0
ARTICLE |

Oncology FREE

Judith E. Karp, MD; Samuel Broder, MD
JAMA. 1992;268(3):391-393. doi:10.1001/jama.1992.03490030103045
Text Size: A A A
Published online

Molecular oncology continues to unravel the fundamental interplay among normally occurring, growth-promoting genes (oncogenes), tumor suppressor genes, and cell cycle regulators that determines the balance between cellular growth and differentiation. Mechanisms that perturb this balance can result in malignant transformation and increasingly serve as molecular targets for manipulation.

Recent innovations in molecular technology provide an increasingly sensitive dissection of the normal mechanisms by which tumor suppressor genes modulate cell growth. For example, the protein product of the tumor suppressor gene p53 (located on the short arm of chromosome 17, 17p13) may exert its net growth inhibitory activity by binding to (and altering the function of) specific sequences of DNA.1,2 In response to certain types of DNA damage (eg, UV light), the p53 protein is upregulated, prolonging the G1 phase of the cell cycle and allowing the cell time to repair DNA breaks.3 Cells with aberrant net p53 expression

REFERENCES

Hollstein M, Sidransky D, Vogelstein B, Harris CC.  p53 mutations in human cancers. Science . 1991;;253:49-53.
Levine AJ, Momand J, Finlay CA.  The p53 tumour suppressor gene. Nature . 1991;;351:453-455.
Kastan MB, Onyekwere O, Sidransky D, Vogelstein B, Craig RW.  Participation of p53 protein in the cellular response to DNA damage. Cancer Res . 1991;;51:6304-6311.
Malkin D, Li FP, Strong LC, et al.  Germ line p53 mutations in a familial syndrome of breast cancer, sarcomas, and other neoplasms. Science . 1990;;250:1233-1238.
Brash DE, Rudolph JA, Simon JA, et al.  A role for sunlight in skin cancer: UV-induced p53 mutations in squamous cell carcinoma. Proc Natl Acad Sci U S A . 1991;;88:10124-10128.
Gaidano G, Ballerini P, Gong JZ, et al.  p53 mutations in human lymphoid malignancies: association with Burkitt lymphoma and chronic lymphocytic leukemia. Proc Natl Acad Sci U S A . 1991;;88: 5413-5417.
Hall JM, Lee MK, Newman B, et al.  Linkage of early-onset familial breast cancer to chromosome 17q21. Science . 1990;;250:1684-1689.
Wakefield LM, Sporn MB.  Suppression of carcinogenesis: a role for TGF-beta and related molecules in prevention of cancer.  In: Klein G, ed. Tumor Suppressor Genes . New York, NY: Marcel Dekker, Inc.; 1990;:217-243.
Early Breast Cancer Trialists' Collaborative Group.  Systemic treatment of early breast cancer by hormonal, cytotoxic, or immune therapy. Lancet . 1992;;339:1-15, 71-85.
Groden J, Thliveris A, Samowitz W, et al.  Identification and characterization of the familial adenomatous polyposis coli gene. Cell . 1991;;66:589-600.
Kinzler KW, Nilbert MC, Su L-K, et al.  Identification of FAP locus genes from chromosome 5q21. Science . 1991;;253:661-665.
Nishisho I, Nakamura Y, Miyoshi Y, et al.  Mutations of chromosome 5q21 genes in FAP and colorectal cancer patients. Science . 1991;;253:665-669.
Holmes FA, Walters RS, Theriault RL, et al.  Phase II trial of taxol, an active drug in the treatment of metastatic breast cancer. J Natl Cancer Inst . 1991;;83:1797-1805.
Ringel I, Horwitz SB.  Studies with RP56976 (taxotere): a semisynthetic analogue of taxol. J Natl Cancer Inst . 1991;;83:288-291.
Golumbek PT, Lazenby AJ, Levitsky HI, et al.  Treatment of established renal cell cancer by tumor cells engineered to secrete interleukin-4. Science . 1991;;254:713-716.
Asher AL, Mule JJ, Kasid A, et al.  Murine tumor cells transduced with the gene for tumor necrosis factor-alpha. J Immunol . 1991;;146:3227-3234.

