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Bevacizumab improves outcomes in patients with metastatic CRC; however, its impact on surgical complications and hepatic regeneration after liver resection remains to be determined. \u003C\u002Fjats:p>\u003C\u002Fjats:sec>\u003Cjats:sec>\u003Cjats:title>Patients and Methods\u003C\u002Fjats:title>\u003Cjats:p> Fifty-six patients with metastatic CRC with liver metastases potentially curable by resection were eligible for this single-center, nonrandomized phase II trial. Eligibility criteria defined patients at high risk of early recurrence. Patients received biweekly bevacizumab plus capecitabine and oxaliplatin for six cycles. The sixth cycle of therapy did not include bevacizumab, resulting in 5 weeks between the last administration of bevacizumab and surgery. \u003C\u002Fjats:p>\u003C\u002Fjats:sec>\u003Cjats:sec>\u003Cjats:title>Results\u003C\u002Fjats:title>\u003Cjats:p> Objective response to neoadjuvant chemotherapy was achieved in 41 patients (73%). Fifty-two patients underwent liver resection including 11 with synchronous primary tumor resection. No increased intraoperative bleeding events or wound-healing complications were observed and only three patients (6%) required perioperative blood transfusions. Further surgery was necessary in a single patient. Postoperative liver function and regeneration were normal in all but one patient. No postoperative mortality occurred and morbidity was encountered in 11 patients (20%). The mean length of postoperative hospitalization was 9 days (± 4.0). \u003C\u002Fjats:p>\u003C\u002Fjats:sec>\u003Cjats:sec>\u003Cjats:title>Conclusion\u003C\u002Fjats:title>\u003Cjats:p> These data suggest that bevacizumab can be safely administered until 5 weeks before liver resection in patients with metastatic CRC without increasing the rate of surgical or wound healing complications or severity of bleeding. 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Oncogene 10:1413,1995-1416,",{},{"id":20,"text":1257,"url":20,"identifiers":1258},"10.1200\u002FJCO.2006.10.5437",{"doi":1257},{"id":20,"text":1260,"url":20,"identifiers":1261},"10.1038\u002Fncponc0509",{"doi":1260},{"id":20,"text":1263,"url":20,"identifiers":1264},"10.1158\u002F0008-5472.CAN-07-0589",{"doi":1263},{"id":20,"text":1266,"url":20,"identifiers":1267},"10.1038\u002Fnature00766",{"doi":1266},{"id":20,"text":1269,"url":20,"identifiers":1270},"10.1200\u002FJCO.2007.11.5956",{"doi":1269},{"id":20,"text":1272,"url":20,"identifiers":1273},"10.1038\u002Fnrm1261",{"doi":1272},{"id":20,"text":1275,"url":20,"identifiers":1276},"10.1038\u002Fnrc1387",{"doi":1275},{"id":1278,"createTime":1279,"updateTime":1280,"relativeEntities":1281,"slug":1282,"properties":1283,"entityType":233,"verifyStatus":234,"verifyTime":1298,"verifyNote":235,"languages":1299,"translateLanguages":20,"viewCount":21,"primaryUrl":1300,"fullTextUrl":20,"authors":1301,"publicationType":355,"publisherRelationship":1421,"citationCount":21,"citationInfo":1479,"publishDate":1482,"publishYear":1480,"citationAnalyzeStatus":19,"lastCitationAnalyze":1280,"indexDatabases":1483,"openAccess":20,"references":1484,"isForceReanalyzing":525},"eb5abb9a-8864-4873-8115-384f2fcb3a18","2024-09-03T13:01:53.432+00:00","2026-07-22T12:42:05.940+00:00",[],"Phase-II-Study-of-Paclitaxel-Plus-Gemcitabine-in-Refractory-Germ-Cell-Tumors-E9897-A-Trial-of-the-Eastern-Cooperative-Oncology-Group",{"mag":1284,"gsPaper":1286,"openalex":1288,"abstract":1290,"title":1292,"pm":1294,"doi":1296},{"VOID":1285},"2130387174",{"VOID":1287},"[\"7696495263042536442\"]",{"VOID":1289},"W2130387174",{"EN":1291},"\u003Cjats:p> PURPOSE: Despite great success in the treatment of disseminated germ cell tumors, 20% of patients are incurable and become candidates