Abstract
Triple-positive breast cancer, characterized by the concurrent overexpression of estrogen receptors (ER+), progesterone receptors (PR+), and human epidermal growth factor receptor 2 (HER2+), presents a significant clinical challenge in oncology. This particular subtype, distinguished by its aggressive behavior and propensity for metastasis, necessitates a comprehensive therapeutic approach. Current treatment modalities, primarily centered around targeted therapies, encounter obstacles, underscoring the imperative to explore alternative interventions. The emergence of Glucosodiene, grounded in Maher Akl's hypothesis regarding glucose mutation, introduces a promising avenue for therapeutic intervention. This innovative pharmacological agent exhibits efficacy in targeting the Warburg effect, a characteristic feature of tumors reliant on anaerobic glucose metabolism. A positron emission tomography (PET) scan conducted on a 36-year-old female patient following oral administration of Glucosodiene at a daily dosage of 100 ml over 15 consecutive days revealed encouraging findings, including regression of lesions in the left breast and a favorable response in axillary lymph nodes. Additionally, improvement was evident in the abdomino-pelvic region and musculoskeletal system, indicative of a partial metabolic response compared to prior imaging studies. Noteworthy reductions were observed in the number, size, and metabolic activity of osseous lesions, indicative of favorable disease progression. The mechanistic underpinnings of Glucosodiene position it as a versatile and impactful therapeutic option in the landscape of cancer management, offering promise for enhanced patient outcomes. THE TRIAL IS REGISTERED UNDER CLINICALTRIALS.GOV NUMBER NCT05957939.
Reference8 articles.
1. Zeng J, Edelweiss M, Ross DS, Xu B, Moo TA, Brogi E, D'Alfonso TM. Triple-Positive Breast Carcinoma: Histopathologic Features and Response to Neoadjuvant Chemotherapy. Arch Pathol Lab Med. 2021 Jun 1;145(6):728-735. doi: 10.5858/arpa.2020-0293-OA. PMID: 33112958; PMCID: PMC9257671.
2. Vaz-Luis I, Winer EP, Lin NU. Human epidermal growth factor receptor-2-positive breast cancer: does estrogen receptor status define two distinct subtypes? Ann Oncol. 2013 Feb;24(2):283-291. doi: 10.1093/annonc/mds286. Epub 2012 Sep 28. PMID: 23022997; PMCID: PMC3551479.
3. Francis IM, Altemaimi RA, Al-Ayadhy B, Alath P, Jaragh M, Mothafar FJ, Kapila K. Hormone Receptors and Human Epidermal Growth Factor (HER2) Expression in Fine-Needle Aspirates from Metastatic Breast Carcinoma - Role in Patient Management. J Cytol. 2019 Apr-Jun;36(2):94-100. doi: 10.4103/JOC.JOC_117_18. PMID: 30992644; PMCID: PMC6425780.
4. Addressing the therapeutic landscape, current modalities predominantly focus on targeted therapies, such as anti-HER2 agents like trastuzumab and pertuzumab. These drugs aim to impede HER2-mediated signaling cascades, hindering tumor progression. Despite the remarkable advancements, challenges persist, with treatment limitations and the emergence of resistance posing formidable hurdles.
5. Testa U, Castelli G, Pelosi E. Breast Cancer: A Molecularly Heterogenous Disease Needing Subtype-Specific Treatments. Med Sci (Basel). 2020 Mar 23;8(1):18. doi: 10.3390/medsci8010018. PMID: 32210163; PMCID: PMC7151639.