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Clinicians' Perspective in the Use and Adaptability of the Latest Methods of Diagnosis and Treatment for Cancers in Women
Published in Shazia Rashid, Ankur Saxena, Sabia Rashid, Latest Advances in Diagnosis and Treatment of Women-Associated Cancers, 2022
Poly-adenosine diphosphate ribose polymerase (PARP) inhibitors: BRCA1 and BRCA2 genes are essential for maintaining genomic stability by ensuring an error free repair of DNA double-stranded breaks through the homologous recombination (HR) repair pathway. Patients with BRCA1 and BRCA2 mutations have tumour cells which are HR deficient, and hence need an alternative pathway which is modulated by PARP. The three common PARP inhibitors approved by FDA are olaparib, rucaparib and niraparib, and are currently in use for ovarian cancers. Research and development in this direction has yielded fruitful results and is bringing us closer to management of cervical cancer [17].
Regulation of Growth of Airway Smooth Muscle by Second Messenger Systems
Published in Alastair G. Stewart, AIRWAY WALL REMODELLING in ASTHMA, 2020
In some cell types, cGMP may enhance the formation of cyclic adenosine diphosphate ribose (cADPR), a metabolite of NAD that can release Ca2+ by acting on the ryanodine receptor.118–120 In these cells, increases in cGMP induced cell proliferation. Clearly, further studies are needed to define the role of cGMP in modulating cell proliferation.
Advances in Understanding the Mechanisms Underlying Synaptic Plasticity
Published in Avital Schurr, Benjamin M. Rigor, BRAIN SLICES in BASIC and CLINICAL RESEARCH, 2020
Timothy J. Teyler, Idil Cavus, Chris Coussens, Pascal DiScenna, Lawrence Grover, Yi-Ping Lee, Zeb Little
Several alternative sources of Ca2+ exist apart from the well-characterized ionotropic NMDA and VDCC channels. The metabotropic glutamate receptor, recently implicated in LTP induction,26 enhances the production of IP3 which, in turn, can release Ca2+ from intracellular stores. Ca2+ can also be released from intracellular stores via pyridine nucleotides.65 ADP-rybosal cyclase, an enzyme found in brain,69 converts NAD+ into cADP-ribose (cyclic adenosine diphosphate ribose), which activates the brain ryanodine receptor to release Ca2+ from stores.66,67 The ryanodine receptor is present in the hippocampus68 and cerebellum69 and has been isolated from dendritic spines.70 cADP-ribose activates the ryanodine receptor at low submicromolar Ca2+ levels to result in rapid Ca2+ release from an IP3-insensitive pool.71,72 cADP-ribose emerges as an alternative second messenger to IP3 for release of Ca2+ from stores. The involvement of cADP-ribose in synaptic plasticity has not been investigated, but the existence of a separate internal store that can be activated through different second messengers suggests an alternative Ca2+ signaling pathway that may be involved in different forms of synaptic plasticity.
Mirvetuximab soravtansine for platinum-resistant epithelial ovarian cancer
Published in Expert Review of Anticancer Therapy, 2023
Rebecca L. Porter, Ursula A. Matulonis
Epithelial ovarian cancer (EOC) is the 5th leading cause of cancer deaths in women with more than 13,000 deaths estimated in 2023 [1]. Several histological subtypes of epithelial ovarian cancer exist with each histology harboring its own genetic characteristics. High grade serous histology is the most common and the most lethal subtype, accounting for approximately 75% of EOC cases and causing up to 80% of deaths from EOC [2,3]. Most women with high-grade serous ovarian cancer (HGSOC) present with advanced-stage disease for which the standard of care treatment remains the combination of either upfront or interval cytoreductive surgery and platinum- and taxane-based chemotherapy, which together induce remission in ~ 80% of women [4]. Maintenance therapy can be given with bevacizumab added to chemotherapy and continued as maintenance therapy [5,6], and/or poly(adenosine diphosphate-ribose) polymerase (PARP) inhibitors initiated as maintenance after chemotherapy [7–9], depending on clinical and genomic features.
Pathology of breast cancer metastasis and a view of metastasis to the brain
Published in International Journal of Neuroscience, 2023
Md Sakibuzzaman, Shahriar Mahmud, Tanzina Afroze, Sawsan Fathma, Ummul Barakat Zakia, Sabrina Afroz, Farzina Zafar, Maksuda Hossain, Amit Barua, Sabiha Akter, Hasanul Islam Chowdhury, Eram Ahsan, Shayet Hossain Eshan, Tasnuva Tarannum Fariza
BRCA1 or BRCA2 germline mutations significantly increase the risk of developing breast cancer [27–31]. BRCA1 and BRCA2 are tumor suppressor genes that participate in the repair process of DNA double-stranded breaks in the homologous recombination repair cycle. Poly-adenosine diphosphate-ribose polymerase enzyme is the key to this repair process. Mutations in these genes, therefore, disrupt the DNA repair process and eventually cause tumor growth [29]. Most patients with BRCA1 germline mutations commonly have the propensity to develop the TN subtype [32]. Most patients with BRCA2 germline mutations commonly have the propensity to develop the HR+/HER2− subtype [28]. BRCA1 mutations are pathologically more aggressive than BRCA2 mutations due to less frequent expression of hormone receptors [27,30]. Germline BRCA1 and BRCA2 mutation carriers have distinct features for central nervous system (CNS) metastasis. BRCA1 and BRCA2 associated breast cancers, therefore, carry a remarkably higher propensity of CNS metastasis [28,30] depending on different subtypes [31]. Patients with HR-positive breast cancers and BRCA2 mutations develop both parenchymal and leptomeningeal disease of CNS. Song et al. [28] showed that BRCA1 mutation alone may not cause CNS metastases. In Albiges et al.’s [30] study, one-third of BRCA1 mutation carriers experienced both parenchymal and leptomeningeal diseases of CNS if associated with TN subtype. Song et al. [28] found a causal relationship between BRCA2 function loss and CNS metastasis homing and/or growth.
Immune-based combinations for metastatic triple negative breast cancer in clinical trials: current knowledge and therapeutic prospects
Published in Expert Opinion on Investigational Drugs, 2022
Alessandro Rizzo, Angela Dalia Ricci, Laura Lanotte, Lucia Lombardi, Alessandro Di Federico, Giovanni Brandi, Gennaro Gadaleta-Caldarola
Poly adenosine diphosphate-ribose polymerase (PARP) inhibitors represent a novel and exciting class of anticancer agents whose use is rapidly expanding in several solid tumors, including ovarian cancer, pancreatic cancer, and breast cancer [38–42]. Of note, PARP inhibitors such as olaparib, talazoparib, niraparib, and veliparib, are able to increase cytosolic DNA, leading to the recruitment and activation of STINGs and the expression of inflammatory cytokines, including interferon [43,44]. In addition, DNA damage repair (DDR) aberrations are able to impair the physiological process of repair, hesitating in genomic stability loss and accumulation of DNA damages. Based on this rationale, recent years have seen the emerging of a large number of trials investigating combination therapies of ICIs plus PARP inhibitors, with these agents widely explored in malignancies with DDR deficiency [45,46]; these tumors are associated with increased inflammation and infiltration of tumors by immune cells, something that further supports the use and investigation of these molecules [47,48].