Figures

Tables

Interactive Graphics

Video

Country-Specific Mortality and Growth Failure in Infancy and Yound Children and Association With Material Stature

Use interactive graphics and maps to view and sort country-specific infant and early dhildhood mortality and growth failure data and their association with maternal

Hollstein M, Sidransky D, Vogelstein B, Harris CC.  p53 mutations in human cancers. Science . 1991;;253:49-53.
Levine AJ, Momand J, Finlay CA.  The p53 tumour suppressor gene. Nature . 1991;;351:453-455.
Kastan MB, Onyekwere O, Sidransky D, Vogelstein B, Craig RW.  Participation of p53 protein in the cellular response to DNA damage. Cancer Res . 1991;;51:6304-6311.
Malkin D, Li FP, Strong LC, et al.  Germ line p53 mutations in a familial syndrome of breast cancer, sarcomas, and other neoplasms. Science . 1990;;250:1233-1238.
Brash DE, Rudolph JA, Simon JA, et al.  A role for sunlight in skin cancer: UV-induced p53 mutations in squamous cell carcinoma. Proc Natl Acad Sci U S A . 1991;;88:10124-10128.
Gaidano G, Ballerini P, Gong JZ, et al.  p53 mutations in human lymphoid malignancies: association with Burkitt lymphoma and chronic lymphocytic leukemia. Proc Natl Acad Sci U S A . 1991;;88: 5413-5417.
Hall JM, Lee MK, Newman B, et al.  Linkage of early-onset familial breast cancer to chromosome 17q21. Science . 1990;;250:1684-1689.
Wakefield LM, Sporn MB.  Suppression of carcinogenesis: a role for TGF-beta and related molecules in prevention of cancer.  In: Klein G, ed. Tumor Suppressor Genes . New York, NY: Marcel Dekker, Inc.; 1990;:217-243.
Early Breast Cancer Trialists' Collaborative Group.  Systemic treatment of early breast cancer by hormonal, cytotoxic, or immune therapy. Lancet . 1992;;339:1-15, 71-85.
Groden J, Thliveris A, Samowitz W, et al.  Identification and characterization of the familial adenomatous polyposis coli gene. Cell . 1991;;66:589-600.
Kinzler KW, Nilbert MC, Su L-K, et al.  Identification of FAP locus genes from chromosome 5q21. Science . 1991;;253:661-665.
Nishisho I, Nakamura Y, Miyoshi Y, et al.  Mutations of chromosome 5q21 genes in FAP and colorectal cancer patients. Science . 1991;;253:665-669.
Holmes FA, Walters RS, Theriault RL, et al.  Phase II trial of taxol, an active drug in the treatment of metastatic breast cancer. J Natl Cancer Inst . 1991;;83:1797-1805.
Ringel I, Horwitz SB.  Studies with RP56976 (taxotere): a semisynthetic analogue of taxol. J Natl Cancer Inst . 1991;;83:288-291.
Golumbek PT, Lazenby AJ, Levitsky HI, et al.  Treatment of established renal cell cancer by tumor cells engineered to secrete interleukin-4. Science . 1991;;254:713-716.
Asher AL, Mule JJ, Kasid A, et al.  Murine tumor cells transduced with the gene for tumor necrosis factor-alpha. J Immunol . 1991;;146:3227-3234.
CME Course for:


You need to register in order to view this quiz.


To understand the clinical management of acute heart failure syndromes.
Accreditation Information The American Medical Association is accredited by the Accreditation Council for Continuing Medical Education to provide continuing medical education for physicians.
The AMA designates this journal-based CME activity for a maximum of 1 AMA PRA Category 1 CreditTM per course. Physicians should claim only the credit commensurate with the extent of their participation in the activity.
Physicians who complete the CME course and score at least 80% correct on the quiz are eligible for AMA PRA Category 1 CreditTM.
Note: You must get at least of the answers correct to pass this quiz.
Note: You must get at least of the answers correct to pass this quiz.
You have not filled in all the answers to complete this quiz
The following questions were not answered:
Sorry, you have unsuccessfully completed this CME quiz with a score of
The following questions were not answered correctly:
For CME Course: A Proposed Model for Initial Assessment and Management of Acute Heart Failure Syndromes
Indicate what changes(s) you will implement in your practice, if any, based on this CME course.
To view and print your certificate and access a summary of your CME courses go to My CME.
NOTE:
Citing articles are presented as examples only. In non-demo SCM6 implementation, integration with CrossRef’s “Cited By” API will populate this tab (http://www.crossref.org/citedby.html).
Submit a Response

Some tools below are only available to our subscribers or users with an online account.

Related Content

Customize your page view by dragging & repositioning the boxes below.