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Journal articles on the topic 'Cancer, n.e.c'

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Author: Grafiati

Published: 10 December 2022

Last updated: 28 January 2023

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1

Cohn, Allen Lee, Michael Seiden, Kathryn N. Kurtzman, Earl Hubbell, Samuel Gross, Oliver Venn, Eric T. Fung, et al. "The Circulating Cell-free Genome Atlas (CCGA) Study: Follow-up (F/U) on non-cancer participants with cancer-like cell-free DNA signals." Journal of Clinical Oncology 37, no. 15_suppl (May 20, 2019): 5574. http://dx.doi.org/10.1200/jco.2019.37.15_suppl.5574.

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5574 Background: A noninvasive cell-free DNA (cfDNA)-based cancer detection assay offers the hope of a blood test that might reduce morbidity and mortality of cancers, particularly those without recommended screening tests (eg, some gynecologic cancers). CCGA (NCT02889978) is a prospective, multi-center, longitudinal, case-control study evaluating models for discriminating cancer versus non-cancer. Here, we report F/U of control participants (pts) who demonstrated a cancer-signal in CCGA. Methods: Clinically evaluable samples (N = 2508) from pts enrolled without a cancer diagnosis (dx; NC) and treatment-naive pts with newly diagnosed cancer (C) were divided into training (n = 1564; 580 NC, 984 C) and test (n = 944; 368 NC, 576 C) sets. Classification performance (cancer/non-cancer) was assessed via 3 prototype assays: whole-genome bisulfite (WGBS), whole-genome (WGS), and targeted (507 gene) sequencing. Notable outlier NC pts were identified with cancer-like scores in either ≥2 assay classification results or by the presence of known cancer drivers with ≥1 assay classification result suggesting cancer. All pts are currently in F/U in accordance with study protocol (to date: 80% with > 10 mo and 15% with > 22 mo F/U). Results: Among training and test sets, 8 ( < 1%) NC pts were identified with a cancer-like signal. To-date, 2 have been diagnosed with a gynecologic malignancy: 1 stage IIIc clear cell endometrial carcinoma and 1 stage IIIc ovarian cancer, 3 and 2 months (mo) post-enrollment [PE], respectively. Among C pts in the study, sensitivity (at 98% specificity; WGBS) in these cancer types was: uterine/endometrial: 11% (n = 27 train) and 22% (n = 9 test); ovarian: 82% (n = 17) and 71% (n = 7). In addition, a third NC pt was diagnosed with a stage IV lung cancer 15 mo PE. Conclusions: This cfDNA-based assay detected a cancer-like signal that anticipated a clinical presentation of cancer in undiagnosed pts as early as 15 months prior to the actual dx. High specificity ( > 99%) requires accounting for undiagnosed cancers in study design and analysis. Together, these data suggest that this prototype assay may have high performance detecting a variety of gynecological and other cancers. Clinical trial information: NCT02889978.

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Furihata, Chie, Akira Yamakoshi, Akiko Hatta, Masae Tatematsu, Hitoshi Iwata, Kenshi Hayashi, Kazuo Umezawa, and Taijiro Matsushima. "Induction of c-fos and c-myc oncogene expression in the pyloric mucosa of rat stomach by N-methyl-N′-nitro-N-nitrosoguanidine and taurocholate." Cancer Letters 83, no. 1-2 (August 1994): 215–20. http://dx.doi.org/10.1016/0304-3835(94)90322-0.

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3

DIAS, P., P. KUMAR, H. B. MARSDEN, H. R. GATTAMANENI, and S. KUMAR. "N-and c-myc Oncogenes in Childhood Rhabdomyosarcoma." JNCI Journal of the National Cancer Institute 82, no. 2 (January 17, 1990): 151. http://dx.doi.org/10.1093/jnci/82.2.151.

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4

Borrello, Maria G., Giusi Carbone, Marco A. Pierotti, Alessandra Molla, and Giuseppe Della Porta. "Activated c-K-ras and c-N-ras oncogenes in 3-methylcholanthrene-induced BALB/c fibrosarcomas." Carcinogenesis 9, no. 8 (1988): 1517–19. http://dx.doi.org/10.1093/carcin/9.8.1517.

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5

Putzrath, Resha. "Studying Cancer Human Carcinogenesis Curtis C. Harris Herman N. Autrup." BioScience 35, no. 1 (January 1985): 51. http://dx.doi.org/10.2307/1310088.

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6

Lin, D. X., M. Friesen, C. Malaveille, D. E. G. Shuker, and H. Bartsch. "Urinary excretion of S-benzylmercapturic acid as an indicator of N-nitroso-N-methylbenzylamine exposure." Cancer Letters 57, no. 3 (May 1991): 193–98. http://dx.doi.org/10.1016/0304-3835(91)90156-c.

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7

di Luccio, Eric, Masayo Morishita, and Takaaki Hirotsu. "C. elegans as a Powerful Tool for Cancer Screening." Biomedicines 10, no. 10 (September 23, 2022): 2371. http://dx.doi.org/10.3390/biomedicines10102371.

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Regular cancer screening is critical for early cancer detection. Cancer screening tends to be burdensome, invasive, and expensive, especially for a comprehensive multi-organ check. Improving the rate and effectiveness of routine cancer screenings remain a challenge in health care. Multi-cancer early detection (MCED) is an exciting concept and a potentially effective solution for addressing current issues with routine cancer screening. In recent years, several technologies have matured for MCED, such as identifying cell-free tumor DNA in blood or using organisms such as Caenorhabditis elegans as a tool for early cancer detection. In Japan, N-NOSE is a commercially available multi-cancer detection test based on the chemotaxis of C. elegans using a urine sample showing 87.5% sensitivity and 90.2% specificity. In this review, we focus on using C. elegans as a powerful biosensor for universal cancer screening. We review N-NOSE clinical research results, spotlighting it as an effective primary cancer screening test.

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Williams, Morwen, Adam I. Green, Julio Fernandez-Cestau, David L. Hughes, Maria A. O'Connell, Mark Searcey, Benoît Bertrand, and Manfred Bochmann. "(C^Npz^C)AuIII complexes of acyclic carbene ligands: synthesis and anticancer properties." Dalton Trans. 46, no. 39 (2017): 13397–408. http://dx.doi.org/10.1039/c7dt02804k.

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Tishchenko, V. K., V. M. Petriev, E. D. Stepchenkova, P. V. Shegai, S. A. Ivanov, and A. D. Kaprin. "The influence of temperature on biodistribution of N,N,N’,N’- ethylenediaminetetrakis(methylene phosphonic) acid labeled with gallium-68." Journal of Physics: Conference Series 2058, no. 1 (October 1, 2021): 012042. http://dx.doi.org/10.1088/1742-6596/2058/1/012042.

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Abstract Bone metastases are serious complication in the progression of various types of cancer. It determines the requirement of modern nuclear diagnostic tools, including positron emission tomography (PET). In this study the biodistribution of EDTMP labeled with gallium-68 (68Ga-EDTMP) prepared at different temperature (20, 50, and 95 °C) was investigated. All experimental studies were performed in healthy intact Wistar rats by measuring the radioactivity in organs and tissues with gamma counter. All 68Ga-EDTMP formulations accumulated predominantly in bones. Only in tibia the uptake of 68Ga-EDTMP prepared at 95 °C was higher (p < 0.05) than 68Ga-EDTMP prepared at 20 °C, but in other bones there weren’t any statistical differences in uptake of 68Ga-EDTMP formulations. The amounts of 68Ga-EDTMP formulations in soft organs and tissues were lower when compared with bones. In conclusion, a temperature of reaction mixture had an influence on the biodistribution of 68Ga-EDTMP in bones.

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Chu, Pei-Yi, Hsing-Ju Wu, Shin-Mae Wang, Po-Ming Chen, Feng-Yao Tang, and En-Pei Isabel Chiang. "MAT2A Localization and Its Independently Prognostic Relevance in Breast Cancer Patients." International Journal of Molecular Sciences 22, no. 10 (May 20, 2021): 5382. http://dx.doi.org/10.3390/ijms22105382.

