Impact Of Cancer Therapy Research Articles

Management of IBD in the Elderly Patient With Cancer.

The management of inflammatory bowel disease (IBD) in patients with known or recently treated cancer has become a common dilemma in our ageing population. Older patients are commonly excluded from prospective trials, and co-morbid status and polypharmacy may muddy our understanding of the impact of therapies on these patients. Immunosuppression (anti-TNF therapy, antimetabolite therapy) carries a relative contra-indication in the setting of known cancer as it is expected to increase cancer risk and increase propagation of in situ cancer. Recent studies have sought to investigate this risk by looking from two sides-the impact of cancer therapies on IBD outcomes and the risk of cancer occurrence/recurrence in patients on IBD therapies. In this chapter, we review this data and determine the safety of commonly used IBD therapies in this potentially vulnerable elderly population.

Caring for cancer survivors: more than just checking the blood pressure and measuring the ejection fraction.

The generation that has come of age since President Richard Nixon signed the National Cancer Act of 1971 (the historical beginning of the ‘war on cancer’), has realized a progressive change in the approach to this disease, which for many has evolved into a chronic illness. While some diagnostic groups have lagged behind, the focused research and supportive care efforts placed on cancer have significantly advanced 5-year survival rates. Overall survival rates have increased from <50 to nearly 70%, with the most impressive gains being realized among those diagnosed in childhood. The majority of children treated for cancer are now expected to become long-term survivors, contributing many life-years saved to society. An unforeseen circumstance, at least at the beginning of this ‘war,’ has been the impact of cancer therapy upon the long-term health and social well being of survivors. Understanding the late effects of cancer therapy has become a focus of research for academic cancer centers, with most also offering clinical programs to advance the care and quality of life of this growing population. The cardiovascular effects of cancer therapy can be varied and most often related to anthracyclines and/or radiation exposures; however, multiple other agents have also been implicated [1]. Early, on-therapy, anthracycline cardiotoxicity is rare (<1%), while chronic toxicity is more common, dose dependent and progressive. Exposure to increasing doses of anthracyclines has been shown to be a risk factor in both adult and pediatric patients. In a retrospective analysis of three treatment studies using high doses of anthracyclines, Swain et al. identified a 5% prevalence of congestive heart failure (CHF) at a cumulative dose of 400 mg/m 2 rising to 48% at doses of 700 mg/m 2 [2]. Similar findings have been reported among those treated for childhood cancer [3,4]; however, at much lower doses. Among participants in the Childhood Cancer Survivor Study, those exposed to anthracyline doses greater than 250 mg/m 2 were five-times more likely to report CHF than those not exposed [5]. The introduction of newer agents such as monoclonal antibodies and tyrosine kinase inhibitors has further improved cancer care

Abstract 4434: Role of Deubiquitinase Usp9x in pancreatic cancers: Tumor promoter or tumor suppressor

