Magnetic resonance imaging (MRI): MRI scans use radio waves and strong magnets instead of x-rays to take pictures. The energy from the radio waves is absorbed and then released in a pattern formed by the type of tissue and by certain diseases. A computer translates the pattern of radio waves given off by the tissues into a very detailed image of parts of the body. Not only does this produce cross sectional slices of the body like a CT scanner, it can also produce slices that are parallel with the length of your body. MRI images are particularly useful in examining pelvic tumors. They are also helpful in detecting cancer that has spread to the brain or spinal cord. A contrast material might be injected into a vein just as with CT scans, but is used less often. MRI scans take longer than CT scans − often up to an hour. Also, you have to be placed inside a tube-like piece of equipment, which is confining and can upset people with claustrophobia (a fear of enclosed spaces). Special, “open” MRI machines that are not so confining may be an option for some patients; the downside of these is that the images may not be as good. The machine also makes a thumping noise that some people find disturbing. Some places provide headphones with music to block this noise out. A mild sedative is helpful for some people.

Intravenous urography: Intravenous urography (also known as intravenous pyelogram or IVP) is an x-ray of the urinary system taken after a special dye is injected into a vein. This dye is removed from the bloodstream by the kidneys and passes through the ureters and into the bladder (the ureters are the tubes that connect the kidneys to the bladder). This test finds abnormalities in the urinary tract, such as changes caused by spread of cervical cancer to the pelvic lymph nodes, which may compress or block a ureter. IVP is rarely used currently to evaluate patients with cervical cancer. You will not usually need an IVP if you have already had a CT or MRI.

Positron emission tomography: Positron emission tomography (PET) uses glucose (a form of sugar) that contains a radioactive atom. Cancer cells in the body absorb large amounts of the radioactive sugar and a special camera can detect the radioactivity. This test can help see if the cancer has spread to lymph nodes. PET scans can also be useful if your doctor thinks the cancer has spread but doesn’t know where. PET scans can be used instead of other types of x-rays because they scan your whole body. Some machines combine a CT scan and a PET scan to even better pinpoint the tumor. This test is rarely used for patients with early cervical cancer, but may be used to look for more advanced disease.

Preventive vaccines work
Target infectious agents that cause or contribute to the development of cancer. They are similar to traditional vaccines, which help prevent infectious diseases such as measles or polio by protecting the body against infection. Both cancer preventive vaccines and traditional vaccines are based on antigens that are carried by the infectious agents and that are relatively easy for the immune system to recognize as foreign.

Vaccines for cancer represent an alternative approach to the use of therapeutics. In contrast to traditional vaccines that prevent disease, cancer vaccines enlist the patient’s immune system to destroy existing cancer cells. While simple in concept, the development of products has proven difficult. Problems lie in eliciting sufficient, tumor-selective stimulation of an immune system that is already tolerant of cancer cells. Commercially sponsored cancer vaccines first entered clinical studies in the early-1980s and so companies had at least some experience in the area by 1990.

Preventive Vaccines Been Approved For Use In The United States:-
In 2006, the U.S. Food and Drug Administration (FDA) approved the vaccine known as Gardasil®, which protects against infection by two types of HPV—specifically, types 16 and 18—that cause approximately 70 percent of all cases of cervical cancer worldwide. At least 17 other types of HPV are responsible for the remaining 30 percent of cervical cancer cases. Gardasil also protects against HPV types 6 and 11, which are responsible for about 90 percent of all cases of genital warts. However, these two HPV types do not cause cervical cancer.

In 2008, the FDA expanded Gardasil’s approval to include its use in the prevention of HPV-associated vulvar and vaginal cancers.

Gardasil, manufactured by Merck & Company, is based on HPV antigens that are proteins. These proteins are used in the laboratory to make four different types of “virus-like particles,” or VLPs, which correspond to HPV types 6, 11, 16, and 18. The four types of VLPs are then combined to make the vaccine. Because Gardasil targets four HPV types, it is called a quadrivalent vaccine. In contrast with traditional vaccines, which are often composed of weakened, whole microbes, the VLPs in Gardasil are not infectious. However, they are still able to stimulate the production of antibodies against HPV types 6, 11, 16, and 18.

A second HPV vaccine manufactured by GlaxoSmithKline and known by the name Carvarix® has also been developed. Although Carvarix has been approved for use in Europe, it has not yet been approved by the FDA for use in the United States. In contrast with Gardasil, Carvarix is a bivalent vaccine. It is composed of VLPs made with proteins from HPV types 16 and 18. Therefore, it provides protection only against these two HPV types.