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(1) Background: methionine cycle is not only essential for cancer cell proliferation but is also critical for metabolic reprogramming, a cancer hallmark. Hepatic and extrahepatic tissues methionine adenosyltransferases (MATs) are products of two genes, MAT1A and MAT2A that catalyze the formation of S-adenosylmethionine (SAM), the principal biological methyl donor. Glycine N-methyltransferase (GNMT) further utilizes SAM for sarcosine formation, thus it regulates the ratio of SAM:S-adenosylhomocysteine (SAH). (2) Methods: by analyzing the TCGA/GTEx datasets available within GEPIA2, we discovered that breast cancer patients with higher MAT2A had worse survival rate (p = 0.0057). Protein expression pattern of MAT1AA, MAT2A and GNMT were investigated in the tissue microarray in our own cohort (n = 252) by immunohistochemistry. MAT2A C/N expression ratio and cell invasion activity were further investigated in a panel of breast cancer cell lines. (3) Results: GNMT and MAT1A were detected in the cytoplasm, whereas MAT2A showed both cytoplasmic and nuclear immunoreactivity. Neither GNMT nor MAT1A protein expression was associated with patient survival rate in our cohort. Kaplan–Meier survival curves showed that a higher cytoplasmic/nuclear (C/N) MAT2A protein expression ratio correlated with poor overall survival (5 year survival rate: 93.7% vs. 83.3%, C/N ratio ≥ 1.0 vs. C/N ratio < 1.0, log-rank p = 0.004). Accordingly, a MAT2A C/N expression ratio ≥ 1.0 was determined as an independent risk factor by Cox regression analysis (hazard ratio = 2.771, p = 0.018, n = 252). In vitro studies found that breast cancer cell lines with a higher MAT2A C/N ratio were more invasive. (4) Conclusions: the subcellular localization of MAT2A may affect its functions, and elevated MAT2A C/N ratio in breast cancer cells is associated with increased invasiveness. MAT2A C/N expression ratio determined by IHC staining could serve as a novel independent prognostic marker for breast cancer.

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Bhattarai, Nimisha, Jieqiong Wang, Daniel Nguyen, Xiaoxiao Yang, Linh Helmers, Jennifer Paruch, Li Li, et al. "Abstract 6372: Nanodrug delivery system for non-genotoxic p53 activator INZ-C." Cancer Research 82, no. 12_Supplement (June 15, 2022): 6372. http://dx.doi.org/10.1158/1538-7445.am2022-6372.

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Abstract p53 is a known tumor suppressor protein whose gene is altered in 50% of all human cancers, while its function is inactivated in the many cancers harboring wild type p53, making it an attractive target for targeted cancer therapies. In this regard, our lab had previously discovered a small molecule, Inauhzin (INZ C), as a potent non-genotoxic p53 activator. In an effort to improve the bioavailability and efficacy, we have now encapsulated the INZ C small molecule in a chitosan/cyclodextrin nanoparticle delivery system. Evaluation of in vitro/in vivo activity and protien expression suggests nanoparticle encapsulation of INZ-C (n-INZ-C) improved p53 induction and inhibition of cell growth in lung and colorectal cancers, while maintaining a minimal effect for MEF and Wi38 normal cells. These results are consistent with the significantly reduced cellular uptake observed for normal cells as compared to the cancer cells. H/E staining of tissues for mice treated with n-INZ-C reveals no toxicity to other organs as well. Additionally, n-INZ-C demonstrates the ability to block migration of cells in vitro as demonstrated by both wound healing and trans-well migration assays. Our in vivo pharmacokinetic evaluation suggests nanoparticle encapsulation doubles the half-life of INZ-C from 2.5 to 5 h. These results suggest that nanoparticle encapsulation improved activity and bioavailability of INZ-C while maintaining the non-toxic nature of INZ-C in normal cells. In addition, we unveiled GRP78 as a potential new target of INZ-C and found out that knockdown of GRP78 can alleviate the inhibitory effect of INZ-C on lung and colorectal cancer proliferation. Further studies now focus on revealing the mechanism of enhanced cellular uptake for INZ-C in cancer cells as comapred to normal cells. Thus, these results demonstrate that we have established a nanoparticle system that could enhance the bioavailability and efficacy of INZ-C as a potential anti-cancer therapeutic and also identified a novel target of INZ-C. Citation Format: Nimisha Bhattarai, Jieqiong Wang, Daniel Nguyen, Xiaoxiao Yang, Linh Helmers, Jennifer Paruch, Li Li, Yiwei Zhang, Kun Meng, Alun Wang, Janarthanan Jayawickramarajah, Binghe Wang, Shelya Zeng, Hua Lu. Nanodrug delivery system for non-genotoxic p53 activator INZ-C [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2022; 2022 Apr 8-13. Philadelphia (PA): AACR; Cancer Res 2022;82(12_Suppl):Abstract nr 6372.

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12

Reno, Elaine M., James M. Haughian, Twila A. Jackson, Alicia M. Thorne, and Andrew P. Bradford. "c-Jun N-terminal kinase regulates apoptosis in endometrial cancer cells." Apoptosis 14, no. 6 (May 8, 2009): 809–20. http://dx.doi.org/10.1007/s10495-009-0354-6.

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13

Shulin, Wang, Zhang Yaozheng, and Yokihiro Matsugama. "C-erbB-2, p53, N-ras expression in hepatocellular carcinoma." Chinese Journal of Cancer Research 8, no. 3 (September 1996): 178–82. http://dx.doi.org/10.1007/bf02675484.

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14

Hurd, Cliff, Richard T. Waldron, and Enrique Rozengurt. "Protein kinase D complexes with C-Jun N-terminal kinase via activation loop phosphorylation and phosphorylates the C-Jun N-terminus." Oncogene 21, no. 14 (March 2002): 2154–60. http://dx.doi.org/10.1038/sj.onc.1205290.

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15

D'Angelo, Sandra, Meredith Deutscher, Maura Dickler, and David M. Weinstock. "Hepatitis C Virus Infection Does Not Preclude Standard Breast Cancer–Directed Therapy." Clinical Breast Cancer 9, no. 1 (February 2009): 51–52. http://dx.doi.org/10.3816/cbc.2009.n.009.

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16

Ramón, Jorge, Laura Rodriguez Rey, Luis Eduardo García, Darío Sánchez Cabrero, Oliver Higuera, Alejandro Gallego, Leticia Ruiz Gimenez, and Nuria Rodriguez Salas. "Prevalence & pathogenic features of hereditary breast/ovarian cancer syndromes: Implementation of a genetic/familiar cancer risk assessment unit." Journal of Clinical Oncology 38, no. 15_suppl (May 20, 2020): e13645-e13645. http://dx.doi.org/10.1200/jco.2020.38.15_suppl.e13645.

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e13645 Background: Currently studies found more than 25 genes associated with inherited Breast/Ovarian cancer. This syndrome shows morphologic, immunophenotic and molecular differences in comparison with sporadic ones. For example, BRCA1/2 are commonly ductal invasive carcinomas, with high grade of differentiation and high mitotic index, showing expression of basal o myoepithelial markers and overexpression of cell cycle proteins. Our study describe the outcomes since the implementation of Genetic/Familiar cancer risk assessment a tertiary hospital. Methods: A retrospective chart review was performed among all patients evaluated in Genetic counseling clinic in our hospital, since September 2008 to March 2019. Patients who fulfill criteria for Breast/Ovarian Cancer syndromes were included. We were specially interested in those with pathogenic, likely pathogenic or uncertain significance variants. All variants were named according to the practice of the BIC database, and the GenBank entries. Description on clinical features of tumor and frequency of implicated genes are considered for statistical analysis. All data were calculated in Stata IC 15. Results: 320 patients were eligible, 62,2% (n = 199) had cancer diagnosis. The most frequent tumor diagnosis was breast, 68,8% (n = 137), featured by: ductal carcinoma (82,5%), high grade differentiation (55,2%), triple negative (22,6%), local/locally advanced stage (86,13%) and bilateral component (16,1%). 11,6% had Breast cancer and 3,4% Ovarian cancer as second malignancies, respectively. Variant alterations were found in 24 different genes. BRCA 2 had the highest frequency (40,9%; n = 139 variants detected), BRCA 1 (24,7%; n = 84), ATM(7,4%; n = 25), PALB2(5,3%;n = 18) and BRIP1(2,9%, n = 10). 230 variants (68,3%) were pathogenic or likely pathogenic variants. Pathogenic mutation variant distribution in BRCA2 were c.3264dupT (n = 12); c.6275_6276delTT (n = 8); c.9026_9030delATCAT (n = 8). The most frequent mutations in BRCA1 were: c.1674delA (n = 7); c.302-1G > A (n = 4); c.3331_3334delCAAG(n = 4). Among all patient with BRCA 1/2 mutations, 30,7% were undergone to prophylactic surgery, without statistical association with survival (p = 0,310). Conclusions: Our findings support literature about highly relation between BRCA1/2 and Breast/Ovarian Cancer. In our population, BRCA2 showed high frequency of pathogenic mutations. Patients with BRCA mutations and prophylactic mastectomy did not show statistical benefit in survival.

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Portal, M. M., G. O. Ferrero, and B. L. Caputto. "N-Terminal c-Fos tyrosine phosphorylation regulates c-Fos/ER association and c-Fos-dependent phospholipid synthesis activation." Oncogene 26, no. 24 (December 11, 2006): 3551–58. http://dx.doi.org/10.1038/sj.onc.1210137.

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Watson, Patrice, Rita Lieberman, Carrie Snyder, Vanessa J. Clark, Henry T. Lynch, and Jeffrey T. Holt. "Detecting BRCA2 Protein Truncation in Tissue Biopsies to Identify Breast Cancers That Arise in BRCA2 Gene Mutation Carriers." Journal of Clinical Oncology 27, no. 24 (August 20, 2009): 3894–900. http://dx.doi.org/10.1200/jco.2008.20.5211.