Abstract Deubiquitinase Usp9x has been shown to promote tumor cell survival and resistance to chemo- and radiotherapy through effects on the Mcl-1 pro-survival protein. It is predicted that a small molecule Usp9x inhibitor could have a major impact in cancer therapy. However, recent data has raised caution about therapeutic targeting of Usp9X in cancer. In a study to identify genes that reduce the latency of pancreatic tumor formation in a mutant Kras model, Pérez-Mancera et al. 2012 reported that the Usp9x locus was frequently inactivated in pancreatic cancer cells, resulting in protection from anoikis and enhanced transformation. In order to clarify the role of Usp9X in pancreatic cancer, we used a newly created cell line 4668 established from mouse pancreatic tumors with doxycycline (DOX) inducible expression of KrasG12D and Tp53R172H. Stable Usp9x knockdown (KD) in 4668 cells had no effect on their proliferation or phenotype in 2D cultures. However, withdrawal of DOX from DOX-treated Usp9x KD 4668 cells resulted in 4-fold increase in colony formation, unlike DOX depleted control KD 4668 cells which undergo apoptosis resulting in colony disintegration. DOX treated control KD and Usp9x KD 4668 cells did not show any difference in basal 3D colony formation. These results suggest that Usp9x loss in the absence of continuous mutant Kras/p53 expression is sufficient to sustain 3D cancer cell growth, confirming a tumor suppressor role for Usp9x in a Kras mouse model of pancreatic cancer. To determine if Usp9x also plays a tumor suppressor role in human pancreatic tumors, we did Usp9x KD in three human pancreatic cancer cell lines with varied Kras mutational status; BxPC3 (wild type), PANC1 (heterozygous) and MIA-PACA2 (homozygous) which expressed high basal levels of Usp9x. MIA-PACA2-Usp9x KD cells undergo apoptosis and caspase activation. In contrast, BxPC3-Usp9x KD cells showed no effect on growth in 2D or in 3D culture. However, PANC1-Usp9x KD cells showed more rapid (38% p=0.004) 2D growth, but 3D colony formation was consistently reduced by &amp;gt;50%, (p=0.03). These results suggest that the effect of Usp9x loss in established human pancreatic tumor cells is distinct from that detected in a murine pancreatic tumor model. Distinctions may be partially dependent on their Kras mutational status or Usp9x substrate utilization in human vs. murine cells. To further assess the clinical relevance of our observations, Usp9x KD was evaluated in four recently established, low passage number human pancreatic patient tumor cell lines (UM2, UM6, UM16, UM76). Usp9x KD did not affect 2D growth but fully suppressed 3D colony growth. This activity was phenocopied by our small molecule Usp9x inhibitor, EOAI3402143 (G9), with nM efficacy. Together, these results suggest that possible species distinctions exist in the tumorigenic functions of Usp9x and necessitate further assessment of its role in pancreatic tumor development and treatment. Citation Format: Anupama Pal, Marina Pasca di Magliano, Moshe Talpaz, Michelle Dziubinski, Diane Simeone, Nicholas J. Donato. Role of Deubiquitinase Usp9x in pancreatic cancers: Tumor promoter or tumor suppressor. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 4434. doi:10.1158/1538-7445.AM2014-4434

Cardiac complications and manifestations of chemotherapy for cancer

The use of potent chemotherapeutic agents and radiotherapy to target cancer cells has certainly improved outcomes for oncology patients. However, there is increasing recognition of the importance of cardiotoxic side...

The impact of cancer therapy on cognition in the elderly

Cancer and cancer therapy-related cognitive impairment (formerly known as chemobrain or chemo-fog) are often described in the literature. In the past, studies have failed to prove the existence of cancer therapy-related cognitive dysfunction. However, more recently, prospective trials have shown that patients undergoing chemotherapy do display impairment in specific cognitive domains. Aging confers an increased risk of developing cancer, as well as cognitive impairment. The Geriatric Oncology clinic of the Segal Cancer Centre, Jewish General Hospital in Montreal was founded in 2006 to address the unique needs of older cancer patients. We will describe two cases of cancer therapy-related cognitive impairment from our Geriatric Oncology clinic. The first case is that of a 75 year old male diagnosed with stage III non-small cell lung carcinoma who complained of forgetfulness since starting carboplatin-paclitaxel. The second case is that of a 65 year old female diagnosed with stage I, estrogen-receptor-positive breast cancer who had undergone lumpectomy followed by adjuvant cyclophosphamide, methotrexate and fluorouracil chemotherapy, radiation therapy and was on exemestane when she was evaluated. We will also briefly review the literature of cancer therapy-related cognitive impairment.

A Cell-Penetrating Bispecific Antibody for Therapeutic Regulation of Intracellular Targets

The therapeutic use of antibodies is restricted by the limited access of antibodies to intracellular compartments. To overcome this limitation, we developed a cell-penetrating monoclonal antibody, mAb 3E10, as an intracellular delivery vehicle for the intracellular and intranuclear delivery of antibodies constructed as bispecific single-chain Fv fragments. Because MDM2 is an important target in cancer therapy, we selected monoclonal antibody (mAb) 3G5 for intracellular transport. mAb 3G5 binds MDM2 and blocks binding of MDM2 to p53. Here, we show that the resulting 3E10-3G5 bispecific antibody retains cell-penetrating and MDM2-binding activity, increases tumor p53 levels, and inhibits growth of MDM2-addicted tumors. The use of cell-penetrating bispecific antibodies in targeted molecular therapy will significantly broaden the spectrum of accessible intracellular targets and may have a profound impact in cancer therapy.