for investigational therapy. Paclitaxel and gemcitabine have shown activity as single agents in refractory germ cell tumors and can be combined with manageable toxicity. \u003C\u002Fjats:p>\u003Cjats:p> PATIENTS AND METHODS: Patients with germ cell tumors believed to be incurable with chemotherapy or surgery were treated with paclitaxel 110 mg\u002Fm\u003Cjats:sup>2\u003C\u002Fjats:sup> and gemcitabine 1,000 mg\u002Fm\u003Cjats:sup>2\u003C\u002Fjats:sup> intravenously on days 1, 8, and 15 of a 4-week cycle for a maximum of six cycles. Patients were evaluated for response and toxicity. \u003C\u002Fjats:p>\u003Cjats:p> RESULTS: Twenty-eight of 30 enrolled patients were assessable. Toxicity was primarily hematologic but was manageable with only a single case of neutropenic fever. Six (21.4%) of 28 patients responded, including three complete responses. Two of the complete responders were continuously disease-free at 15+ and 25+ months. \u003C\u002Fjats:p>\u003Cjats:p> CONCLUSION: Paclitaxel plus gemcitabine is an active regimen in refractory germ cell tumors, with an acceptable toxicity profile. This regimen has the possibility for long-term disease-free survival in this refractory patient population. \u003C\u002Fjats:p>",{"EN":1293},"Phase II Study of Paclitaxel Plus Gemcitabine in Refractory Germ Cell Tumors (E9897): A Trial of the Eastern Cooperative Oncology Group",{"VOID":1295},"11919245",{"VOID":1297},"10.1200\u002Fjco.2002.07.158","2024-09-03T13:01:53.431+00:00",[237],"https:\u002F\u002Fascopubs.org\u002Fdoi\u002F10.1200\u002FJCO.2002.07.158",[1302,1321,1338,1355,1372,1389,1406],{"id":1303,"sortIndex":21,"researcher":20,"roles":1304,"affiliations":1305,"properties":1314,"displayName":1318,"givenName":20,"familyName":20},"65bdefe6-c50f-445f-a1af-64a757dedd7a",[],[1306],{"id":1307,"sortIndex":21,"affiliation":1308,"properties":20},"24fd046c-80c4-4e17-b56b-650038289a96",{"id":1307,"createTime":20,"updateTime":20,"relativeEntities":1309,"slug":20,"properties":1310,"entityType":20,"verifyStatus":20,"verifyTime":20,"verifyNote":20,"languages":20,"translateLanguages":20,"viewCount":20,"url":20,"parentIds":1313,"statistic":20},[],{"title":1311},{"EN":1312},"From the Indiana University Medical Center and Walther Cancer Institute, Indianapolis, IN; Dana-Farber Cancer Institute, Boston, MA; Northwestern University, Chicago, IL; University of Pennsylvania, Philadelphia, PA; and University of Wisconsin, Madison, WI.",[],{"orcid":1315,"title":1317,"openalex":1319},{"VOID":1316},"https:\u002F\u002Forcid.org\u002F0000-0001-7903-9706",{"EN":1318},"Stuart Hinton",{"VOID":1320},"A5024682890",{"id":1322,"sortIndex":259,"researcher":20,"roles":1323,"affiliations":1324,"properties":1331,"displayName":1335,"givenName":20,"familyName":20},"8a2bdbad-632f-4b5d-a5ea-64181bc76710",[],[1325],{"id":1307,"sortIndex":21,"affiliation":1326,"properties":20},{"id":1307,"createTime":20,"updateTime":20,"relativeEntities":1327,"slug":20,"properties":1328,"entityType":20,"verifyStatus":20,"verifyTime":20,"verifyNote":20,"languages":20,"translateLanguages":20,"viewCount":20,"url":20,"parentIds":1330,"statistic":20},[],{"title":1329},{"EN":1312},[],{"orcid":1332,"title":1334,"openalex":1336},{"VOID":1333},"https:\u002F\u002Forcid.org\u002F0000-0002-1105-8852",{"EN":1335},"Paul J. 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Clin Cancer Res 3:  2630,1997-2632,",{},{"id":20,"text":1489,"url":20,"identifiers":1490},"10.1056\u002FNEJM199707243370406",{"doi":1489},{"id":20,"text":1492,"url":20,"identifiers":1493},"10.1200\u002FJCO.1998.16.7.2500",{"doi":1492},{"id":20,"text":1495,"url":20,"identifiers":1496},"10.1200\u002FJCO.1989.7.7.932",{"doi":1495},{"id":20,"text":1498,"url":20,"identifiers":1499},"10.1200\u002FJCO.2000.18.19.3346",{"doi":1498},{"id":20,"text":1501,"url":20,"identifiers":1502},"10.1023\u002FA:1008286305312",{"doi":1501},{"id":20,"text":1504,"url":20,"identifiers":1505},"10.1200\u002FJCO.2000.18.6.1181",{"doi":1504},{"id":20,"text":1507,"url":20,"identifiers":1508},"Miller  JC,   Einhorn  LH:   Phase II study of daily oral etoposide in refractory germ cell tumors.  