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Purpose Mutations in the BRCA2 gene are dominantly inherited but cause cancers when the wild-type allele has loss of heterozygosity (LOH) within the cancer. Because most disease-associated BRCA2 mutations are protein-truncating mutations, a test for truncated BRCA2 proteins should identify most BRCA2 hereditary cancers. Methods We have developed a tissue truncation test to identify truncated BRCA2 proteins in breast cancer tissue biopsies in vivo that does not use amplification or genetic manipulations. N-terminal and C-terminal antibodies are used to visualize protein truncation by demonstrating that the beginning of the protein is present but the end (ie, terminus) is absent. Results A quantitative C-terminal immunostaining score or a C-terminal to N-terminal truncation ratio correctly classified 20 of 21 breast cancers arising in BRCA2 mutation carriers and 57 of 58 cancers arising outside the context of a multiple-case breast cancer family. This represents a sensitivity of 95% and a specificity of 98%. Because of the presence of C-terminal BRCA2 protein and atypical clinical features of the misclassified cancer in a BRCA2 mutation carrier, we performed polymerase chain reaction and sequence analyses on this cancer. The results showed continued presence of the BRCA2 wild-type allele in the cancer, which indicated that intact BRCA2 protein was present in this cancer. Conclusion This immunohistochemistry-based test (which takes only 4 hours) appears to identify BRCA2 hereditary cancer with high accuracy. The test also appears to diagnose the biochemical loss of BRCA2 protein in cancers (ie, BRCA2-mutant genotype), which will usually but not always agree with the presence of a germline BRCA2 mutation found by susceptibility testing by DNA sequencing of blood samples.

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Snyder, Jeremy, Marco Zenone, and Timothy Caulfield. "Crowdfunding for complementary and alternative medicine: What are cancer patients seeking?" PLOS ONE 15, no. 11 (November 20, 2020): e0242048. http://dx.doi.org/10.1371/journal.pone.0242048.

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Background Complementary and alternative medicine (CAM) is increasingly being integrated into conventional medical care for cancer, used to counter the side effects of conventional cancer treatment, and offered as an alternative to conventional cancer care. Our aim is to gain a broader understanding of trends in CAM interventions for cancer and crowdfunding campaigns for these interventions. Methods GoFundMe campaigns fundraising for CAM were retrieved through a database of crowdfunding campaign data. Search terms were drawn from two National Institutes of Health lists of CAM cancer interventions and a previous study. Campaigns were excluded that did not match these or related search terms or were initiated outside of June 4th, 2018 to June 4th, 2019. Results 1,396 campaigns were identified from the US (n = 1,037, 73.9%), Canada (n = 165, 11.8%), and the UK (n = 107, 7.7%). Most common cancer types were breast (n = 344, 24.6%), colorectal (n = 131, 9.4%), and brain (n = 98, 7.0%). CAM interventions sought included supplements (n = 422, 30.2%), better nutrition (n = 293, 21.0%), high dose vitamin C (n = 276, 19.8%), naturopathy (n = 226, 16.2%), and cannabis products (n = 211, 15.1%). Mexico (n = 198, 41.9%), and the US (n = 169, 35.7%) were the most common treatment destinations. Conclusions These findings confirm active and ongoing interest in using crowdfunding platforms to finance CAM cancer interventions. They confirm previous findings that CAM users with cancer tend to have late stage cancers, cancers with high mortality rates, and specific diseases such as breast cancer. These findings can inform targeted responses where facilities engage in misleading marketing practices and the efficacy of interventions is unproven.

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Tatematsu, Masae, Kumiko Ogawa, Toru Hoshiya, Yutaka Shichino, Toshio Kato, Katsumi Imaida, and Nobuyuki Ito. "Induction of Adenocarcinomas in the Glandular Stomach of BALB/c Mice Treated with N-Methyl-N-nitrosourea." Japanese Journal of Cancer Research 83, no. 9 (September 1992): 915–18. http://dx.doi.org/10.1111/j.1349-7006.1992.tb01999.x.

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Kim, Jung-Mi, Jung-Dae Kim, Rina Yu, Byung-Sam Kim, Mi-Kyung Shin, and In-Seob Han. "Effects of capsaicin on induction of c-jun proto-oncogene expression in Fisher-344 rats by N-methyl-N′-nitro-N-nitrosoguanidine." Cancer Letters 142, no. 2 (August 1999): 155–60. http://dx.doi.org/10.1016/s0304-3835(99)00154-8.

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Luzzatto, Lucio, Flavia Colonna, and Irene Reilly. "The “n-1” model for myelodysplastic syndromes." Leukemia Research 16, no. 1 (January 1992): 57–59. http://dx.doi.org/10.1016/0145-2126(92)90101-c.

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Musto, Pellegrino. "Hepatitis C Virus Infection and B-Cell Non-Hodgkin's Lymphomas: More Than a Simple Association." Clinical Lymphoma 3, no. 3 (December 2002): 150–60. http://dx.doi.org/10.3816/clm.2002.n.021.

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Lahn, Michael, Chen Su, Shuyu Li, Marcio Chedid, Kimberly R. Hanna, Jeremy R. Graff, George E. Sandusky, et al. "Expression Levels of Protein Kinase C-α in Non–Small-Cell Lung Cancer." Clinical Lung Cancer 6, no. 3 (November 2004): 184–89. http://dx.doi.org/10.3816/clc.2004.n.032.

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Ma, Liandong, Yuzhi Tong, Zhaohui Yang, Qianxiang Zhou, Honghua Yan, Ye Chen, Dong Chen, Ru Xu, Yini Wang, and Jun Qin. "Abstract A03: Discovery and evaluation of GT19630, a c-Myc/n-Myc degrader, for targeting c-Myc-driven B-cell malignancies, acute myeloid leukemia (AML) and n-Myc driven cancers." Blood Cancer Discovery 3, no. 5_Supplement (September 6, 2022): A03. http://dx.doi.org/10.1158/2643-3249.lymphoma22-a03.

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Abstract Myc family members (MYC, MYCN and MYCL) are oncogenic transcriptional factors, which form dimers with Max to activate transcription activities to drive tumor initiation and progression. c-Myc deregulation has been identified in 80% of all tumor types, including B-cell malignancies, AML and a variety of solid tumors. N-Myc genetic alterations have been identified in small cell lung cancer, neuroblastoma, neuroendocrine prostate cancers and sarcoma. Myc-deregulation has been directly linked to the poor clinical outcome in these cancers, which makes Myc a therapeutic target for pharmacological inhibition. Here we described GT19630, a c-Myc/n-Myc degrader. GT19630 selectively degraded c-Myc proteins in c-Myc dependent blood cancer cells (IC50=1.5 nM) as compared to growth-factor regulated c-Myc in hematopoietic progenitor cells (TF-1) (IC50=52.5 nM). Similar selectivity of GT19630 has been demonstrated in cell proliferation and granulocyte–macrophage progenitor colony forming unit (GM-CFU) assays with the IC50s of 26.2 and 39.0 nM, respectively. GT19630 was shown to degrade c-Myc via proteasome degradation system and degraded CRBN-dependent endogenous neo-substrates of GSPT1, CK1α and IKZF1. GT19630 reduced transcriptional factors including c-Myc, Max, MXI1, SWF/SNF family members/associated proteins; ARID1A, SMARCE1, and SMARCC1 in transcriptional factor response element (TFRE) assays. Moreover, GT19630 inhibited the cell proliferation with IC50<10 nM in 74% of B-cell malignant cell lines (20/27) bearing deregulated c-Myc. Importantly, GT19630 was demonstrated to degrade Myc proteins completely and induced tumor regression or tumor eradication in AML, lymphoma and multiple myeloma (MM) animal xenograft tumor at lowest dose of 0.3 mpk/qd. In addition, GT19630 demonstrated an even-driven pharmacology in vivo and induced complete AML tumor regression with an intermittent dosing regimen of 3d on/7d off. Furthermore, GT19630 degraded n-Myc in SCLC, and neuroblastoma cells and demonstrated target-engaged efficacy in SCLC tumor models. Finally, GT19630 demonstrated favorable PK and safety profiles in rat after Rx for 14 days. In conclusion, GT19630 is a potent c-Myc/n-Myc degrader, which induced complete tumor regression and eradicated lymphoma cells in c-Myc/n-Myc dependent animal models (lymphoma, MM and AML and SCLC) without heme toxicity in vivo. GT19630 has achieved favorable PK profile and therapeutic index, which help advance this compound to IND-enabling stage. Citation Format: Liandong Ma, Yuzhi Tong, Zhaohui Yang, Qianxiang Zhou, Honghua Yan, Ye Chen, Dong Chen, Ru Xu, Yini Wang, Jun Qin. Discovery and evaluation of GT19630, a c-Myc/n-Myc degrader, for targeting c-Myc-driven B-cell malignancies, acute myeloid leukemia (AML) and n-Myc driven cancers [abstract]. In: Proceedings of the Third AACR International Meeting: Advances in Malignant Lymphoma: Maximizing the Basic-Translational Interface for Clinical Application; 2022 Jun 23-26; Boston, MA. Philadelphia (PA): AACR; Blood Cancer Discov 2022;3(5_Suppl):Abstract nr A03.