Cardiac response to doxorubicin and dexrazoxane in intact and ovariectomized young female rats at rest and after swim training

The impact of cancer therapies on adult cardiac function is becoming a concern as more children survive their initial cancer. Cardiovascular disease is now a significant problem to adult survivors of childhood cancer. Specifically, doxorubicin (DOX) may be particularly harmful in young girls. The objective of this study was to characterize DOX damage and determine the ability of dexrazoxane (DEX) to reduce DOX-mediated cardiac damage in sedentary and swim-trained female rats. Female Sprague-Dawley rats were left intact or ovariectomized (OVX) at weaning then injected with DEX (60 mg/kg) before DOX (3 mg/kg), DOX alone, or PBS. Rats were separated into sedentary and swim cohorts. Body weight was reduced in DOX:DEX- but not PBS- or DOX-treated rats. Echocardiographic parameters were similar in sedentary rats. Swim training revealed greater concentric remodeling in DOX-treated rats and reduced fractional shortening in DOX:DEX-treated rats. Calsequestrin 2 was reduced with DOX and increased with DOX:DEX postswim. Sarco(endo)plasmic reticulum Ca(2+)-ATPase 2a was reduced and calsequestrin 2 reduced further by swim training only in intact rats. OVX rats were heavier and developed eccentric remodeling post-swim with DOX and eccentric hypertrophy with DOX:DEX. Changes in SERCA2a and calsequestrin 2 expression were not observed. Ovariectomized DOX- and DOX:DEX-treated rats stopped growing during swim training. DEX coinjection did not relieve DOX-mediated cardiotoxicity in intact or hormone-deficient rats. DOX-mediated reductions in growth, cardiac function, and expression of calcium homeostasis proteins were exacerbated by swim. DEX coadministration did not substantially relieve DOX-mediated cardiotoxicity in young female rats. Ovarian hormones reduce DOX-induced cardiotoxicity.

Impact of cancer therapies on ovarian reserve

To determine whether measures of ovarian reserve differ between females exposed to cancer therapies in a dose-dependent manner as compared with healthy controls of similar age and late reproductive age. Cross-sectional analysis of data from a prospective cohort study. University medical center. Seventy-one cancer survivors aged 15-39 years; 67 healthy, similarly aged unexposed subjects; and 69 regularly menstruating women of late reproductive age (40-52 years). None. Early follicular-phase hormones (FSH, E(2), inhibin B, antimüllerian hormone [AMH]) and ovarian ultrasound measurements (ovarian volume and antral follicle counts [AFC]) were compared using multivariable linear regression. In adjusted models, FSH, AMH, and AFC differed between exposed vs. unexposed subjects (FSH 11.12 mIU/mL vs. 7.25 mIU/mL; AMH 0.81 ng/mL vs. 2.85 ng/mL; AFC 14.55 vs. 27.20). In participants with an FSH <10 mIU/mL, survivors had lower levels of AMH and AFC compared with controls. Alkylating agent dose score was associated with increased levels of FSH and decreased levels of AMH. Exposure to pelvic radiation was associated with impairment in FSH, AMH, AFC, and ovarian volume. Antimüllerian hormone was similar in women previously exposed to high-dose cancer therapy and 40-42-year-old controls. Measures of ovarian reserve are impaired in a dose-dependent manner among cancer survivors compared with unexposed females of similar age. Reproductive hormone levels in menstruating survivors exposed to high-dose therapy are similar to those in late-reproductive-age women. The predictive value of measures for pregnancy and menopause must be studied. CLINICALTRIALS.GOV IDENTIFIER: NCT01143844.