Semin Oncol 17:  36,1990-39,",{},{"id":20,"text":1510,"url":20,"identifiers":1511},"10.1200\u002FJCO.1994.12.11.2277",{"doi":1510},{"id":20,"text":1513,"url":20,"identifiers":1514},"10.1016\u002F1078-1439(95)00064-X",{"doi":1513},{"id":20,"text":1516,"url":20,"identifiers":1517},"10.1093\u002Foxfordjournals.annonc.a010473",{"doi":1516},{"id":20,"text":1519,"url":20,"identifiers":1520},"10.1002\u002F(SICI)1097-0142(19980401)82:7\u003C1381::AID-CNCR23>3.0.CO;2-1",{"doi":1519},{"id":20,"text":1522,"url":20,"identifiers":1523},"10.1200\u002FJCO.1999.17.2.509",{"doi":1522},{"id":20,"text":1525,"url":20,"identifiers":1526},"10.1200\u002FJCO.1999.17.2.512",{"doi":1525},{"id":20,"text":1528,"url":20,"identifiers":1529},"Einhorn  L,   Raghavan  D,   Kindler  H,  et al:   A phase I trial of gemcitabine plus paclitaxel combination therapy in patients with refractory solid tumors.  Proc Am Soc Clin Oncol 17:  207a,1998  (abstr 796)",{},{"id":20,"text":1531,"url":20,"identifiers":1532},"10.1016\u002F0197-2456(89)90015-9",{"doi":1531},{"id":20,"text":1534,"url":20,"identifiers":1535},"10.1056\u002FNEJM198706043162302",{"doi":1534},{"id":20,"text":1537,"url":20,"identifiers":1538},"10.7326\u002F0003-4819-109-7-540",{"doi":1537},{"id":20,"text":1540,"url":20,"identifiers":1541},"10.1200\u002FJCO.1998.16.4.1287",{"doi":1540},{"id":20,"text":1543,"url":20,"identifiers":1544},"10.1200\u002FJCO.2000.18.6.1173",{"doi":1543},{"id":20,"text":1546,"url":20,"identifiers":1547},"10.1200\u002FJCO.2000.18.12.2413",{"doi":1546},{"id":20,"text":1549,"url":20,"identifiers":1550},"Pizzocaro  G,   Nicolai  N,   Salvioni  R,  et al:   Paclitaxel, cisplatin, gemcitabine (TPG) third line therapy in metastatic germ cell tumors (GCT) of the testis.  Proc Am Soc Clin Oncol 20:  194a,2001  (abstr 773)",{},{"id":20,"text":1552,"url":20,"identifiers":1553},"Hartmann  J,   Schleucher  N,   Metzner  B,  et al:   Phase I\u002FII study of sequential high dose VIP plus paclitaxel (T) in patients (pts) with ’poor prognosis’ germ cell tumor (GCT).  Proc Am Soc Clin Oncol 20:  173a,2001  (abstr 691)",{},{"id":20,"text":1555,"url":20,"identifiers":1556},"Cebotaru  C,   Todor  N,   Iancu  D,  et al:   Phase II paclitaxel, ifosfamide and cisplatin as first-line chemotherapy in high risk germ cell tumours.  Proc Am Soc Clin Oncol 20:  194a,2001  (abstr 775)",{},{"id":1558,"createTime":1559,"updateTime":1560,"relativeEntities":1561,"slug":1562,"properties":1563,"entityType":233,"verifyStatus":234,"verifyTime":1578,"verifyNote":235,"languages":1579,"translateLanguages":20,"viewCount":21,"primaryUrl":1580,"fullTextUrl":20,"authors":1581,"publicationType":355,"publisherRelationship":1821,"citationCount":1879,"citationInfo":1880,"publishDate":1883,"publishYear":1881,"citationAnalyzeStatus":19,"lastCitationAnalyze":1884,"indexDatabases":1885,"openAccess":20,"references":1886,"isForceReanalyzing":525},"66d0cbad-b165-43cc-814b-0e80929b7c50","2024-09-12T07:17:14.999+00:00","2026-07-14T04:59:35.444+00:00",[],"Topotecan-versus-paclitaxel-for-the-treatment-of-recurrent-epithelial-ovarian-cancer-",{"mag":1564,"gsPaper":1566,"openalex":1568,"abstract":1570,"title":1572,"pm":1574,"doi":1576},{"VOID":1565},"1913802169",{"VOID":1567},"[\"8187434381318355020\"]",{"VOID":1569},"W1913802169",{"EN":1571},"\u003Cjats:sec>\u003Cjats:title>PURPOSE\u003C\u002Fjats:title>\u003Cjats:p> Topotecan and paclitaxel were evaluated in a randomized, multicenter