TKIs), including imatinib and nilotinib, have a non-specific target, namely plateletderived growth factor receptor (PDGFR), which indirectly affects blood potassium and calcium levels in CML patients. The clinical manifestations of these changes vary from being visible only in laboratory tests to displaying a variety of clinical signs and symptoms.

The study aims to summarize the literature and explore the strength of evidence for PD-L1 expression difference in basal like TNBC and non-basal like TNBC, and association of PD-L1 expression with disease free survival and overall survival in each group. A systematic search of the original research literature through November 29^th, 2020, reported according to PRISMA guideline. Eligible studies investigated must have a primary outcome and at least one secondary outcome. Two reviewers independently searched, selected, and assessed quality of studies and risk of bias. Any discrepancies will be resolved by consensus or by consulting a third and fourth author. A total of 6813 articles were screened from which five articles were selected and assessed for quality of studies and risk of bias. Of 5 articles, no similar findings are found regarding the level of PD-L1 expression and its correlation with recurrence and overall survival. There is not enough substantial evidence to support the difference PD-L1 protein expression level in basal and non-basal like TNBC and its association with recurrence and overall survival. Hence, further studies are needed specifically to focus on this problem.

Cell-to-cell communication is a pivotal aspect of cancer biology. Recently, extracellular vesicles (EVs)have been shown to play essential roles in intercellular communications between cancer cells and the surrounding microenvironment owing to cancer development. EVs are small membrane-bound vesicles secreted by various cells containing proteins, lipids, mRNAs, and non-coding RNAs (microRNAs and long non-coding RNAs), which contribute to cancer cell development and progression. Here, we provide an overview of current research direction on EVs, especially biomolecules in EVs, and also point out the novel diagnostics, monitoring, predicting, and therapeutic aspects using EVs against cancer.

BACH1 encodes for a protein that belongs to RecQ DEAH helicase family and interacts with the BRCT repeats of BRCA1. The N-terminus of BACH1 functions in DNA metabolism as DNA-dependent ATPase and helicase. The C-terminus consists of BRCT domain, which interacts with BRCA1 and this interaction is one of the major regulator of BACH1 function. BACH1 plays important roles both in phosphorylated as well as dephosphorylated state and functions in coordination with multiple signaling molecules. The active helicase property of BACH1 is maintained by its dephosphorylated state. Imbalance between these two states enhances the development and progression of the diseased condition. Currently BACH1 is known as a tumor suppressor gene based on the presence of its clinically relevant mutations in different cancers. Through this review we have justified it to be named as an oncogene. In this review, we have explained the mechanism of how BACH1 in collaboration with BRCA1 or independently regulates various pathways like cell cycle progression, DNA replication during both normal and stressed situation, recombination and repair of damaged DNA, chromatin remodeling and epigenetic modifications. Mutation and overexpression of BACH1 are significantly found in different cancer types. This review enlists the molecular players which interact with BACH1 to regulate DNA metabolic functions, thereby revealing its potential for cancer therapeutics. We have identified the most mutated functional domain of BACH1, the hot spot for tumorigenesis, justifying it as a target molecule in different cancer types for therapeutics. BACH1 has high potentials of transforming a normal cell into a tumor cell if compromised under certain circumstances. Thus, through this review, we justify BACH1 as an oncogene along with the existing role of being a tumor suppressant.

Since the identification of BRCA1 and BRCA2 genes 3 decades ago, genetic testing and genetic counseling have become an integral part of routine clinical practice. The risk of breast cancer among carriers of germline pathogenic variants, like BRCA1 and BRCA2, is well established. Risk-reducing interventions, including bilateral mastectomies and salpingo-oophorectomies are both effective and have become more acceptable. Many researchers and professional societies view current guidelines as restrictive and may miss many at-risk women, and are calling to expand testing to include all patients with breast cancer, regardless of their personal or family history of cancer, while others are calling for wider adoption to even include all healthy women at age 30 or older. This review will address expanding testing in two directions; horizontally to include more patients, and even healthy women, and vertically to include more genes using next-generation sequencing-based multi-gene panel testing.