Question: Give the name of the relatively new class of cancer drugs that can overcome many of the issues seen with the use of cytotoxics?
About the article "Chemotherapy", section "Cytotoxics and targeted therapies".

Candidate passages:
Targeted therapies are a relatively new class of cancer drugs that can overcome many of the issues seen with the use of cytotoxics.
They are divided into two groups: small molecule and antibodies.
The massive toxicity seen with the use of cytotoxics is due to the lack of cell specificity of the drugs.
They will kill any rapidly dividing cell, tumor or normal.
Targeted therapies are designed to affect cellular proteins or processes that are utilised by the cancer cells.
This allows a high dose to cancer tissues with a relatively low dose to other tissues.
As different proteins are utilised by different cancer types, the targeted therapy drugs are used on a cancer type specific, or even on a patient specific basis.
Although the side effects are often less severe than that seen of cytotoxic chemotherapeutics, life-threatening effects can occur.
Initially, the targeted therapeutics were supposed to be solely selective for one protein.
Now it is clear that there is often a range of protein targets that the drug can bind.
An example target for targeted therapy is the protein produced by the Philadelphia chromosome, a genetic lesion found commonly in chronic myelomonocytic leukemia.
This fusion protein has enzyme activity that can be inhibited by imatinib, a small molecule drug.
Ruthenium has numerous properties that qualify it as an antineoplastic drug contender.
While platinum-based compounds have served as very successful anti-cancer drugs, they have several limitations including their side effects, as well as ineffectiveness against certain types of cancer.
It is thought that some of these issues can be resolved with the use of a ruthenium substitute.
Though most ruthenium complexes are only in the beginning stages of become approved anti-cancer drugs, many of their properties give it promising advantages over many platinum based drugs now in use. 
Healthcare workers exposed to anti-neoplastic agents take precautions to keep their exposure to a minimum.
There is a limitation in cytotoxics dissolution in Australia and the United States to 20 dissolutions per pharmacist/nurse, since pharmacists that prepare these drugs or nurses that may prepare or administer them are the two occupational groups with the highest potential exposure to antineoplastic agents.
In addition, physicians and operating room personnel may also be exposed through the treatment of patients.
Hospital staff, such as shipping and receiving personnel, custodial workers, laundry workers, and waste handlers, all have potential exposure to these drugs during the course of their work.
The increased use of antineoplastic agents in veterinary oncology also puts these workers at risk for exposure to these drugs.
Routes of entry into the users body are skin absorption, inhalation and ingestion.
The long term effects of exposure include chromosomal abnormalities and infertility. 
Many different topical and systemic medications have been studied, including anti-inflammatories, antimycotics (target Candida species), carotenoids (precursors to vitamin A, e.g.
beta carotene), retinoids (drugs similar to vitamin A), and cytotoxics, but none have evidence that they prevent malignant transformation in an area of leukoplakia.
Vitamins C and E have also been studied with regards a therapy for leukoplakia.
Some of this research is carried out based upon the hypothesis that antioxidant nutrients, vitamins and cell growth suppressor proteins (e.g.
p53) are antagonistic to oncogenesis.
High doses of retinoids may cause toxic effects.
Other treatments that have been studied include photodynamic therapy. 
While the role in folate as a cancer treatment is well established, its long-term effectiveness is diminished by cellular response.
In response to decreased tetrahydrofolate (THF), the cell begins to transcribe more DHF reductase, the enzyme that reduces DHF to THF.
Because methotrexate is a competitive inhibitor of DHF reductase, increased concentrations of DHF reductase can overcome the drugs inhibition.
Many new drugs are under development to reduce antifolate drug resistance.