The public health benefits of vaccines against HPV types 16 and 18 may extend beyond reducing the risks of cervical cancer, vaginal cancer, and vulvar cancer. Evidence suggests that chronic infection by one or both of these virus types is also associated with cancers of the anus, penis, and or pharynx.

The FDA has approved one other type of cancer preventive vaccine, which protects against HBV infection. Chronic HBV infection can lead to liver cancer. The first HBV vaccine was approved in 1981, making it the first cancer preventive vaccine to be successfully developed and marketed. Today, most children in the United States are vaccinated against HBV shortly after birth.

Many scientists believe that microbes cause or contribute to between 15 percent and 25 percent of all cancers diagnosed worldwide each year, with the percentages being lower in developed countries than in developing countries. The International Agency for Research on Cancer (IARC) has classified several microbes as carcinogenic (causing or contributing to the development of cancer in people), including HPV and HBV. These infectious agents—bacteria, viruses, and parasites—and the cancer types with which they are most strongly associated are listed in the table below.

Infectious Agents

Type of

Associated Cancer(s)

hepatitis B virus (HBV)


hepatocellular carcinoma (a type of liver cancer)

hepatitis C virus (HCV)


hepatocellular carcinoma (a type of liver cancer)

human papillomavirus (HPV) types 16 and 18, as well as other HPV types


cervical cancer; vaginal cancer; vulvar cancer;
oropharyngeal cancer(cancers of the base of the tongue, tonsils, or upper throat); anal cancer; penile cancer

Epstein-Barr virus


Burkett lymphoma; non-Hodgkin lymphoma; Hodgkin lymphoma; nasopharyngealcarcinoma(cancer of the upper part of the throat behind the nose)

human T-cell lymph tropic virus 1 (HTLV1)


acute T-cell leukemia

Helicobacter pylori


stomach cancer

schistosomes (Schistosoma hematobium)


bladder cancer

liver flukes (Opisthorchis viverrini)


cholangio carcinoma (a type of liver cancer)

Cancer treatment vaccines are designed to treat cancers that have already occurred. They are intended to delay or stop cancer cell growth; cause tumor shrinkage; prevent cancer from coming back; or eliminate cancer cells that are not killed by other forms of treatment, such as surgery, radiation therapy, or chemotherapy. Most important is the fact that cancer cells carry normal self antigens in addition to any cancer-associated antigens. Furthermore, cancer cells sometimes undergo genetic changes that lead to the loss of cancer-associated antigens. Finally, cancer cells can produce chemical messages that suppress specific anticancer immune responses by killer T cells. As a result, even when the immune system recognizes a growing cancer as a threat, the cancer may still escape a strong attack by the immune system.

The FDA has not approved any type of cancer treatment vaccine. Producing effective treatment vaccines has proved much more difficult and challenging than developing cancer preventive vaccines. Although researchers have identified many cancer-associated antigens, these molecules vary widely in their capacity to stimulate a strong anticancer immune response. Two major areas of research aimed at developing better cancer treatment vaccines involve the discovery of new cancer-associated antigens that may prove more effective in stimulating immune responses than the already known antigens and the development of new methods to enhance the ability of cancer-associated antigens to stimulate the immune system. Research is also under way to determine how to combine multiple antigens within a single cancer treatment vaccine to produce optimal anticancer immune responses. In addition, researchers are trying to identify the mechanisms by which cancer cells evade or suppress anticancer immune responses. Gardasil for type 6 and 11 and carvarix, a second HPV vaccine manufactured by Glaxosmithklime for type 16 and 18. Research can use certain immune system cells and their product antibodies created in lab. e.g. – Dendritic cells and costimulatory molecules, idiotype vaccines, anti-id.

Side effects of vaccine-inflammation, pain swelling, itching, rashes, flu, fever, chill, weakness, dizziness, nausea, vomiting, fatigue, headache, hypersensitivity. In addition, researchers are trying to identify the mechanisms by which cancer cells evade or suppress anticancer immune responses.

•Every year more than 270000 women die from cervical cancer, more than 85% of these deaths are in low and middle income countries.

•Cervical cancer is caused by sexually-acquired infection with Human papillomavirus (HPV).  Most people are infected with HPV shortly after onset of sexual activity.

•accination against HPV in girls 9 to 13 years old combined with regular screening in women  over age 000 new cervical cancer cases diagnosed every year.