study of patients with advanced epithelial ovarian carcinoma who had progressed during or after one platinum-based regimen. \u003C\u002Fjats:p>\u003C\u002Fjats:sec>\u003Cjats:sec>\u003Cjats:title>PATIENTS AND METHODS\u003C\u002Fjats:title>\u003Cjats:p> Patients received either topotecan (1.5 mg\u002Fm2) as a 30-minute infusion daily for 5 days every 21 days (n = 112) or paclitaxel (175 mg\u002Fm2) infused over 3 hours every 21 days (n = 114). Patients had bidimensionally measurable disease and were assessed for efficacy and toxicity. \u003C\u002Fjats:p>\u003C\u002Fjats:sec>\u003Cjats:sec>\u003Cjats:title>RESULTS\u003C\u002Fjats:title>\u003Cjats:p> Response rate was 23 of 112 (20.5%) in topotecan-treated patients and 15 of 114 (13.2%) in paclitaxel-treated patients (P = .138). Disease stabilization for at least 8 weeks was noted in 30% of patients with topotecan and 33% of patients with paclitaxel. Median durations of response to topotecan and paclitaxel were 32 and 20 weeks, respectively (P = .222) and median times to progression were 23 and 14 weeks, respectively (P = .002). Median survival was 61 weeks for topotecan and 43 weeks for paclitaxel (P = .515). Response rates for topotecan and paclitaxel were 13.3% versus 6.7% (P = .303) in resistant patients (not responded to prior platinum-based therapy or progressed within 6 months of an initial response) and 28.8% versus 20.0% (P = .213) in sensitive patients (progressed > 6 months after response). Neutropenia was significantly more frequent on the topotecan arm 79% versus paclitaxel arm 23% (P < .01). It was short-lasting and noncumulative in both arms. 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Medical records and standardized self-report measures were maintained prospectively. After 10 years, 137 survivors and nontransplant controls, case-matched on age, sex, and race, completed self-report of medical problems, symptoms, and health-related quality of life.\u003C\u002Fjats:p>\u003C\u002Fjats:sec>\u003Cjats:sec>\u003Cjats:title>Results\u003C\u002Fjats:title>\u003Cjats:p>Survivors and controls had similar rates of hospitalization and most diseases, but survivors reported an average of 3.5 medical problems versus 1.7 for controls (P < .001). Survivors reported more musculoskeletal stiffness, cramps, weakness and joint swelling (P < .001), cataract surgery (P < .001), hepatitis C (P = .004), sexual problems for men (P = .01) and women (P < .001), restrictions in social function (P = .002), memory and attention concerns (P = .003), urinary frequency or leaking (P = .006), use of psychotropic medication (P = .009), and denial of life and health insurance (P < .001). 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Medical records of all members of the cohort were abstracted to obtain chemotherapeutic agents administered; the cumulative dose of drug administered for several drugs of interest; and the doses, volumes, and dates of administration of all radiation therapy. \u003C\u002Fjats:p>\u003C\u002Fjats:sec>\u003Cjats:sec>\u003Cjats:title>Results\u003C\u002Fjats:title>\u003Cjats:p> There were 5,149 female CCSS participants, and there were 1,441 female siblings of CCSS participants who were age 15 to 44 years. The relative risk (RR) for survivors of ever being pregnant was 0.81 (95% CI, 0.73 to 0.90; P < .001) compared with female siblings. In multivariate models among survivors only, those who received a hypothalamic\u002Fpituitary radiation dose ≥ 30 Gy (RR, 0.61; 95% CI, 0.44 to 0.83) or an ovarian\u002Futerine radiation dose greater than 5 Gy were less likely to have ever been pregnant (RR, 0.56 for 5 to 10 Gy; 95% CI, 0.37 to 0.85; RR, 0.18 for > 10 Gy; 95% CI, 0.13 to 0.26). Those with a summed alkylating agent dose (AAD) score of three or four or who were treated with lomustine or cyclophosphamide were less likely to have ever been pregnant. \u003C\u002Fjats:p>\u003C\u002Fjats:sec>\u003Cjats:sec>\u003Cjats:title>Conclusion\u003C\u002Fjats:title>\u003Cjats:p> This large study demonstrated that fertility is decreased among female CCSS participants. 