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Pracht, Marc, Ariane Mogha, Alain Fautrel, Alexandra Lespagnol, Nicolas Mouchet, Francois Le Gall, Emmanuel Oger, Marie-Dominique Galibert, and Thierry Lesimple. "C-kit, B-raf, and N-ras mutations in melanoma subtypes." Journal of Clinical Oncology 30, no. 15_suppl (May 20, 2012): e19037-e19037. http://dx.doi.org/10.1200/jco.2012.30.15_suppl.e19037.

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e19037 Background: The recent understanding of melanomas’ molecular pathways improved their classification and clinical strategies. Initial studies showed that B-Raf/N-Ras mutations (respectively V600E and Q61) are the most frequent alterations being present in 70 to 80% of melanomas, characterizing non Chronic Sun-induced Damage skins (CSD). These include Superficial Spreading Melanomas (SSM) and Nodular Melanomas (NM). Other studies showed that c-Kit mutations are present at low rate (20-40%) in Acro-Lentiginous Melanomas (ALM), Mucous Melanomas (MM) and in melanomas arising on CSD skins. C-kit mutation pattern is complex with four exons being affected leading to numerous mutations. Because c-Kit targeted therapy is a critical clinical issue, we aimed to identify the most frequent mutations to propose appropriate screening test and adapted therapy. Methods: 186 melanoma samples corresponding to an homogeneous white-caucasian population (Brittany, France) were screened. c-Kit exons 11, 13,17 and 18 were sequenced, c-Kit copy number was quantified by q-PCR and level of c-Kit determined by immunohistochemistry (CD117). Samples were also analyzed for B-Raf mutations (codon 464, 466, 469, 600) and for N-Ras mutations (codon 12, 13, 61) by pyrosequencing. Results: Detectedmutations are shown in the table. Uveal melanomas (n=13) were never mutated. These mutations were never overlaped and comparable profiles were obtained between the primary tumour, nodes or metastatic lesions from a same patient. Conclusions: C-Kit mutations are much less common than in other previously described populations especially for MM or ALM. B-Raf/N-Ras mutations appeared also less frequent than waited in non-CSD , reaching 46% in SSM. Interestingly our population presents a high incidence of N-Ras mutations, especially in SSM and NM. Screening of B-Raf/N-Ras mutations is fundamental not only for SSM but also for NM, CSD and ALM for prescribing targeted therapies such as MEK-inhibitors. [Table: see text]

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Wang, Y., and S. R. McAlpine. "N-terminal and C-terminal modulation of Hsp90 produce dissimilar phenotypes." Chemical Communications 51, no. 8 (2015): 1410–13. http://dx.doi.org/10.1039/c4cc07284g.

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Chambers, Laura, Xuefei Jia, and Mariam Alhilli. "Impact of neoadjuvant chemotherapy on survival in women with endometrial cancer: A National Cancer Database analysis." Journal of Clinical Oncology 38, no. 15_suppl (May 20, 2020): e18094-e18094. http://dx.doi.org/10.1200/jco.2020.38.15_suppl.e18094.

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e18094 Background: To evaluate overall survival (OS), prognostic factors for survival, and treatment outcomes in patients with Stage III/IV endometrial cancer (EC) undergoing neoadjuvant chemotherapy +/- surgery compared to surgery followed by adjuvant chemotherapy. Methods: The National Cancer Database (NCDB) was queried to identify patients with Stage III/IV EC who were treated with chemotherapy. Univariable and multivariable Cox proportional hazards analyses were used to determine independent prognostic factors for OS. Survival was measured from date of diagnosis to the date of last contact or death. Results: From 2004-2012, 31,726 women with stage III/IV EC were identified. . Treatment groups consisted of: 3424 (10.8%) chemotherapy alone (C), 26926 (84.9%) surgery followed by chemotherapy (S+C), and 1412 (4.4%) neoadjuvant chemotherapy followed by surgery (NACT+S). The median age at diagnosis was 64 years (19-90), and 65.8% (n = 35402) of patients had Stage III disease. Reasons for no surgery were: not part of primary treatment plan (77.7%; n = 5859), contraindicated due to patient factors (11.3%, n = 850) or patient refusal (3.6%; n = 268). The majority of patients (86.8%) received multiple chemotherapy agents and 1988 (6.3%) received single agent chemotherapy. Charlson-Deyo score was 0 for 75.3% (n = 2578) of C, 76.7% (n = 20652) of S+C and 77.8% (n = 1098) of NACT+S patients (p < 0.001). Compared to patients who received C alone, S+C and NACT+S were associated with improved median OS (10.9 months vs. 63.3 (HR 0.27 CI 0.26-0.28, p < 0.001) and 24.6 months (HR 0.50, 95% CI 0.47-0.54, p < 0.001), respectively). On multivariate analysis advanced age (HR 1.03, p < 0.001), stage IV disease (HR 2.70, p < 0.001), Charlson Deyo Score (1 – HR 1.13, p < 0.001; 2 – HR 1.32, p < 0.001), and African American race (HR 1.53, p < 0.001) were associated with worse OS.Private insurance (HR 0.87, p < 0.001), income > $63,000 (HR 0.86, p < 0.001) and treatment with S+C (HR = 0.32, p < 0.001) or NACT+S (HR 0.44, p < 0.001) versus C alone were predictive of improved OS. Conclusions: In this analysis of the NCDB, receipt of chemotherapy alone is associated with markedly worse OS than S+C or NACT +S in stage III/IV patients. . Socioeconomic factors including African American race, insurance status and income are independent predictors for survival in this cohort. Where feasible, surgery should be should be incorporated into treatment planning for women with Stage III/IV EC.

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Wyrwicz, Lucjan, Elena Elimova, Steven I. Blum, Hong Xiao, Eric Davenport, Jinyi Wang, Shannon Hunter, Mingshun Li, Kaoru Kondo, and Markus H. Moehler. "Health-related quality of life (HRQOL) in patients (pts) with advanced gastric cancer/gastroesophageal junction cancer (GC/GEJC) or esophageal adenocarcinoma (EAC): Interim results of nivolumab plus chemotherapy (N+C) versus (C) from CheckMate 649." Journal of Clinical Oncology 39, no. 15_suppl (May 20, 2021): 4066. http://dx.doi.org/10.1200/jco.2021.39.15_suppl.4066.

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4066 Background: CheckMate 649 (NCT02872116) is a randomized, open label phase 3 study in first line (1L) GC/GEJC/EAC. Prespecified interim results showed statistically significant improvement in overall survival (OS) and progression-free survival (PFS) for N+C vs C in all randomized pts and pts whose tumors expressed programmed death-ligand 1 combined positive score (CPS) ≥ 5. We present interim HRQOL results for CPS ≥ 5 pts, included as exploratory in the study. Methods: HRQOL was assessed using EQ-5D-3L (EQ-5D) and Functional Assessment of Cancer Therapy–Gastric Cancer (FACT-Ga). Assessments were performed at baseline (BL), every 6 weeks during treatment, and during follow-up. Change from BL EQ-5D Visual Analog Scale (VAS), Utility Index (UI) and FACT-Ga scores were analyzed using mixed models. Time to first symptom deterioration (TTSD), time until definitive deterioration (TuDD), and time to improvement (TTI) were estimated with Kaplan-Meier estimators and stratified Cox models; deterioration/improvement was based on prespecified meaningful change thresholds. Results: 1,581 pts were randomized to N+C (n = 789) and C (n = 792); of those, 955 pts had CPS ≥ 5 (N+C [n = 473] and C [n = 482]). Among 821 pts with BL and post BL PROs (N+C [n = 421] and C [n = 400]), BL scores for FACT-Ga total were similar for N+C and C. Least-squares mean differences from BL favored N+C at most visits for EQ-5D and FACT-Ga total and GaCS, and were comparable for other FACT subscales (data not shown). TTI largely favored N+C (most hazard ratios (HR) > 1) but was not significantly different between treatments. For TTSD, pts treated with N+C had decreased risk of deterioration (HR < 1) in EQ-5D UI, FACT-Ga total, and GaCS. TuDD showed statistically significant delays in deterioration (HR with confidence intervals [CI] < 1) for all scores. Conclusions: Pts with 1L GC/GEJC/EAC experienced better HRQOL with N+C compared with C alone. Change from BL in EQ-5D and FACT-Ga total and GaCS favored N+C at most visits. N+C decreased deterioration risk compared to C with OS and PFS improvement, suggesting favorable benefits in 1L GC/GEJC/EAC pts with CPS ≥ 5. Clinical trial information: NCT02872116. [Table: see text]

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Kumar, R., P. Mende, A. R. Tricker, M. Siddiqi, and R. Preussmann. "N-Nitroso compounds and their precursors in Brassica oleracea." Cancer Letters 54, no. 1-2 (October 1990): 61–65. http://dx.doi.org/10.1016/0304-3835(90)90092-c.

