Annual Review of Medicine
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CAR T Cell Therapy for Solid Tumors The field of cancer immunotherapy has been re-energized by the application of chimeric antigen receptor (CAR) T cell therapy in cancers. These CAR T cells are engineered to express synthetic receptors that redirect polyclonal T cells to surface antigens for subsequent tumor elimination. Many CARs are designed with elements that augment T cell persistence and activity. To date, CAR T cells have demonstrated tremendous success in eradicating hematologic malignancies (e.g., CD19 CARs in leukemias). However, this success has yet to be extrapolated to solid tumors, and the reasons for this are being actively investigated. We characterize some of the challenges that CAR T cells have to surmount in the solid tumor microenvironment and new approaches that are being considered to overcome these hurdles.
Annual Review of Medicine - Tập 68 Số 1 - Trang 139-152 - 2017
Aspirin in the Prevention of Cardiovascular Disease and Cancer More than a century after its synthesis, daily aspirin, given at a low dose, is a milestone treatment for the secondary prevention of cardiovascular disease (CVD). Its role in primary prevention of CVD is still debated. Older randomized controlled trials showed that aspirin reduced the low incidence of myocardial infarction but correspondingly increased the low incidence of serious gastrointestinal bleeds without altering mortality. More recent trials see the benefit attenuated, perhaps obscured by other cardioprotective practices, while the bleeding risk remains, especially in older patients. Indirect evidence, both preclinical and clinical, suggests that aspirin may protect against sporadic colorectal cancer and perhaps other cancers. However, further studies are still necessary to warrant the consumption of aspirin for primary prevention of CVD and cancer by apparently healthy individuals.
Annual Review of Medicine - Tập 72 Số 1 - Trang 473-495 - 2021
RU486 (MIFEPRISTONE): Mechanisms of Action and Clinical Uses ▪ Abstract RU486 (mifepristone) has proved to be a remarkably active antiprogesterone and antiglucocorticosteroid agent in human beings. The mechanism of action involves the intracellular receptors of the antagonized hormones (progesterone and glucocorticosteroids). At the molecular level, the most important features are high binding affinity to the receptor, interaction of the phenylaminodimethyl group in the 11β-position with a specific region of the receptor binding pocket, and RU486-induced transconformation differences in the ligand-binding domain. These particularities have consequences at different steps of the receptor function as compared with agonists. However, the reasoning cannot be limited to the RU486-receptor interaction, and, for instance, there is the possibility of a switch from antagonistic property to agonist activity, depending on the intervention of other signaling pathways. It would be desirable to have derivatives with only one of the two antagonistic properties (antiprogestin, antiglucocorticosteroid) in spite of similarities between steroid structures, receptors involved, and responsive machineries in target cells. Clinically, the RU486-plus-prostaglandin method is ready to be used on a large scale and is close to being as convenient and safe as any medical method of abortion may be. The early use of RU486 as a contragestive as soon as a woman fears a pregnancy she does not want will help to defuse the abortion issue. Research should now be conducted to define an efficient and convenient contraceptive method with RU486 or other antiprogestins. The usefulness of RU486 for obstetric indications, including facilitation of difficult delivery, has to be assessed rapidly. Gynecologic trials, particularly in leiomyomata, should also be systematically continued. The very preliminary results obtained with tumors, including breast cancers, indicate that further studies are necessary.
Annual Review of Medicine - Tập 48 Số 1 - Trang 129-156 - 1997
Mechanisms of Cancer Drug Resistance ▪ Abstract The design of cancer chemotherapy has become increasingly sophisticated, yet there is no cancer treatment that is 100% effective against disseminated cancer. Resistance to treatment with anticancer drugs results from a variety of factors including individual variations in patients and somatic cell genetic differences in tumors, even those from the same tissue of origin. Frequently resistance is intrinsic to the cancer, but as therapy becomes more and more effective, acquired resistance has also become common. The most common reason for acquisition of resistance to a broad range of anticancer drugs is expression of one or more energy-dependent transporters that detect and eject anticancer drugs from cells, but other mechanisms of resistance including insensitivity to drug-induced apoptosis and induction of drug-detoxifying mechanisms probably play an important role in acquired anticancer drug resistance. Studies on mechanisms of cancer drug resistance have yielded important information about how to circumvent this resistance to improve cancer chemotherapy and have implications for pharmacokinetics of many commonly used drugs.
Annual Review of Medicine - Tập 53 Số 1 - Trang 615-627 - 2002
Growth Considerations in the Radiation Therapy of Children with Cancer
Annual Review of Medicine - Tập 30 Số 1 - Trang 405-415 - 1979
Growth and Physiological Development During Adolescence
Annual Review of Medicine - Tập 19 Số 1 - Trang 283-300 - 1968
HUMAN LYMPHOCYTE AND LYMPHOMA HOMING RECEPTORS
Annual Review of Medicine - Tập 38 Số 1 - Trang 467-476 - 1987
PROGNOSIS IN CONGESTIVE HEART FAILURE ▪ Abstract Prognostic variables such as the ejection fraction and peak oxygen consumption can be used to place patients with heart failure in risk strata. Some vasodilators have been shown to improve survival at all stages of heart failure with the probability of benefit increasing as the prognosis worsens. Quantitative estimates of survival among groups defined by prognostic variables and treatments should be used to make more informed benefit-to-risk assessments.
Annual Review of Medicine - Tập 45 Số 1 - Trang 341-350 - 1994
HIGH-ALTITUDE PULMONARY EDEMA: Current Concepts ▪ Abstract High-altitude pulmonary edema (HAPE) occurs in unacclimatized individuals who are rapidly exposed to altitudes in excess of 2450 m. It is commonly seen in climbers and skiers who ascend to high altitude without previous acclimatization. Initial symptoms of dyspnea, cough, weakness, and chest tightness appear, usually within 1–3 days after arrival. Common physical signs are tachypnea, tachycardia, rales, and cyanosis. Descent to a lower altitude, nifedipine, and oxygen administration result in rapid clinical improvement. Physiologic studies during the acute stage have revealed a normal pulmonary artery wedge pressure, marked elevation of pulmonary artery pressure, severe arterial unsaturation, and usually a low cardiac output. Pulmonary arteriolar (precapillary) resistance is elevated. A working hypothesis of the etiology of HAPE suggests that hypoxic pulmonary vasoconstriction is extensive but not uniform. The result is overperfusion of the remaining patent vessels with transmission of the high pulmonary artery pressure to capillaries. Dilatation of the capillaries and high flow results in capillary injury, with leakage of protein and red cells into the alveoli and airways. HAPE represents one of the few varieties of pulmonary edema where left ventricular filling pressure is normal.
Annual Review of Medicine - Tập 47 Số 1 - Trang 267-284 - 1996
The Expanded Biology of Serotonin Serotonin is perhaps best known as a neurotransmitter that modulates neural activity and a wide range of neuropsychological processes, and drugs that target serotonin receptors are used widely in psychiatry and neurology. However, most serotonin is found outside the central nervous system, and virtually all of the 15 serotonin receptors are expressed outside as well as within the brain. Serotonin regulates numerous biological processes including cardiovascular function, bowel motility, ejaculatory latency, and bladder control. Additionally, new work suggests that serotonin may regulate some processes, including platelet aggregation, by receptor-independent, transglutaminase-dependent covalent linkage to cellular proteins. We review this new “expanded serotonin biology” and discuss how drugs targeting specific serotonin receptors are beginning to help treat a wide range of diseases.
Annual Review of Medicine - Tập 60 Số 1 - Trang 355-366 - 2009
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