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LBA8002 \u003C\u002Fjats:p>\u003Cjats:p> Background: B when added to chemotherapy, and E alone, each lead to improved survival in the treatment of patients (pts) with NSCLC (Sandler et al, NEJM 2006, 355:2542–2550; Shepherd et al, NEJM 2005, 353:123–132). Pre-clinical and clinical data (Herbst, J Clin Oncol 2007, 25: 4743–4750) suggest that the combination of B and E may improve the efficacy of NSCLC treatment. This potential was demonstrated in the BETA (B in combination with E compared with E alone for treatment of advanced NSCLC after failure of standard first-line chemotherapy) trial, a phase III trial in which progression free survival (PFS) was improved for patients treated with B + E (Hainsworth, Thoracic Oncol 2008, 3(11) Supp. 4:S302). Methods: The ATLAS study was designed to evaluate B + E (150 mg daily) versus B alone, following B + platin-containing doublet chemotherapy, in pts with stage IIIb\u002FIV NSCLC. Enrolled pts were B-eligible, including pts with treated brain metastases, and pts anticoagulated with low molecular weight heparin(s). Pts with peripheral and\u002For extra-thoracic squamous tumors were also eligible. Pts received 4 cycles of B (15 mg\u002Fkg every 3 weeks) with chemotherapy. Pts who had not experienced disease progression (DP) or significant toxicity were then randomized to receive B + E or B + placebo (P). The primary objective of ATLAS was to compare PFS in pts receiving B + E versus B + placebo. Secondary objectives included the assessment of safety, and overall survival. A data safety monitoring committee (DSMC) monitored safety and efficacy. Results: 1,160 patients were enrolled and 768 randomized from May 2005 to May 2008. The DSMC recommended stopping the trial at the second planned interim efficacy analysis, because it met the primary endpoint. The median PFS after randomization was 4.8 mos for (B + E) vs. 3.7 mos for (B + P), HR= 0.722 (95% CI: 0.592–0.881), p = 0.0012. The safety profile for B + E was consistent with known profiles for B and E. Conclusions: E added to B treatment after chemotherapy with B significantly improves the PFS of patients treated in the first-line setting for locally advanced, recurrent, or metastatic NSCLC. \u003C\u002Fjats:p>\u003Cjats:p> [Table: see text] \u003C\u002Fjats:p>",{"EN":2730},"A randomized, double-blind, placebo-controlled, phase IIIb trial (ATLAS) comparing bevacizumab (B) therapy with or without erlotinib (E) after completion of chemotherapy with B for first-line treatment of locally advanced, recurrent, or metastatic non-small cell lung cancer (NSCLC)",{"VOID":536},{"VOID":2733},"10.1200\u002Fjco.2009.27.18_suppl.lba8002",[237],"https:\u002F\u002Fascopubs.org\u002Fdoi\u002F10.1200\u002Fjco.2009.27.18_suppl.lba8002",[2737,2754,2769,2784],{"id":2738,"sortIndex":21,"researcher":20,"roles":2739,"affiliations":2740,"properties":2749,"displayName":2751,"givenName":20,"familyName":20},"722871e0-4ac4-4be1-b77f-6284df5ced18",[],[2741],{"id":2742,"sortIndex":21,"affiliation":2743,"properties":20},"6088d706-6863-4957-b146-9f4c2af23eda",{"id":2742,"createTime":20,"updateTime":20,"relativeEntities":2744,"slug":20,"properties":2745,"entityType":20,"verifyStatus":20,"verifyTime":20,"verifyNote":20,"languages":20,"translateLanguages":20,"viewCount":20,"url":20,"parentIds":2748,"statistic":20},[],{"title":2746},{"EN":2747},"Memorial Sloan-Kettering Cancer Center, New York, NY; Genentech, Inc., South San Francisco, CA; University of California, Los Angeles, Los Angeles, CA",[],{"title":2750,"openalex":2752},{"EN":2751},"V. 