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Takahashi, Ryota, Yoshihiro Hirata, Kosuke Sakitani, Wachiko Nakata, Hiroto Kinoshita, Yoku Hayakawa, Hayato Nakagawa, et al. "Therapeutic effect of c-Jun N-terminal kinase inhibition on pancreatic cancer." Cancer Science 104, no. 3 (January 24, 2013): 337–44. http://dx.doi.org/10.1111/cas.12080.

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Zhou, Xue-Quan, Anja Busemann, Michael S. Meijer, Maxime A. Siegler, and Sylvestre Bonnet. "The two isomers of a cyclometallated palladium sensitizer show different photodynamic properties in cancer cells." Chemical Communications 55, no. 32 (2019): 4695–98. http://dx.doi.org/10.1039/c8cc10134e.

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This report demonstrates that changing the position of the carbon-metal bond in a polypyridyl cyclopalladated complex, i.e. going from PdL1 (N^N^C^N) to PdL2 (N^N^N^C), dramatically influences the photodynamic properties of the complex in cancer cells.

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Maruzzo, Marco, Alberto Bortolami, Dario Palleschi, Andrea Zivi, Maurizio Nicodemo, Donata Sartori, Rocco De Vivo, et al. "Use of nivolumab (N) and cabozantinib (C) for treatment of the metastatic renal cell carcinoma (mRCC) in the Veneto region: Results of AMOUR study." Journal of Clinical Oncology 39, no. 6_suppl (February 20, 2021): 290. http://dx.doi.org/10.1200/jco.2021.39.6_suppl.290.

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290 Background: Second (2L) or third-line (3L) treatment options for mRCC have dramatically changed in the last years. The standard of care as per Italian Regulatory Agencies approvals is N or C. To date, there are no criteria for the choice between N and C, which both demonstrated OS gain in the pivotal trials. Methods: We planned a retrospective, real world analysis of the use of N and C as 2L and 3L treatment in 17 Oncology Units of Veneto Region. All consecutive patients (pts) with mRCC treated in advanced setting in 2017-2018 were included. Results: We identified 170 pts, 73% males, median age 68.4 years. All pts started a 2L treatment while only 59% received a 3L treatment. In our cohort, patients with NLR > 3 at treatment start had a shorter OS (43 vs 90 months (mos), p < 0.0001); IMDC classification maintained its prognostic role. In 2L, N was administrated in 108 pts (63%), C in 29 pts (17%); in 3L N was administrated in 42 pts (25%), C in 49 pts (29%). Reported oncologists’ reasons for 2L choice were: change of mechanism of action compared to first line (28%), response to previous TKI (21.2%), intolerance to TKI (17.6%), previous toxicity (12.9%), tumor burden (11.2%), age of the patient (4.1%). Median OS and PFS in 2L were 28.4 and 6.6 mos for N, 16.8 and 6.6 mos for 2L C. Median OS and PFS in 3L were 27 and 5.2 mos for N, 16.6 and 7.5 mos for C. 46 pts received the sequence of drugs N > C, 12 the opposite sequence C > N. Median OS for N > C vs C > N were 96.6 vs 36 mos (p > 0.0001); median PFS for both the sequences were similar at 5.7 mos (p = ns). The cost per patient of the sequence N > C is 51.606 € while for the sequence C > N is 31.480,00 €. Between the two sequences a cost effectiveness per month of survival analysis was performed: the cost per month of OS for the sequence N > C was 534,18 € while for the sequence C > N was 874,46 €, heavily higher. Conclusions: In our real-world setting cohort, most of the pts received N as 2L treatment and a minority received C. Outcome of single drug are superimposable to published literature. With the limits of the retrospective nature of the study, with a cost per month of OS lower a much longer OS, the sequence N > C appear to be a better treatment strategy.

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Alkrekshi, Akram, Raul Arroyo Suarez, and Ahmad Nader Kassem. "Excess body weight association with various cancer: A United States population-based study 2021." Journal of Clinical Oncology 39, no. 15_suppl (May 20, 2021): e18558-e18558. http://dx.doi.org/10.1200/jco.2021.39.15_suppl.e18558.

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e18558 Background: Excess body weight (EW) is a rising healthcare issue affecting over two-thirds of the United States (US) population, and it is a risk factor for various cancer. Methods: We used Explorys, IBM, a US database that includes ̃ 73 million patients. We evaluated non-gastrointestinal cancers prevalence based on age (18-64 and ≥ 65 years; for female cancers 18-49 and ≥ 50 years), race; Caucasians (C) and African-Americans (AA), and weight; normal weight (N) with BMI 18.5- 24.9 kg/m2 and EW for BMI ≥ 25 kg/m2. Compared to NW, the odds ratio (OR) and 95% confidence interval (CI) for multiple cancer rates in the EW group were calculated. p-value of <0.001 was considered significant (S) and > 0.001 as non-significant (NS). Results: A population of 26.9 million was included. C 85.6%, AA 14.4%. See table. Conclusions: A strong association between EW and urological cancers (prostate, bladder, renal), non-Hodgkin's lymphoma, multiple myelomas (MM), breast cancer, endometrial cancer, ovarian cancer in C 18-64 yrs but not in C ≥ 65 yrs with the exception for kidney cancer. A similar finding in AA 18-64 yrs for cancers of prostate, renal, breast, uterus, and MM compared to AA ≥ 65 yrs. EW is possibly more oncogenic earlier in life, especially in C.[Table: see text]

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Saura, Cristina, Mafalda Oliveira, Yin-Hsun Feng, Ming-Shen Dai, Sara A. Hurvitz, Sung-Bae Kim, Beverly Moy, et al. "Neratinib + capecitabine versus lapatinib + capecitabine in patients with HER2+ metastatic breast cancer previously treated with ≥ 2 HER2-directed regimens: Findings from the multinational, randomized, phase III NALA trial." Journal of Clinical Oncology 37, no. 15_suppl (May 20, 2019): 1002. http://dx.doi.org/10.1200/jco.2019.37.15_suppl.1002.

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1002 Background: NALA (ClinicalTrials.gov NCT01808573) is a multinational, randomized, open-label, phase III trial of neratinib (an irreversible pan-HER tyrosine kinase inhibitor [TKI]) + capecitabine (N+C) vs lapatinib (a reversible dual TKI) + capecitabine (L+C) in patients with stage IV HER2+ metastatic breast cancer (MBC) who had received ≥2 prior HER2-directed regimens for MBC. Methods: Patients were randomized 1:1 to N (240 mg qd po) + C (750 mg/m2 bid po) or L (1250 mg qd po) + C (1000 mg/m2 bid po). Co-primary endpoints were centrally assessed progression-free survival (PFS) and overall survival (OS). Secondary endpoints were investigator-assessed PFS; objective response rate (ORR); duration of response (DoR); clinical benefit rate (CBR); time to intervention for symptomatic metastatic central nervous system (CNS) disease; safety; and patient-reported health outcomes. Results: 621 patients were randomized (307 to N+C; 314 to L+C). The risk of disease progression or death was reduced by 24% with N+C vs L+C (HR = 0.76; 95% CI 0.63–0.93; p = 0.006); 6- and 12-month PFS rates were 47.2% vs 37.8% and 28.8% vs 14.8% for N+C vs L+C, respectively. OS rates at 6 and 12 months were 90.2% vs 87.5% and 72.5% vs 66.7% for N+C vs L+C, respectively (HR = 0.88; 95% CI 0.72–1.07; p = 0.2086). ORR in patients with measurable disease at screening was improved with N+C vs L+C (32.8% vs 26.7%; p = 0.1201), as was CBR (44.5% vs 35.6%; p = 0.0328) and DoR (HR = 0.50; 95% CI 0.33–0.74; p = 0.0004). Time to intervention for symptomatic CNS disease (overall cumulative incidence 22.8% vs 29.2%; p = 0.043) was delayed with N+C vs L+C. Treatment-emergent adverse events (TEAEs) were similar between arms, but there was a higher rate of grade 3 diarrhea with N+C vs L+C (24.4% vs 12.5%). TEAEs leading to neratinib/lapatinib discontinuation were lower with neratinib (10.9%) than with lapatinib (14.5%). Conclusions: N+C significantly improved PFS with a trend towards improved OS vs L+C. N+C also resulted in a delayed time to intervention for symptomatic CNS disease. Tolerability was similar between the two arms, with no new safety signals observed. Clinical trial information: NCT01808573.