Abstract ED02-04: Intersection of cancer, aging, and survivorship

Abstract Cancer is a disease associated with aging, with approximately 60% of cancer diagnoses occurring in patients age 65 and older. Of 10.8 million cancer survivors in the US, approximately 6.8 million are age 65 or older. With the aging of the baby boomer population and rises in life expectancy, the number of cancer cases and the number of cancer survivors is anticipated to grow over the coming decades.1 Optimal care of this growing population of older adult cancer survivors will require an understanding of the interaction between cancer, cancer therapy, and the aging process. In particular there is a gap in knowledge regarding whether cancer and/or cancer treatment accelerates the aging process, and if so whether the accelerated aging is transient or permanent. This lecture will provide an overview of the available data regarding the intersection between aging and survivorship, as well as specific considerations in the assessment and treatment of older adult survivors. Cancer and cancer treatment has a potential long term impact on the health status and physical function of older adults.2–3 The Health and Retirement study evaluated the health and functional status of older cancer survivors in comparison to controls. Older cancer survivors were less likely to report excellent or good health (P&amp;lt;0.001), reported more mobility limitations (P&amp;lt;0.001), and reported more limitations with activities of daily living (P=0.01). Among older cancer survivors, obesity, lack of exercise, and poor diet are associated with a poorer quality of life.4 A randomized study tested the benefits of an exercise and diet intervention in older cancer survivors and demonstrated that the intervention was associated with a decrease in self-reported functional decline.5 Older cancer survivors have an increased number of comorbid conditions in comparison to individuals without a history of cancer.2 The NIA/NCI Collaborative Study on Cancer and Comorbidity in the Elderly provided summary data on the comorbidity of 7,600 patients age 55 and older with a history of cancer. The most common comorbid conditions included hypertension (43%), heart conditions (39%) and arthritis (35%).6 Patients may be at increased risk for specific comorbid conditions based on their preexisting comorbid conditions and the therapeutic exposures received. For example, therapy with doxorubicin is associated with an increased risk of congestive heart failure and cardiomyopathy.7–8 Risk factors include a history of diabetes mellitus, coronary artery disease, and hypertension. Therapy with an aromatase inhibitor is associated with a loss in bone mineral density and this risk is most pronounced in patients with pre-existing bone loss.9 These examples highlight the need to better understand the association between a history of cancer, patient characteristics (including pre-existing comorbid conditions), specific therapeutic exposure, and the subsequent development or acceleration of comorbid conditions. Although our knowledge of the potential survivorship issues facing older adults is growing, several gaps in knowledge remain.10 As the number of cancer survivors is on the rise, it is critical to improve our evidence-based knowledge to identify and reduce the risk of late side effects from treatment. Prospective longitudinal studies of the long term impact of cancer therapies and interventions to decrease the risk are needed.

Anthracyclines induce the accumulation of mutant p53 through E2F1-dependent and -independent mechanisms

Mutant p53 frequently accumulates in cancer cells and promotes tumor cell invasion, as part of its gain of function. Its accumulation is partially due to enhanced stability, but little is known about how the mRNA levels of mutant p53 can be regulated. Likewise, the impact of cancer therapy on the levels of mutant p53 is poorly understood. We show here that the anthracyclines doxorubicin, daunorubicin and epirubicin further increase the amounts of mutant p53 mRNA and protein in cancer cells. Moreover, we show for the first time that the transcription factor E2F1 associates with the promoter DNA of TP53. Upon genotoxic treatment, E2F1 contributed to the expression of mutant p53, both directly and through induction of TAp73. In contrast, the anthracycline idarubicin and also another topoisomerase inhibitor, etoposide, failed to increase the levels of p53 mRNA, despite their ability to induce the synthesis of TAp73 mRNA. Instead, a natural antisense transcript of TP53, WRAP53, was strongly augmented by idarubicin and etoposide, but only less so by the other anthracyclines under study. RNA corresponding to the first exon of WRAP53 was mainly found in cell nuclei and it reduced the levels of mutant p53. Taken together, this suggests a reciprocal activation pattern of TP53 and WRAP53 by different chemotherapeutics. Reducing the levels of mutant p53 by small-interfering RNA increased chemosensitivity, and idarubicin prevented cell survival more efficiently than the mutant p53-inducing doxorubicin. We conclude that even closely related anthracyclines induce the synthesis of different, opposing transcripts from the TP53 locus. When using these drugs for cancer therapy, the increased levels of mutant p53 may augment its gain of function and thus favor unwanted chemoresistance and tumor progression.

Capecitabine is associated with lower chemotherapy-related expenditures than those associated with gemcitabine in women with metastatic breast cancer.

