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Immunomodulatory Therapies
Published in David E. Thurston, Ilona Pysz, Chemistry and Pharmacology of Anticancer Drugs, 2021
To use a vaccination approach to prevent or treat cancer, the vaccine is usually targeted toward a well-defined proteinaceous antigen on the surface of the tumor cells, and so subunit vaccines have been an important element of many studies in this area. However, tumor cells usually evolve multiple mechanisms to evade the immune system and then divide uncontrollably to the point where they cause damage to tissues and organs. Therefore, a vaccination approach is very challenging as tumor cells can rapidly evolve modifications to a targeted antigen, or down-regulate its production, to evade an enhanced immune response produced through a vaccination therapy. This is discussed in more detail below.
Ganglioside GD2 Specific Antibodies in the Diagnosis and Therapy of Human Neuroblastoma
Published in John T. Kemshead, Pediatric Tumors: Immunological and Molecular Markers, 2020
Nai-Kong V. Cheung, Floro D. Miraldi
Ganglioside GD2 is a glycolipid antigen present on most neuroblastomas tested.7,8 It is a surface antigen estimated at 10 million molecules per cell. Except for the brain, this antigen is present only at low levels in restricted tissues of the normal body. We have described murine monoclonal antibodies (MAb) specific for this ganglioside, GD2, that bind strongly to human NB irrespective of whether they are from established cell lines, fresh patient tumors, or tumors xenografted and passaged in athymic nude mice.9 None of the non-NB bone marrow samples we tested reacted with these antibodies.10 Using conventional fluorescent microscopy, as few as 0.01% tumor cells can be detected. The detection of metastatic NB by these MAb correlates with the results of in vitro clonogenic assays10. Histochemical staining using Wright-Giemsa and Hematoxylin-Eosin have thus far been unable to monitor microscopic disease quantitatively so as to be able to measure the impact of intensivechemotherapy. The detection of micrometastasis in the bone marrow will be a convenient method to evaluate the overall metastatic disease in the patient. Our antibodies to GD2 seem useful in detecting extremely low levels of metastatic disease in the bone marrow of patients with NB. They may allow a quantitative measure of the extent and the chemoresponse of microscopic disease. They may also be useful in identifying the time of minimal disease for optimal bone marrow transplantation as well as for adjuvant monoclonal antibody immunotherapy.
Dopamine and Tumorigenesis in Reproductive Tissues
Published in Nira Ben-Jonathan, Dopamine, 2020
Tumors are masses of mutated and dysfunctional cells that may cause pain and disfigurement, invade organs, and potentially spread throughout the body. Tumors grow because of DNA malfunctions, mainly in genes that regulate cell growth or cell death. Some of these mutations can lead to rapid, unchecked growth by producing tumors that expand quickly and damage nearby organs and tissue. Transformed cells can produce enzymes that dissolve the surrounding tissue and grow beyond their normal boundaries, a process that is defined as invasiveness. Moreover, many tumor cells can be released into the blood stream, invade remote organs and grow at distant locations, a process that is defined as metastasis.
RANK pathway in cancer: underlying resistance and therapeutic approaches
Published in Journal of Chemotherapy, 2023
Stephen Paget proposed the “seed and soil” theory more than a century ago to explain the association between CTCs (seed) and metastatic sites (soil) [59]. Tumor cells spread more easily to certain organs than others, depending on where they come from [60]. Breast cancer metastases are most commonly disseminated through the bone. Even if some osteoblastic or mixed lesions are present, most BC metastases are bone lytic. About 80–90% of all bone metastases occur as a result of osteolysis. According to recent research, BC cells and the bone microenvironment may interact, but the exact mechanism by which the cancer cells migrate to the bone has yet to be discovered [61]. Chemokines can be used to direct cancer cells from the blood to the bone for radiation therapy. Growth factors are released by the mineralized bone matrix when it comes into contact with breast cancer cells. In a calcified bone matrix, tumor cells proliferate and become more aggressive. Cancer cells may benefit from PDGF, BMP, and calcium in the bone matrix [62,63]. It has been shown that bone-derived IGF promotes cancer cell proliferation and survival by activating the Akt/NF-kB signaling pathway [64,65]. In addition to its involvement in initiating the vicious cycle, TGF-β, which ranks second in abundance in the bone’s extracellular matrix, also plays a significant part in its maintenance.
Complexity of Tumor Microenvironment: Therapeutic Role of Curcumin and Its Metabolites
Published in Nutrition and Cancer, 2022
Sahdeo Prasad, Priyanka Saha, Bilash Chatterjee, Anis Ahmad Chaudhary, Rajiv Lall, Amit K Srivastava
Tumor cells grow and divide rapidly, which results in the accumulation of waste products, the creation of an acidic environment, and nutrition and oxygen deficiency. In order to cope with these unfavorable environments, tumor cells create their surrounding niche into a hospitable environment by interacting with cellular and non-cellular components. Components of TME such as CAFs, CAA, ECM and endothelial cells favor the tumor cells for their growth, survival, metastasis, and angiogenesis. These TME factors also promote tumor inflammation and induce signaling pathways that support escaping of tumor cells from host immune response. Thus, TME is clearly complex vicinity that favors the tumor growth, metastasis, and therapy resistance, while impeding anti-tumor immunity. Therefore, TME can be considered as a therapeutic target for the effective management of cancer. As described above, curcumin and its metabolites as well as curcumin derivatives have multiple effects in modulating the complexity of TME. They interfere with the interactions of the TME with tumor cells by inhibiting inflammatory factors, CAFs and CAA, increase anticancer immunity that results in suppression of growth, proliferation, metastasis and angiogenesis along with induction of apoptosis in cancer cells. Overall, curcumin normalizes the surrounding TME network as well as modulates the immune system, and increases antitumor activity. However, further studies are still required for the clinical implementation of curcumin and its metabolites in order to directly benefit cancer patients.
Role of poorly differentiated cluster in gastric cancer: is it a new prognosis factor?
Published in Scandinavian Journal of Gastroenterology, 2022
L. Sorrentino, N. De Ruvo, F. Serra, M. Salati, A. A. Ricciardolo, L. R. Bonetti, R. Gelmini
Nowadays, gastric cancer is still a challenge in the matter of therapies and survival due to the high rate of recurrence and metastasis after surgery [15]. Among the unfavorable prognostic factors, the diffuse signet-ring histotype and the presence of lymph node metastases at the time of diagnosis represent some of the dismal significance [16]. In epithelial tumors, it is well known that multiple biological and molecular factors promote the lymphatic spread of neoplastic cells. These factors include the spreading of neoplastic cells identified at the tumor's advancement and morphologically recognizable in tumor budding and clusters of poorly differentiated tumor cells (PDCs) [17]. PDCs have recently been described in gastric carcinoma in a cohort of 88 patients with intestinal-type tumors. It has been suggested to be a relevant prognostic factor associated with perineural invasion, lymph node metastasis, and high LNR [12].