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One of the leading causes of death worldwide these days is cancer, and new anticancer drugs have been developed to treat it with all the vigor of advancement of science and technology. Unfortunately, these drugs are very expensive and besides they cause great economic hardship for cancer patients, and society as a whole. On the other hand, the deployment of hazardous chemicals, and especially the common commercial solvents in the production of anti-cancer drugs, causes environmental pollution thus contributing to the drug purification costs. Herein, recent FDA-approved anticancer drugs in 2020-2021, their mechanism of action, financial challenges, and associated environmental hazards are deliberated, with possible solutions that may reduce not only the costs of the drugs but also the environmental pollution involved in synthesis of anticancer drugs via greener pathways by appropriate substitution

This article is from Pharmaceuticals , volume 3 . Abstract There is compelling evidence that nonsteroidal anti-inflammatory drugs (NSAIDs) and cyclooxygenase-2 selective inhibitors have antineoplastic activity, but toxicity from cyclooxygenase (COX) inhibition and the suppression of physiologically important prostaglandins limits their use for cancer chemoprevention. Previous studies as reviewed here suggest that the mechanism for their anticancer properties does not require COX inhibition, but instead involves an off-target effect. In support of this possibility, recent molecular modeling studies have shown that the NSAID sulindac can be chemically modified to selectively design out its COX-1 and COX-2 inhibitory activity. Unexpectedly, certain derivatives that were synthesized based on in silico modeling displayed increased potency to inhibit tumor cell growth. Other experiments have shown that sulindac can inhibit phosphodiesterase to increase intracellular cyclic GMP levels and that this activity is closely associated with its ability to selectively induce apoptosis of tumor cells. Together, these studies suggest that COX-independent mechanisms can be targeted to develop safer and more efficacious drugs for cancer chemoprevention.

This article is from Pharmaceuticals , volume 3 . Abstract There is compelling evidence that nonsteroidal anti-inflammatory drugs (NSAIDs) and cyclooxygenase-2 selective inhibitors have antineoplastic activity, but toxicity from cyclooxygenase (COX) inhibition and the suppression of physiologically important prostaglandins limits their use for cancer chemoprevention. Previous studies as reviewed here suggest that the mechanism for their anticancer properties does not require COX inhibition, but instead involves an off-target effect. In support of this possibility, recent molecular modeling studies have shown that the NSAID sulindac can be chemically modified to selectively design out its COX-1 and COX-2 inhibitory activity. Unexpectedly, certain derivatives that were synthesized based on in silico modeling displayed increased potency to inhibit tumor cell growth. Other experiments have shown that sulindac can inhibit phosphodiesterase to increase intracellular cyclic GMP levels and that this activity is closely associated with its ability to selectively induce apoptosis of tumor cells. Together, these studies suggest that COX-independent mechanisms can be targeted to develop safer and more efficacious drugs for cancer chemoprevention.

Investigational New Drugs the Journal of New Anticancer Agents 2004: Volume 22 , Issue CONTENTS. Digitized from IA1631514-06 . Previous issue: sim_investigational-new-drugs_2002-11_20_4 . Next issue: sim_investigational-new-drugs_2004-01_22_1 . Note: This issue has no cover

Investigational New Drugs the Journal of New Anticancer Agents 1989: Volume 7 , Issue CONTENTS. Digitized from IA1631514-06 . Next issue: sim_investigational-new-drugs_1989-04_7_1 . Note: This issue has no cover

Investigational New Drugs the Journal of New Anticancer Agents 1989: Volume 7 , Issue CONTENTS. Digitized from IA1631514-06 . Next issue: sim_investigational-new-drugs_1989-04_7_1 . Note: This issue has no cover

Investigational New Drugs the Journal of New Anticancer Agents 1991: Volume 9 , Issue CONTENTS. Digitized from IA1631514-06 . Previous issue: sim_investigational-new-drugs_1990_8_supplement . Next issue: sim_investigational-new-drugs_1991-02_9_1 . Note: This issue has no cover

Investigational New Drugs the Journal of New Anticancer Agents 1997: Volume 15 , Issue CONTENTS. Digitized from IA1631514-06 . Previous issue: sim_investigational-new-drugs_1996_14_4 . Next issue: sim_investigational-new-drugs_1997_15_1 . Note: This issue has no cover

Investigational New Drugs the Journal of New Anticancer Agents 1990: Volume 8 , Issue CONTENTS. Digitized from IA1631514-06 . Previous issue: sim_investigational-new-drugs_1989-11_7_4 . Next issue: sim_investigational-new-drugs_1990-02_8_1 . Note: This issue has no cover

Investigational New Drugs the Journal of New Anticancer Agents 1990: Volume 8 , Issue CONTENTS. Digitized from IA1631514-06 . Previous issue: sim_investigational-new-drugs_1989-11_7_4 . Next issue: sim_investigational-new-drugs_1990-02_8_1 . Note: This issue has no cover

Investigational New Drugs the Journal of New Anticancer Agents 1999: Volume 17 , Issue CONTENTS. Digitized from IA1631514-06 . Previous issue: sim_investigational-new-drugs_1999_16_4 . Next issue: sim_investigational-new-drugs_1999_17_1 . Note: This issue has no cover

Investigational New Drugs the Journal of New Anticancer Agents 1995 - 1996: Volume 13 , Issue CONTENTS. Digitized from IA1631514-06 . Previous issue: sim_investigational-new-drugs_1994_12_4 . Next issue: sim_investigational-new-drugs_1995_13_1 . Note: This issue has no cover