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Crudele, Julie M., Geerte L. Van Sluis, Paris Margaritis, Joshua I. Siner, Michael Sliozberg, Jenna Maurer, Armida Faella, et al. "Insights Into the Mechanism of Zymogen Protein C Protection Against Cancer Progression." Blood 120, no. 21 (November 16, 2012): 3350. http://dx.doi.org/10.1182/blood.v120.21.3350.3350.

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Abstract Abstract 3350 Cancer is frequently associated with activation of coagulation, and a procoagulant state facilitates tumor metastasis. Recent studies have suggested that the activated protein C (aPC) pathway plays a role in modulating tumor metastasis, and this protection likely requires both the anticoagulant and cytoprotective effects of aPC. Notably, our early work revealed that the inactive precursor, zymogen PC (zyPC), can even more effectively protect against metastasis. The aim of this study was therefore to explore mechanisms through which zyPC could prevent metastatic cancer progression in a murine cancer model. A liver gene transfer model using viral vectors was utilized to achieve a wide range of sustained expression of wildtype (WT) or mutant murine zyPCs. C57BL/6 experimental mice expressing stable levels of zyPCs and age and gender matched control mice receiving PBS were injected intravenously with 2.5×105 murine melanoma B16F10 cells, which metastasize to the lungs. After 3 weeks the number of pulmonary tumors was determined. Expression of WT zyPC in C57BL/6s decreased the rates of metastasis in a dose-dependent manner compared to PBS controls (p<0.01; n=8–18/group). These effects were noted even in mice injected with low vector dose (200% zyPC expression). Conversely, when PC-deficient mice (3% of normal, n=7) were administered B16F10s without zyPC-expression, they did not survive the full 3 weeks, while their littermate controls (PC > 50% of normal, n=6) did despite high rates of metastasis. These data clearly demonstrate the protective role of zyPC in tumor progression. We then tested modified zyPCs to identify the critical functions responsible for our observations in this tumor model. Two mutants with minimal anticoagulant function, R15Q and S195A, were generated. zyPC-R15Q is unable to dock to the thrombin-thrombomodulin complex active site and so cannot be converted to aPC. Compared to PBS controls (n=7), mice expressing zyPC-R15Q still showed a significant decrease in the number of tumor foci (p<0.001; 75–99% reduction; n=13) similar to the WT zyPC (p=0.28; n=8). Mice expressing zyPC-S195A (n=12), which has a mutation in the serine protease active site, also showed a significant decrease in the number of tumor foci compared to PBS controls (n=8; p<0.05; 90–99% reduction). As with the R15Q, mutating the S195 did not affect the ability of zyPC to protect against metastasis (p=0.22). Next, we tested the importance of the main PC/aPC cellular receptors in our model. Binding to endothelial protein C receptor (EPCR) enhances activation of PC. We inhibited this binding by injecting anti-EPCR blocking antibody 1560 (J Thromb Haemost. 2005 3:1351) intraperitoneally one hour prior to the B16F10 cells. zyPC-expressing mice that received anti-EPCR antibody (n=22) still had a significant reduction in tumor rates compared to PBS controls (n=10; p<0.01; 45–75% reduction). Moreover, mice expressing zyPC had similar levels of protection whether they received the anti-EPCR antibody or an isotype control (n=22–24; p=0.31). EPCR binding not only increases activation of PC, it also mediates the cytoprotective effect by clustering with and facilitating the activation of the signaling protease-activated receptor 1 (PAR1). PAR1 −/− mice expressing zyPC (n=21) challenged with B16F10 cells still had reduced rates of metastasis compared to PAR1 −/− PBS controls (n=15; p<0.01; 67% reduction). The zyPC protection in PAR1 null mice was comparable to that in PAR1 +/− littermate controls (n=10; p=0.619). Collectively, these findings suggest a distinct mechanism by which zyPC modulates tumor progression independent of EPCR and PAR1, both of which are required for aPC-mediated protection. Despite elevated circulating levels of PC, zyPC-expressing mice did not suffer from increased blood loss following tail clipping or show prolonged activated partial thromboplastin times (aPTTs) compared to hemostatically normal mice. In conclusion, zyPC protects against metastatic cancer progression in a dose-dependent manner. Our data show for the first time that this zyPC effect is independent of its anticoagulant function. Furthermore, protection is not mediated through EPCR or PAR1, suggesting an alternative pathway by which zyPC limits tumor progression. These findings suggest that WT zyPC and variants with little to no anticoagulant function are safe and efficacious in preventing metastatic cancer progression. Disclosures: Van Sluis: PCT patent pending: Protein C: A Zymogen for Anti-Cancer Treatment Patents & Royalties. High:PCT patent pending: Protein C: A Zymogen for Anti-Cancer Treatment Patents & Royalties. Spek:PCT patent pending: Protein C: A Zymogen for Anti-Cancer Treatment Patents & Royalties. Arruda:PCT patent pending: Protein C: A Zymogen for Anti-Cancer Treatment Patents & Royalties.

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Wiench, Karin, Eva Frei, Peter Schroth, and Manfred Wiessler. "1-C-Glucuronidation of N-nitrosodiethylamine and N-nitrosomethyl-n-pentylamine in vivo and in primary hepatocytes from rats pretreated with inducers." Carcinogenesis 13, no. 5 (1992): 867–72. http://dx.doi.org/10.1093/carcin/13.5.867.

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Lee, Sang-Haak, Tingan Chen, Jun Zhou, Jennifer Hofmann, and Gerold Bepler. "Protein Kinase C-β Gene Variants, Pathway Activation, and Enzastaurin Activity in Lung Cancer." Clinical Lung Cancer 11, no. 3 (May 2010): 169–75. http://dx.doi.org/10.3816/clc.2010.n.021.

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Shi, Liu, Yu Xiong, and Xiaoyan Hu. "MicroRNA-1254 Suppresses Epithelial-Mesenchymal Transition by Upregulating c-Cellular Myelocytomatosis Oncogene (c-Myc) and Alleviates Drug Resistance in Lung Cancer." Journal of Biomaterials and Tissue Engineering 11, no. 11 (November 1, 2021): 2146–52. http://dx.doi.org/10.1166/jbt.2021.2794.

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Drug resistance is a huge challenge during the management of diseases. MicroRNA (miRNA) dys-regulation is known to contribute to tumor progression. Herein we aimed to explore miR-1254’s role in drug resistance in lung cancer. In the present study, we used Pabolizumab to treat drug-resistant and non-drug resistant lung cancer cells followed by analysis of miR-1254 expression by RT-qPCR, epithelial-mesenchymal transition (EMT) related protein and c-Myc expression by western blot, E-cadherin and N-cadherin level by immunofluorescence. Additionally, mouse model of lung cancer was treated with miR-1254 mimic and/or Pabolizumab to assess miR-1254’s role in lung cancer in vivo. Drug-resistant lung cancer cells exhibited significantly increased viability upon treatment with Pabolizumab with decreased miR-1254 expression. Besides, Pabolizumab upregulated E-caderin and downregulated N-cadherin. Importantly, miR-1254 bound to c-Myc in cancer cells. In the presence of miR-1254 mimic or siRNA (si)-c-Myc, the chemosensitivity of lung cancer cells was increased whereas miR-1254 inhibitor augmented cell resistance to Pabolizumab. Furthermore, the chemosensitivity induced by c-Myc could be depleted by miR-1254 inhibitor. Combined treatment of miR-1254 mimic and Pabolizumab significantly decreased tumor weight and volume, and reduced c-Myc level. In conclusion, miR-1254 might suppress EMT by inhibiting c-Myc expression in lung cancer and decrease drug resistance.

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Oelgeschläger, Michael, Elisabeth Kowenz-Leutz, Sabine Schreek, Achim Leutz, and Bernhard Lüscher. "Tumorigenic N-terminal deletions of c-Myb modulate DNA binding, transactivation, and cooperativity with C/EBP." Oncogene 20, no. 50 (November 2001): 7420–24. http://dx.doi.org/10.1038/sj.onc.1204922.

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Kramer, Mario W., Annika Heinisch, Gerd Wegener, Mahmoud Abbas, Inga Peters, Christoph A. J. von Klot, Hossein Tezval, Thomas R. W. Herrmann, Markus A. Kuczyk, and Axel S. Merseburger. "C-reactive protein prior to cystectomy: An external validation of the TNR-C score." Journal of Clinical Oncology 32, no. 4_suppl (February 1, 2014): 344. http://dx.doi.org/10.1200/jco.2014.32.4_suppl.344.