•Sur vival rates for cervical cancer can be further improved by establishing effective cancer treatment programmes.

1.Pardoll DM. Cancer immunology. In: Abeloff MD, Armitage JO, Niederhuber JE, Kastan MB, McKenna WG, editors. Abeloff's Clinical Oncology. 4th ed. Philadelphia: Churchill Livingstone, 2008.
2.Murphy KM, Travers P, Walport M, editors. Janeway's Immunobiology. 7th ed. New York: Garland Science, 2007.
3.Waldmann TA. Effective cancer therapy through immunomodulation. Annual Review of Medicine 2006; 57:65–81.
4.Emens LA. Cancer vaccines: On the threshold of success. Expert Opinion on Emerging Drugs 2008; 13(2):295–308.
5.Sioud M. An overview of the immune system and technical advances in tumor antigen discovery and validation. Methods in Molecular Biology 2007; 360:277–318.
6.Pazdur MP, Jones JL. Vaccines: An innovative approach to treating cancer. Journal of Infusion Nursing 2007; 30(3):173–178.
7.Lollini PL, Cavallo F, Nanni P, Forni G. Vaccines for tumour prevention. Nature Reviews Cancer 2006; 6(3):204–216.
8.Frazer IH, Lowy DR, Schiller JT. Prevention of cancer through immunization: Prospects and challenges for the 21st century. European Journal of Immunology 2007; 37(Suppl 1):S148–S155.
9.Doorbar J. Molecular biology of human papillomavirus infection and cervical cancer. Clinical Science 2006; 110(5):525–541.
10.Lowy DR, Schiller JT. Prophylactic human papillomavirus vaccines. Journal of Clinical Investigation 2006; 116(5):1167–1173.
11.Barr E, Sings HL. Prophylactic HPV vaccines: New interventions for cancer control. Vaccine 2008; August 9 [Epub ahead of print].
12.U.S. Centers for Disease Control and Prevention. A comprehensive immunization strategy to eliminate transmission of hepatitis B virus infection in the United States: Recommendations of the Advisory Committee on Immunization Practices (ACIP) Part 1: Immunization of infants, children, and adolescents. Morbidity and Mortality Weekly Report 2005; 54(No. RR–16):1–23.
13.Parkin DM. The global health burden of infection-associated cancers in the year 2002. International Journal of Cancer 2006; 118(12):3030–3044.
14.Mueller NE. Cancers caused by infections: Unequal burdens. Cancer Epidemiology, Biomarkers & Prevention 2003; 12(3):237s.
15.International Agency for Research on Cancer (2008). IARC monographs on the evaluation of carcinogenic risks to humans. Overall evaluations of carcinogenicity to humans: Group 1: Carcinogenic to humans. Retrieved October 3, 2008, from: Rivoltini L, Canese P, Huber V, et al. Escape strategies and reasons for failure in the interaction between tumour cells and the immune system: How can we tilt the balance towards immune-mediated cancer control? Expert Opinion on Biological Therapy 2005; 5(4):463–476.
16.Rosenberg SA, Yang JC, Restifo NP. Cancer immunotherapy: Moving beyond current vaccines. Nature Medicine 2004; 10(9):909–915.
17.Renkvist N, Castelli C, Robbins PF, Parmiani G. A listing of human tumor antigens recognized by T cells. Cancer Immunology and Immunotherapy 2001; 50(1):3–15.
18.Parmiani G, Russo V, Marrari A, et al. Universal and stemness-related tumor antigens: Potential use in cancer immunotherapy. Clinical Cancer Research 2007; 13(19):5675–5679.
19.Parmiani G, De Filippo A, Novellino L, Castelli C. Unique tumor antigens: Immunobiology and use in clinical trials. The Journal of Immunology 2007; 178(4):1975–1979.
20.Lollini PL, Forni G. Cancer immunoprevention: Tracking down persistent tumor antigens. Trends in Immunology 2003; 24(2):62–66.
21.Schlom J, Arlen PM, Gulley JL. Cancer vaccines: Moving beyond current paradigms. Clinical Cancer Research 2007; 13(13):3776–3782.
22.Banchereau J, Steinman RM. Dendritic cells and the control of immunity. Nature 1998; 392(6673):245–252.
23.Finn OJ. Cancer immunology. The New England Journal of Medicine 2008; 358(25):2704–2715.