Investigational New Drugs the Journal of New Anticancer Agents 2000: Volume 18 , Issue CONTENTS. Digitized from IA1631514-06 . Previous issue: sim_investigational-new-drugs_1999_17_4 . Next issue: sim_investigational-new-drugs_2000-02_18_1 . Note: This issue has no cover

This article is from Journal of Translational Medicine , volume 11 . Abstract In recent years an increasing number of publications have emphasized the growing importance of hydrogen ion dynamics in modern cancer research, from etiopathogenesis and treatment. A proton [H+]-related mechanism underlying the initiation and progression of the neoplastic process has been recently described by different research groups as a new paradigm in which all cancer cells and tissues, regardless of their origin and genetic background, have a pivotal energetic and homeostatic disturbance of their metabolism that is completely different from all normal tissues: an aberrant regulation of hydrogen ion dynamics leading to a reversal of the pH gradient in cancer cells and tissues (↑pHi/↓pHe, or “proton reversal”). Tumor cells survive their hostile microenvironment due to membrane-bound proton pumps and transporters, and their main defensive strategy is to never allow internal acidification because that could lead to their death through apoptosis. In this context, one of the primary and best studied regulators of both pHi and pHe in tumors is the Na+/H+ exchanger isoform 1 (NHE1). An elevated NHE1 activity can be correlated with both an increase in cell pH and a decrease in the extracellular pH of tumors, and such proton reversal is associated with the origin, local growth, activation and further progression of the metastatic process. Consequently, NHE1 pharmaceutical inhibition by new and potent NHE1 inhibitors represents a potential and highly selective target in anticancer therapy. Cariporide, being one of the better studied specific and powerful NHE1 inhibitors, has proven to be well tolerated by humans in the cardiological context, however some side-effects, mainly related to drug accumulation and cerebrovascular complications were reported. Thus, cariporide could become a new, slightly toxic and effective anticancer agent in different human malignancies.

Engineered transfer RNAs (tRNA) can be used to reprogram the genetic code and synthesize proteins of interest with new cellular properties. We developed a new class of tRNA mutants that promote numerous and harmful amino acid substitutions upon entering human cells and induce apoptosis. Our objective is to target this tRNA prototype (called killer-tRNA) specifically to cancer cells but sparing healthy blood stem cells and progenitors thereby developing the killer-tRNA as a potential therapeutic agent. Because the killer tRNAs share the exact same feature as all cellular tRNAs, they are undetectable and cannot be cleared by any defense mechanism, thereby constituting a perfect molecular Trojan horse for cell damage and cell death. We aim to test nanocarriers containing killer-tRNAs to human blood cancer cells (acute myeloid leukemia and multiple myeloma) via the high-affinity folate receptors. Since the action of the killer-tRNA is on the synthesis of cellular proteins, it is not restricted to specific stages of cancer. Killer-tRNA can be used to reduce growth of the primary tumor, limit metastatic spread or target tumors at anatomical sites where surgery is difficult to perform.

Investigational New Drugs the Journal of New Anticancer Agents 1996: Volume 14 , Issue CONTENTS. Digitized from IA1631514-06 . Previous issue: sim_investigational-new-drugs_1995-1996_13_4 . Next issue: sim_investigational-new-drugs_1996_14_1 . Note: This issue has no cover

Investigational New Drugs the Journal of New Anticancer Agents 1992: Volume 10 , Issue CONTENTS. Digitized from IA1631514-06 . Previous issue: sim_investigational-new-drugs_1991-11_9_4 . Next issue: sim_investigational-new-drugs_1992-04_10_1 . Note: This issue has no cover

Investigational New Drugs the Journal of New Anticancer Agents 2001: Volume 19 , Issue CONTENTS. Digitized from IA1631514-06 . Previous issue: sim_investigational-new-drugs_2000-11_18_4 . Next issue: sim_investigational-new-drugs_2001-02_19_1 . Note: This issue has no cover

Investigational New Drugs the Journal of New Anticancer Agents 2005: Volume 23 , Issue CONTENTS. Digitized from IA1631514-06 . Previous issue: sim_investigational-new-drugs_2004-11_22_4 . Next issue: sim_investigational-new-drugs_2005-01_23_1 . Note: This issue has no cover

Investigational New Drugs the Journal of New Anticancer Agents 1993: Volume 11 , Issue CONTENTS. Digitized from IA1631514-06 . Previous issue: sim_investigational-new-drugs_1992-11_10_4 . Next issue: sim_investigational-new-drugs_1993-02_11_1 . Note: This issue has no cover

Investigational New Drugs the Journal of New Anticancer Agents 1998 - 1999: Volume 16 , Issue CONTENTS. Digitized from IA1631514-06 . Previous issue: sim_investigational-new-drugs_1997_15_4 . Next issue: sim_investigational-new-drugs_1998_16_1 . Note: This issue has no cover

Investigational New Drugs the Journal of New Anticancer Agents 2002: Volume 20 , Issue CONTENTS. Digitized from IA1631514-06 . Previous issue: sim_investigational-new-drugs_2001-11_19_4 . Next issue: sim_investigational-new-drugs_2002-02_20_1 . Note: This issue has no cover

Investigational New Drugs the Journal of New Anticancer Agents 1994: Volume 12 , Issue CONTENTS. Digitized from IA1631514-06 . Previous issue: sim_investigational-new-drugs_1993-11_11_4 . Next issue: sim_investigational-new-drugs_1994_12_1 . Note: This issue has no cover