Abstract Abstract #6108 Background: There is growing concern about the impact of cancer therapies on escalating medical costs, with considerable focus on the high unit cost of new therapies. The current study quantified the impact of all chemotherapy-related costs (drug acquisition, drug administration, and related complications) on direct medical expenditure among patients with metastatic breast cancer (mBC) who were treated with capecitabine monotherapy or gemcitabine monotherapy.&amp;#x2028; Methods: Women with mBC who were treated with gemcitabine or capecitabine between 1/1/2003 and12/31/2006 were identified from the Thomson Reuters Marketscan® database. Capecitabine users were propensity matched to gemcitabine users to address selection bias and to achieve balanced groups. Complications evaluated included myelosuppression, infection, constitutional symptoms, and GI-related events. The Cox proportional hazards model was used to assess relative risk of an event, while general linear models were used to estimate monthly complication cost, chemotherapy cost, and overall monthly expenditure.&amp;#x2028; Results: A total of 252 capecitabine users were propensity matched 1:1 to gemcitabine users. Mean adjusted monthly expenditure was significantly lower among capecitabine users ($6930 vs $12,716 for gemcitabine, P&amp;lt;.0001). The difference was driven by significantly lower complication costs (P&amp;lt;.0001) and chemotherapy acquisition/administration costs (P&amp;lt;.0001). Among capecitabine patients, 30% of the total mean monthly expenditure was attributed to chemotherapy treatment (15% complication related, 15% acquisition/administration), versus 51% (26% complication related, 25% acquisition/administration) for gemcitabine patients. Lower complication costs during capecitabine treatment episodes were due to reduced frequency of any of the 23 complications evaluated (HR=0.33, P&amp;lt;.0001). Capecitabine users were at a significantly lower risk for myelosuppression (HR=0.28, P&amp;lt;.0001), constitutional symptoms (HR=0.62, P=.001), and GI events, which led to the use of prescription medications or deemed clinically significant (HR=0.24, P&amp;lt;.0001). The decrease in the rate of complications for capecitabine versus gemcitabine users resulted in significantly lower costs associated with myelosuppression ($485 vs $1607, respectively, P&amp;lt;.0001) and GI events ($178 vs $674, respectively, P&amp;lt;.0001). Lower chemotherapy costs during capecitabine treatment episodes versus gemcitabine treatment episodes were driven by significantly reduced costs associated with chemotherapy administration ($68 vs $466, respectively, P&amp;lt;.0001) and drug acquisition ($967 vs $2668, respectively, P&amp;lt;.0001).&amp;#x2028; Conclusion: Patients with mBC who were treated with capecitabine monotherapy incurred significantly lower total health care costs than gemcitabine monotherapy patients. The difference in total cost was driven by lower costs associated with chemotherapy-related complications and chemotherapy acquisition/administration for patients treated with capecitabine. Citation Information: Cancer Res 2009;69(2 Suppl):Abstract nr 6108.

Selenium Compounds and Apoptotic Modulation: A New Perspective in Cancer Therapy

Recent epidemiological studies have demonstrated that selenium may be an effective chemopreventive and anticancer agent with a broad spectrum against several human cancer cells (prostate, colon, bladder, lung, liver, ovarian, leukemia). A wide range of potential mechanisms have been proposed for the antitumorigenic effects of selenium and these include antiandrogen activity, growth inhibitory effects by regulation of p53 and antioxidant function, and through DNA damage. However, apoptosis is one of the most plausible mechanisms for the anticancer activity. The regulating mechanisms of apoptosis are extremely complex and for selenium compounds they mainly involve a mitochondrial pathway, protein kinases, tumor necrosis factor, activation of caspases and reactive oxygen species. The aim of this review is to summarize the current knowledge about more than twenty eight selenium-containing molecules and to discuss the implications for apoptosis and the impact in cancer therapy.

Proactive routine monitoring and intervention to reduce the psychosocial impact of cancer therapy

Much of the psychosocial morbidity experienced by cancer patients goes undetected and therefore untreated. This paper describes infrastructure to routinely screen patients for psychosocial problems and provide targeted intervention in the cancer care setting. Cancer patients will complete a psychosocial screening survey via touchscreen computer at three outpatient visits. A report containing a summary of their responses, score interpretation and recommended management strategies will be printed immediately and placed in their file for follow-up by their health care team. Centres will be able to track changes in their patients psychosocial outcomes over time, and in response to changes in service delivery. Benchmarking reports will be produced annually to feed back performance data to individual centres on their patients' psychosocial outcomes.

The impact of cancer therapy on the endocrine system in survivors of childhood brain tumours

Survival rates are improving following cancer therapy for childhood brain tumours. There is therefore a growing cohort of survivors at risk of late effects of cancer therapy. Endocrine problems are very common in these patients. The recognition and prompt management of these are essential to prevent further morbidity and impairment of quality of life. Cranial radiation can damage hypothalamic-pituitary function, most frequently affecting GH status; however, higher radiation doses may cause more widespread hypothalamic-pituitary damage. Early puberty secondary to cranial irradiation is now being managed with gonadotrophin-releasing hormone analogues to improve final height. Prompt diagnosis and management of GH deficiency may improve final height outcome; continued GH therapy beyond final height aids the achievement of adult body composition (lean body mass and bone mass) and GH therapy in adulthood improves quality of life. Both cranial irradiation alone and with spinal irradiation can result in radiation damage to the thyroid resulting in hypothyroidism and thyroid nodules, a high proportion of which are malignant. Gonadal damage secondary to spinal irradiation and adjuvant chemotherapy may have long-term consequences including infertility.