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344 Background: Systemic inflammation has been described as a common reaction to cancer progression. Besides other malignancies, elevated serum CRP levels have been sparsely reported in bladder cancer patients prior to treatment. The aim of this study was to analyze whether our patient cohort showed association of CRP levels and survival after radical cystectomy as well as for external validation of the recently described TNR-C score. Methods: We retrospectively reviewed charts of patients undergoing radical cystectomy and bilateral pelvic lymphadenectomy between 1996 and 2005 identifying 279 patients of which 194 had preoperative CRP levels and no concomitant infection. CRP levels were defined as elevated if they were >5 mg/l. Cancer-specific outcome was predicted based on the aforementioned CRP-based scoring model (T=T-stage; N=N-stage; R=residual tumor; C=CRP). The mean follow-up was 29 months (0-131). Results: Elevated serum CRP levels were found in 89 (45.9%) patients preoperatively. These patients were more likely to have advanced tumor stages (pT3-4; p<0.01), positive resection margins (p<0.01) and positive lymph nodes (p<0.05). Cancer specific survival was decreased by approx. 17% after 12, 36, and 60 months. In multivariate analysis, CRP was identified as an independent prognostic indicator for poor cancer-specific survival. The 3-year CSS in patients with a TNR-score in the ranges 0-2, 3-6, and 7-10 was 74.0%, 33.3%, and 4.0%, respectively (p<0.001) with a concordance index of 0,833 (p<0.001). Conclusions: Elevated preoperative CRP levels might be used in nomograms to predict poor survival after radical cystectomy. The prognostic impact of the TNR-C score could be validated. However, more evidence, especially from prospective studies is needed.

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Janku, Filip, Siqing Fu, Ravi Murthy, Daniel Karp, David Hong, Apostolia Tsimberidou, Maura Gillison, et al. "383 First-in-man clinical trial of intratumoral injection of clostridium Novyi-NT spores in combination with pembrolizumab in patients with treatment-refractory advanced solid tumors." Journal for ImmunoTherapy of Cancer 8, Suppl 3 (November 2020): A408. http://dx.doi.org/10.1136/jitc-2020-sitc2020.0383.

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BackgroundIntratumorally injected Clostridium novyi-NT (non-toxic), an attenuated strain of C. novyi that lacks production of the lethal alpha toxin, replicates within hypoxic tumor regions and elicits tumor-confined cell lysis. Early clinical and translational data suggest that intratumoral injection of C. novyi-NT is feasible, demonstrates early signals of anti-tumor activity and induction of the host immune response, which supports additional studies in combination with immune checkpoint inhibitors.MethodsThis first-in-human study (NCT03435952) enrolls patients with injectable, treatment-refractory solid tumors to receive a single intratumoral injection of C. novyi-NT across 4 dose cohorts (3 × 104 to 100 × 104 spores, 3+3 dose-escalation design) in combination with intravenous pembrolizumab 200 mg every 3 weeks for up to 24 months to determine dose-limiting toxicities (DLTs), and the maximum tolerated dose (MTD).ResultsAs of August 24, 2020, 9 patients (breast cancer, n=2; colorectal cancer, n=1; fibrous histiocytoma, n=1; anal cancer, n=1; chondrosarcoma, n=1; appendiceal cancer, n=1; tongue squamous cell cancer, n=1; nasopharyngeal cancer, n=1) were treated. There were no DLTs to date. Signs and symptoms of C. novyi-NT germination (infection) including fever, injection site pain, erythema, swelling, tenderness, and in some cases, ulceration, spontaneous drainage, tissue sloughing, bleeding, and malodor were observed in 5 patients. Partial responses were noted in 2 of 9 patients (tongue squamous cell cancer, nasopharyngeal cancer).ConclusionsSingle intratumoral injection of C. novyi-NT in combination with pembrolizumab has been demonstrating manageable toxicity profile and encouraging signals of anticancer activity. The enrolment continues.Trial RegistrationNCT03435952Ethics ApprovalThe study was approved by MD Anderson IRB

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Sofi, Firdoos Ahmad, and Prasad V. Bharatam. "Synthesis of Drugs and Biorelevant N-heterocycles Employing Recent Advances in C-N Bond Formation." Current Organic Chemistry 24, no. 20 (December 2, 2020): 2293–340. http://dx.doi.org/10.2174/1385272824999200909114144.

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C-N bond formation is a particularly important step in the generation of many biologically relevant heterocyclic molecules. Several methods have been reported for this purpose over the past few decades. Well-known named reactions like Ullmann-Goldberg coupling, Buchwald-Hartwig coupling and Chan-Lam coupling are associated with the C-N bond formation reactions. Several reviews covering this topic have already been published. However, no comprehensive review covering the synthesis of drugs/ lead compounds using the C-N bond formation reactions was reported. In this review, we cover many modern methods of the C-N bond formation reactions, with special emphasis on metal-free and green chemistry methods. We also report specific strategies adopted for the synthesis of drugs, which involve the C-N bond formation reactions. Examples include anti-cancer, antidepressant, anti-inflammatory, anti-atherosclerotic, anti-histaminic, antibiotics, antibacterial, anti-rheumatic, antiepileptic and anti-diabetic agents. Many recently developed lead compounds generated using the C-N bond formation reactions are also covered in this review. Examples include MAP kinase inhibitors, TRKs inhibitors, Polo-like Kinase inhibitors and MPS1 inhibitors.

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Sofi, Firdoos Ahmad, and Prasad V. Bharatam. "Synthesis of Drugs and Biorelevant N-heterocycles Employing Recent Advances in C-N Bond Formation." Current Organic Chemistry 24, no. 20 (October 2020): 2293–340. http://dx.doi.org/10.2174/138527282499920090911414.

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C-N bond formation is a particularly important step in the generation of many biologically relevant heterocyclic molecules. Several methods have been reported for this purpose over the past few decades. Well-known named reactions like Ullmann-Goldberg coupling, Buchwald-Hartwig coupling and Chan-Lam coupling are associated with the C-N bond formation reactions. Several reviews covering this topic have already been published. However, no comprehensive review covering the synthesis of drugs/ lead compounds using the C-N bond formation reactions was reported. In this review, we cover many modern methods of the C-N bond formation reactions, with special emphasis on metal-free and green chemistry methods. We also report specific strategies adopted for the synthesis of drugs, which involve the C-N bond formation reactions. Examples include anti-cancer, antidepressant, anti-inflammatory, anti-atherosclerotic, anti-histaminic, antibiotics, antibacterial, anti-rheumatic, antiepileptic and anti-diabetic agents. Many recently developed lead compounds generated using the C-N bond formation reactions are also covered in this review. Examples include MAP kinase inhibitors, TRKs inhibitors, Polo-like Kinase inhibitors and MPS1 inhibitors.

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Latham, Sharissa L., Yolande E. I. O'Donnell, and David R. Croucher. "Non-kinase targeting of oncogenic c-Jun N-terminal kinase (JNK) signaling: the future of clinically viable cancer treatments." Biochemical Society Transactions 50, no. 6 (December 1, 2022): 1823–36. http://dx.doi.org/10.1042/bst20220808.

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c-Jun N-terminal Kinases (JNKs) have been identified as key disease drivers in a number of pathophysiological settings and central oncogenic signaling nodes in various cancers. Their roles in driving primary tumor growth, positively regulating cancer stem cell populations, promoting invasion and facilitating metastatic outgrowth have led JNKs to be considered attractive targets for anti-cancer therapies. However, the homeostatic, apoptotic and tumor-suppressive activities of JNK proteins limit the use of direct JNK inhibitors in a clinical setting. In this review, we will provide an overview of the different JNK targeting strategies developed to date, which include various ATP-competitive, non-kinase and substrate-competitive inhibitors. We aim to summarize their distinct mechanisms of action, review some of the insights they have provided regarding JNK-targeting in cancer, and outline the limitations as well as challenges of all strategies that target JNKs directly. Furthermore, we will highlight alternate drug targets within JNK signaling complexes, including recently identified scaffold proteins, and discuss how these findings may open up novel therapeutic options for targeting discrete oncogenic JNK signaling complexes in specific cancer settings.

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Yao, Ke, Hanyong Chen, Mee-Hyun Lee, Haitao Li, Weiya Ma, Cong Peng, Nu Ry Song, et al. "Licochalcone A, a Natural Inhibitor of c-Jun N-Terminal Kinase 1." Cancer Prevention Research 7, no. 1 (November 19, 2013): 139–49. http://dx.doi.org/10.1158/1940-6207.capr-13-0117.

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Slingerland, R. J., A. H. Van Gennip, J. M. Bodlaender, P. A. Voǔte, and A. B. P. Van Kuilenburg. "Cyclopentenyl cytosine and neuroblastoma SK-N-BE(2)-C cell line cells." European Journal of Cancer 31, no. 4 (January 1995): 627–31. http://dx.doi.org/10.1016/0959-8049(95)00071-p.

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Saura, Cristina, Mafalda Oliveira, Yin-Hsun Feng, Ming-Shen Dai, Shang-Wen Chen, Sara A. Hurvitz, Sung-Bae Kim, et al. "Neratinib Plus Capecitabine Versus Lapatinib Plus Capecitabine in HER2-Positive Metastatic Breast Cancer Previously Treated With ≥ 2 HER2-Directed Regimens: Phase III NALA Trial." Journal of Clinical Oncology 38, no. 27 (September 20, 2020): 3138–49. http://dx.doi.org/10.1200/jco.20.00147.

