THE PROGRESS OF USING CHINESE HERBAL MEDICINES IN CANCER RESEARCH
Kevin Chan, Henry Lee in The Way Forward for Chinese Medicine, 2001
Cancers are populations of cells in the body that have acquired the ability to multiply and spread without the normal restraints. Most cancers take the form of tumors, although not all tumors are cancers. A tumor is simply spontaneous new tissue form that serves no physio-logical purpose. It can be benign like a wart, or malignant, like most lung cancers. Cancer cells can also spread (in a process called metasta-sis), to distant sites via the blood and lymphatic circulation, thereby producing invasive tumors in almost any part of the body. Malignant tumors affect host functions by compression, invasion, and destruction of normal tissues and also by the elaboration of substances that circulate in the blood stream. The effects of a growing tumor in a patient may include fever, anorexia (loss of appetite), weight loss and cachexia (body weight), infection, anemia, and various hormonal and neurological symptoms. Both genetics and lifestyle are potent forces that influence the risk for development cancer or carcinogenesis.
The Evolution of Anticancer Therapies
David E. Thurston, Ilona Pysz in Chemistry and Pharmacology of Anticancer Drugs, 2021
Although significant advances in understanding the transformation of a healthy cell into a tumor cell have been made during the past few decades, understanding of the precise biochemical mechanisms involved is still limited and is a major barrier to discovering more efficacious but less toxic therapeutic agents. In a few cases such as chronic myelogenous leukemia (i.e., Imatinib, GleevecTM), melanoma (i.e., Vemurafenib, ZelborafTM), and lung cancer (i.e., Crizotinib, XalkoriTM), our understanding of oncogenesis has been sufficient to support the development of effective treatments. Major genome sequencing projects have been undertaken to identify the genes mutated in various tumors. However, because the tumors are usually sequenced at a late stage in their development, it is often unclear which of the numerous mutations found represent the best therapeutic targets. Also, after many generations of cell replications during tumor development, late-stage mutations may only be present in a subset of tumor cells. Targeting the protein products of these mutated genes may lead to transient antitumor effects followed by overgrowth of tumor clones that do not contain these particular target mutations. Therefore, the ideal drug targets are initial key oncogenic mutations present in all tumor cells, including tumor stem cells. Targeting these mutations should lead to more substantial therapeutic effects.
Colorectal cancer
J. K. Cowell in Molecular Genetics of Cancer, 2003
Colorectal cancer (CRC) is the largest cancer killer in non-smokers in Westernized countries. There has been very little change in the death rate of the disease in the last 50 years, partly due to increasing incidence but mainly due to lack of substantial improvement in survival which is still only around 37%. This emphasizes the need for prevention strategies which can only develop when the fundamental processes of carcinogenesis are further understood. The largest step towards such an understanding was in 1987 when the APC gene responsible for familial adenomatous polyposis (FAP) was identified on chromosome 5. This was the first colorectal cancer gene to be described, and has led the way to huge research initiatives in the area of CRC genetics. CRC is more sensitive to environmental factors than any other malignancy, and dietary factors play a big part. Another characteristic of CRC is the presence of a premalignant lesion in the form of an adenomatous polyp. Taking all these factors together, primary prevention is likely to be possible, screening for adenomas should save lives, and the study and understanding of underlying genetic and biological processes is extremely important.
Possible Protective Potency of Argun Nut (Medemia argun – An Ancient Egyptian Palm) against Hepatocellular Carcinoma in Rats
Published in Nutrition and Cancer, 2022
Nabil Mohie Abdel-Hamid, Sara Gamal Abd Allah, Mohamed K. Hassan, Amal A.M. Ahmed, Nahla H. Anber, Ibrahim Adel Faried
Cell proliferation is regarded as one of the most important biological mechanisms in oncogenesis. Uncontrolled tumor cell proliferation is the hallmark of almost all types of cancer. One common approach to study the proliferative status of transformed cells is detection of proliferating cell nuclear antigen (PCNA) by immunohistochemistry. PCNA is a key factor in DNA replication and cell-cycle regulation (47). The crucial involvement of PCNA in cellular proliferation and its tight association with cancer transformation resulted in the frequent use of PCNA as a diagnostic and prognostic cell-cycle marker (48). Cancer group showed increased level of PCNA which is an indication of hyperproliferative activity. Whereas, MA treatment significantly decreased the proliferative index as revealed by down regulated protein level expression of PCNA. Moreover, caspases are crucial mediators of apoptosis; among them, caspase‐3 is a principal enzyme in the apoptotic cascade and is often used to detect apoptotic activity (49). The present study estimated a significant accumulation of caspase-3 monoclonal antibody in liver tissue of the HCC group.
ABO Blood Groups, Rh Factor, and Thyroid Cancer Risk: To ‘B’ or Not to ‘B’
Published in Endocrine Research, 2020
Abbas Ali Tam, Didem Özdemir, Sevgül Fakı, Muhammet Cüneyt Bilginer, Reyhan Ersoy, Bekir Çakır
Individual differences in regulation of immune response and disease susceptibility can partly be explained by human leukocyte antigen (HLA) polymorphisms. It is known that HLA class II alleles have a significant effect on autoimmune reactions.36 There is also evidence that HLA might have a role in the development of tumors. Shuxian et al.37 showed that HLA-B*51:01 might be a contributor risk for the development of PTC. In our study, prevalence of lymphocytic thyroiditis was higher in patients with malignant thyroid lesions. Oncogenesis is a multifactorial process influenced by genetic and environmental factors. The fact that some of the people who are exposed to the same environment develops disease and some do not suggest that genetic features play an important role in the developmet of tumor.37 Thus, in the presence of ABO blood group B, autoimmune thyroid disease as a risk factor may contribute to the development of thyroid cancer.
Diagnostic techniques in HPV infections and the need to implement them in plantar lesions: A systematic review
Published in Expert Review of Molecular Diagnostics, 2021
Alberto Aldana-Caballero, Felix Marcos-Tejedor, Raquel Mayordomo
Risk factors associated with oncogenesis have been studied using models. In Alpha papillomavirus types affecting mucosa, carcinogenesis appears to be primarily influenced by the expression of E6 and E7 proteins, which inactivate p53 and pRb suppressor tumor proteins, respectively. Coupled with persistent infection and a stronger mechanism for evading the immune system, this facilitates accumulation of DNA damage and progression to cancer [6]. In oncogenesis of cutaneous lesions, widely studied in beta papillomavirus, it appears that the mechanisms involved are the expression of both E6 and E7 at an early stage, inducing UV mutations in the host genome and progressing to cancer. However, although E6 and E7 genes are present in HR and LR types, in the latter they generally increase viral production and are insufficient for progression to neoplastic lesions [2,6].
Related Knowledge Centers
- Cancer Cell
- Cell Division
- Epigenetics
- Mutation
- Tissue
- Cancer
- Apoptosis
- Cell
- Malignant Transformation
- Genetics