24.Curigliano G, Spitaleri G, Dettori M, et al. Vaccine immunotherapy in breast cancer treatment: Promising, but still early. Expert Review of Anticancer Therapy 2007; 7(9):1225–1241.
25.Tacken PJ, deVries JM, Torensma R, Fidgor CG. Dendritic-cell immunotherapy: From ex vivo loading to in vivo targeting. Nature Reviews Immunology 2007; 7(10):790–802.
26.Garnett CT, Greiner JW, Tsang K-Y, et al. TRICOM vector based cancer vaccines. Current Pharmaceutical Design 2006; 12(3):351–361. Cerio AL, Zabalegui N, Rodríguez-Calvillo M, Inoges S, Bendandi M. Anti-idiotype antibodies in cancer treatment. Oncogene 2007; 26(25):3594–3602.
28.Chiarella P, Massi E, De Robertis M, Signori E, Fazio VM. Adjuvants in vaccines and for immunisation: Current trends. Expert Opinion on Biological Therapy 2007; 7(10):1551–1562.
29.Herr HW, Morales A. History of Bacillus Calmette-Guérin and bladder cancer: An immunotherapy success story. The Journal of Urology 2008; 179(1):53–56.
30.Emens LA. Chemotherapy and tumor immunity: An unexpected collaboration. Frontiers in Bioscience 2008; 13:249–257.
31.Dudley ME, Wunderlich JR, Robbins PF, et al. Cancer regression and autoimmunity in patients after clonal repopulation with antitumor lymphocytes. Science 2002; 298(5594):850–854.
32.Dudley ME, Wunderlich JR, Yang JC, et al. Adoptive cell transfer therapy following non-myeloablative but lymphodepleting chemotherapy for the treatment of patients with refractory metastatic melanoma. Journal of Clinical Oncology 2005; 23(10):2346–2357.
33.Morgan RA, Dudley ME, Wunderlich JR, et al. Cancer regression in patients after transfer of genetically engineered lymphocytes. Science 2006; 314(5796):126–129.
34.Rosenberg SA, Restifo NP, Yang JC, Morgan RA, Dudley ME. Adoptive cell transfer: A clinical path to effective cancer immunotherapy. Nature Reviews Cancer 2008; 8(4):299–308.
35.Ng LG, Mrass P, Kinjyo I, Reiner SL, Weninger W. Two-photon imaging of effector T-cell behavior: Lessons from a tumor model. Immunological Reviews 2008; 221:147–162.
36.Zou W. Regulatory T cells, tumour immunity and immunotherapy. Nature Reviews Immunology 2006; 6(4):295–307
37.Adam E, Kaufman RH, Adler-Storthz K, et al. A prospective study of association of herpes simplex virus and human papillomavirus infection with cervical neoplasia in women exposed to diethylstilbestrol in utero. Int J Cancer. 1985; 35(1):19-26.
38.American Cancer Society. Cancer Facts and Figures 2013. Atlanta, Ga: American Cancern Society; 2013. American Cancer Society. Cancer Prevention and Early Detection Facts and Figures 2010.
39.Fyles A, Keane TJ, Barton M, Simm J. The effect of treatment duration in the local control of cervix cancer. Radiother Oncol m1992; 25:273-279.
40. Girinsky T, Rey A, Roche B, et al. Overall treatment time in advanced cervical carcinomas: a critical parameter in treatment outcome. Int J Radiat Oncol Biol Phys 1993; 27:1051-1056.
41. Lanciano RM, Pajak TF, Martz K, Hanks GE. The influence of treatment time on outcome for squamous cell cancer of the uterine cervix treated with radiation: a patterns-of-care study. Int J Radiat Oncol Biol Phys 1993; 25:391-397.
42.Perez CA, Grigsby PW, Castro-Vita H, Lockett MA. Carcinoma of the uterine cervix. I. Impact of prolongation of overall treatment time and timing of brachytherapy on outcome of radiation therapy. Int J Radiat Oncol Biol Phys 1995; 32:1275-1288
43.Petereit DG, Sarkaria JN, Chappell R, et al. The adverse effect of treatment prolongation in cervical carcinoma. Int J Radiat Oncol Biol Phys 1995; 32:1301-1307.
44. Eifel PJ, Levenback C, Wharton JT, Oswald MJ. Time course and incidence of late complications in patients treated with radiation therapy for FIGO stage IB carcinoma of the uterine cervix. Int J Radiat Oncol Biol Phys 1995; 32:1289-1300.



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