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PURPOSE NALA (ClinicalTrials.gov identifier: NCT01808573 ) is a randomized, active-controlled, phase III trial comparing neratinib, an irreversible pan-HER tyrosine kinase inhibitor (TKI), plus capecitabine (N+C) against lapatinib, a reversible dual TKI, plus capecitabine (L+C) in patients with centrally confirmed HER2-positive, metastatic breast cancer (MBC) with ≥ 2 previous HER2-directed MBC regimens. METHODS Patients, including those with stable, asymptomatic CNS disease, were randomly assigned 1:1 to neratinib (240 mg once every day) plus capecitabine (750 mg/m2 twice a day 14 d/21 d) with loperamide prophylaxis, or to lapatinib (1,250 mg once every day) plus capecitabine (1,000 mg/m2 twice a day 14 d/21 d). Coprimary end points were centrally confirmed progression-free survival (PFS) and overall survival (OS). NALA was considered positive if either primary end point was met (α split between end points). Secondary end points were time to CNS disease intervention, investigator-assessed PFS, objective response rate (ORR), duration of response (DoR), clinical benefit rate, safety, and health-related quality of life (HRQoL). RESULTS A total of 621 patients from 28 countries were randomly assigned (N+C, n = 307; L+C, n = 314). Centrally reviewed PFS was improved with N+C (hazard ratio [HR], 0.76; 95% CI, 0.63 to 0.93; stratified log-rank P = .0059). The OS HR was 0.88 (95% CI, 0.72 to 1.07; P = .2098). Fewer interventions for CNS disease occurred with N+C versus L+C (cumulative incidence, 22.8% v 29.2%; P = .043). ORRs were N+C 32.8% (95% CI, 27.1 to 38.9) and L+C 26.7% (95% CI, 21.5 to 32.4; P = .1201); median DoR was 8.5 versus 5.6 months, respectively (HR, 0.50; 95% CI, 0.33 to 0.74; P = .0004). The most common all-grade adverse events were diarrhea (N+C 83% v L+C 66%) and nausea (53% v 42%). Discontinuation rates and HRQoL were similar between groups. CONCLUSION N+C significantly improved PFS and time to intervention for CNS disease versus L+C. No new N+C safety signals were observed.

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Nierenberg, Jovia L., Linda Kachuri, Taylor B. Cavazos, Rebecca E. Graff, Thomas J. Hoffmann, Jie Zhang, Stacey Alexeeff, et al. "Abstract 1446: Genetic risk factors for the development of multiple primary cancers." Cancer Research 82, no. 12_Supplement (June 15, 2022): 1446. http://dx.doi.org/10.1158/1538-7445.am2022-1446.

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Abstract Introduction: Individuals with one cancer are at greater risk of new primary cancers than the general population. While several hereditary cancer syndromes are known, genetic risk factors for multiple primary cancers in an individual are not well understood. Identification of susceptibility variants to multiple primary tumors could enhance screening for subsequent cancers among those at highest risk. Methods: We conducted a pan-cancer genome-wide association study (GWAS) of multiple primary cancers among participants from 2 prospective cohorts: Kaiser Permanente and the UK Biobank. The primary GWAS within cohorts used logistic regression to estimate associations for diagnosis with ≥2 invasive or in situ primary cancers other than non-melanoma skin (N=11,773, 8,928 invasive only) compared to cancer-free controls (N=420,101). Case-case analyses were conducted to distinguish associations with multiple cancers from single-cancer (N=90,576) susceptibility signals. Regression models were adjusted for age, sex, first 10 genetic ancestry principal components, and array. Cohort-specific GWAS results were meta-analyzed. We highlight genome-wide significant (p<5×10-8) results with consistent effect direction across the 2 studies. Results: We identified 8 variants associated with multiple primary cancers. Discussion: To our knowledge, rs192703567 has no previous cancer associations. Three identified variants are in known cancer predisposition genes (rs2293607 in TERC, rs6983267 in CASC8, rs35850753 in TP53). Three variants (rs34379047, rs612611, and rs9419958) are previously associated with multiple cancers, 2 (rs2293607 and rs6983267) with cancer pleiotropy, and 2 (rs283732 and rs35850753) with individual cancers. Most variants from the cancer-free control analyses had consistent effects in the single-cancer case-case analyses, suggesting pleiotropic mechanisms. Our preliminary findings offer insight into genetic risk factors associated with developing multiple primary cancers. Multiple vs. none Multiple invasive vs. none Multiple vs. single Multiple invasive vs. single Chr Position rsID A1 A2 Gene OR P OR P OR P OR P 3 169482335 rs2293607 T C TERC 1.11 1.0×10-9 1.10 2.2×10-7 1.06 2.0×10-3 1.05 0.01 8 128281644 rs283732 C T Intergenic 1.09 2.3×10-7 1.11 9.2×10-9 1.06 3.8×10-4 1.09 3.9×10-5 8 128413305 rs6983267 G T CASC8 POU5F1B CCAT2 PCAT1 1.08 4.1×10-7 1.09 2.9×10-8 1.00 0.83 1.02 0.34 10 105644473 rs34379047 T A OBFC1 1.16 8.5×10-12 1.19 6.0×10-11 1.19 2.3×10-4 1.10 4.0×10-4 10 105675946 rs9419958 T C STN1 1.14 1.8×10-11 1.16 4.5×10-11 1.08 3.1×10-4 1.09 2.8×10-4 11 69307463 rs612611 G A Intergenic 1.11 3.7×10-8 1.10 5.3×10-6 1.06 9.6×10-4 1.05 0.02 17 7578671 rs35850753 T C TP53 1.27 4.9×10-7 1.34 1.6×10-8 1.16 2.8×10-3 1.24 8.8×10-5 22 40738280 rs192703567 C T Intergenic 1.37 5.2×10-8 1.37 1.8×10-6 1.43 4.9×10-9 1.43 2.8×10-7 Chr=Chromosome; A1=Effect allele; A2=Other allele; OR=Odds ratio. Citation Format: Jovia L. Nierenberg, Linda Kachuri, Taylor B. Cavazos, Rebecca E. Graff, Thomas J. Hoffmann, Jie Zhang, Stacey Alexeeff, Laurel Habel, Douglas Corley, Stephen Van Den Eeden, Elad Ziv, Lori C. Sakoda, John S. Witte. Genetic risk factors for the development of multiple primary cancers [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2022; 2022 Apr 8-13. Philadelphia (PA): AACR; Cancer Res 2022;82(12_Suppl):Abstract nr 1446.

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Satoi, S., H. Yanagimoto, S. Takai, H. Toyokawa, K. Takahashi, N. Terakawa, T. Yamamoto, and Y. Kamiyama. "Circulating dendritic cell as a new prognostic factor in pancreatic cancer patients." Journal of Clinical Oncology 24, no. 18_suppl (June 20, 2006): 4095. http://dx.doi.org/10.1200/jco.2006.24.18_suppl.4095.

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4095 Background: Pancreatic cancer is a cancer with very poor prognosis that might be associated with impaired immune defense. Dendritic cells (DC) are important for immune surveillance and play a central role in protection against infection and malignancy. A defective host antitumor immune response may allow tumor cells to escape from the host immune system. The aim of this study is to determine whether circulating DC could be one of new immunological markers that may predict the prognosis of the pancreatic cancer. Methods: We evaluated pretreatment circulating myeloid-lineage DC (C-DC1) rate in the peripheral blood mononuclear cell and various clinical parameters to determine their prognostic value in 104 pancreatic cancer patients (41 resected and 63 unresected patients) seen at our institution. Results: In unresected patients, univariate analysis demonstrated two risk factors for prognosis of albmin < 3.8g/dl (p = 0.0468), and C-DC1 < 0.27% (p = 0.0006), when all patients were divided by the median value of C-DC1 rate. Consequently, multivariate analysis demonstrated that only C-DC1 was a predominant independent predictor of survival (Hazard ratio; 9.330, 95% Confidential interval; 2.595–33.549, p = 0.0006). In resected patients, C-DC1 in patients with advanced disease (Stages 2b-4, n=28) was significantly lower than that in patients with lower staged cancer (Stage 1–2a, n = 13: 0.43 ± 0.67%, Stage 2b-4: 0.24 ± 0.30%, p < 0.05). The overall survival rates in patients with C-DC1 ≥ 0.27% were significantly longer than those in patients with C-DC1 < 0.27 (C-DC1 ≥ 0.27%, n = 20, 1/3 year survival: 100%/64%. C-DC1 < 0.27, n = 21, 1/3 year survival: 68%/26%. P < 0.05). Conclusions: The C-DC1 less than 0.27% could be one of prognostic factors in patients with pancreatic cancer, and such patients could be targets for the future therapeutic trials. No significant financial relationships to disclose.

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