Changes in sexual function over time in women receiving adjuvant therapy for early stage breast cancer

622 Background: The impact of cancer therapy on sexual functioning has not been systematically studied over time in women undergoing adjuvant therapy for breast cancer. Patients were enrolled in a trial addressing the impact of surgery, chemotherapy (CT), and tamoxifen (TAM)on sexual function. Methods: Within 30 days of initiating adjuvant therapy, and 2, 6, and 12 mos. afterwards, women completed the Sexual History Form (Nowinki & Lopiccolo; Schover & Jensen). Results:75 women were enrolled with a mean age 53.7 yrs; (range 28–82 yrs); 50 (67%) were Caucasian, 22 (29%) African-American, 1 Asian, and 1 unknown. 44 (59%) underwent lumpectomy and radiation (XRT) and 31 (41%) mastectomy. CT alone was administered in 32 (43%), CT and TAM in 14 (19%), and TAM alone 20 (27%). Baseline scores were identical for women undergoing mastectomy vs. lumpectomy/XRT (p=1.0), CT vs. no CT(p=0.13), and any TAM vs. no TAM (p=0.63). After initiation of adjuvant therapy, sexual function worsens initially and improves by 12 mos...

Changes in sexual function over time in women receiving adjuvant therapy for early stage breast cancer

622 Background: The impact of cancer therapy on sexual functioning has not been systematically studied over time in women undergoing adjuvant therapy for breast cancer. Patients were enrolled in a trial addressing the impact of surgery, chemotherapy (CT), and tamoxifen (TAM)on sexual function. Methods: Within 30 days of initiating adjuvant therapy, and 2, 6, and 12 mos. afterwards, women completed the Sexual History Form (Nowinki & Lopiccolo; Schover & Jensen). Results:75 women were enrolled with a mean age 53.7 yrs; (range 28–82 yrs); 50 (67%) were Caucasian, 22 (29%) African-American, 1 Asian, and 1 unknown. 44 (59%) underwent lumpectomy and radiation (XRT) and 31 (41%) mastectomy. CT alone was administered in 32 (43%), CT and TAM in 14 (19%), and TAM alone 20 (27%). Baseline scores were identical for women undergoing mastectomy vs. lumpectomy/XRT (p=1.0), CT vs. no CT(p=0.13), and any TAM vs. no TAM (p=0.63). After initiation of adjuvant therapy, sexual function worsens initially and improves by 12 mos. Differences between lumpectomy/XRT and mastectomy patients were not significant. Scores are expected to increase (worsen) by 3.7 points for lumpectomy/ XRT patients vs.1.8 points for mastectomy patients over the first 6 mos.of therapy, yet by 12 mos. lumpectomy/XRT patients are expected to improve by 5.1 points beyond their initial scores in contrast to mastectomy patients whose scores increase further by 1.4 points. Women receiving TAM had lower sores at 2, 6 and 12 mos. than those not receiving TAM. Women on chemotherapy exhibited the overall pattern of initial decline in sexual function with a rebound to initial level by 12 mos. In contrast, the scores of those not receiving chemotherapy steadily improved over time, an expected improvement of 11.2 points over initial levels by 12 mos. (p=0.11). Conclusions: Surgery and adjuvant therapy may adversely impact patients sexual functioning. Women treated with mastectomy and those receiving CT experienced worsening of sexual functioning, but did return to baseline levels by 12 mos. Supported by NIH CA72554-O2. No significant financial relationships to disclose.

Impact of cancer therapy on survival

Survival rates improved significantly for 28,036 lymphoma and leukemia patients studied between 1950 and 1973. Nine cancers reviewed demonstrated increased one, three and five year survival rates. Greatest improvement was acute lymphocytic leukemia survival. Least improvement was for chronic granulocytic leukemia. Analyses of age-specific trends in U.S. cancer mortality since 1960 indicates death rates decreased 20% for all ages up to 45 years. This included 70% of the population, but less than 10% of all cancer deaths. Age groups over 55 experienced an 8% increase in cancer mortality. Accurate determination of national cancer incidence trends is not presently possible. Available data, representing approximately 15 million population, indicate that cancer incidence rates increased between 1960 and 1973. Age-specific trend analyses indicate unusual divergences. For the group 15 to 29-years-old, incidence increased 28% in 13 years and there was a concomitant decrease of 20% in mortality.