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10 \u003C\u002Fjats:p>\u003Cjats:p> Background: Multiple randomized phase II trials suggest that metastasis-directed therapy (MDT) for oligometastatic prostate cancer (PCa) improves progression-free survival, but the majority of trials lack longer follow-up. We present the updated 5-year results from the STOMP-trial. Methods: In this multicentre, randomised, phase II study, asymptomatic PCa patients were eligible in case of a biochemical recurrence following primary PCa treatment with curative intent and presenting with up to 3 extracranial on choline PET-CT and a serum testosterone levels > 50 ng\u002Fml. Patients were randomly assigned (1:1) to either surveillance or MDT of all detected lesions. Randomisation was balanced dynamically on two factors: PSA doubling time (≤3 vs. > 3 months) and nodal vs non-nodal metastases. The primary endpoint was androgen deprivation therapy (ADT)-free survival. Castrate resistant prostate cancer-free survival (CRPC) was a secondary endpoint. Tests were performed two-sided; p values less than 0.20 were deemed significant. Results: The 5-year ADT-free survival was 8% for the surveillance group and 34% for the MDT group (Figure 1, hazard ratio 0.57 [80% CI: 0.38-0.84], log-rank p = 0.06). There was no significant difference in effect for the different stratification factors (interaction test). The 5-year CRPC-free survival was 53% for the surveillance group and 76% for the MDT group (hazard ratio 0.62 [80% CI: 0.35−1.09]; log−rank p = 0.27). At a median follow for survival of 5.3 years (IQR 4.3-6.3), the 5-year overall survival was 85%, with 6 out of 14 deaths attributed to prostate cancer. Conclusions: The updated STOMP trial outcomes confirm the earlier reported significant difference in ADT free survival in favor of the MDT group compared to surveillance. Prostate-cancer related mortality is low within the first 5 years of diagnosis of oligorecurrent prostate cancer. 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To evaluate and compare psychological outcomes in long-term survivors of pediatric brain cancer and siblings of childhood cancer survivors, and to identify significant correlates of psychological distress. \u003C\u002Fjats:p>\u003C\u002Fjats:sec>\u003Cjats:sec>\u003Cjats:title>Methods\u003C\u002Fjats:title>\u003Cjats:p> One thousand one hundred one adult survivors of childhood brain cancer and 2,817 siblings completed a long-term follow-up questionnaire allowing assessment of symptoms associated with depression, somatization, and anxiety, as well as demographic, health, and medical information. \u003C\u002Fjats:p>\u003C\u002Fjats:sec>\u003Cjats:sec>\u003Cjats:title>Results\u003C\u002Fjats:title>\u003Cjats:p> A large majority of siblings and survivors report few, if any, symptoms of psychological distress. The prevalence of distress approximating clinically significant levels for both survivors (11%) and siblings (5%) reflects rates found in the general population. Yet when accounting for significant sociodemographic, socioeconomic, and health-status variables, survivors of childhood brain cancer, in the aggregate, appear to report significantly higher global distress and depression scores than do siblings. As in the general population, higher levels of distress among survivors and siblings were associated with female sex, low household income, lower educational attainment, being unmarried, not being employed in the past 12 months, and poor physical health status. No diagnostic or treatment-related variables were directly and significantly associated with increases in distress symptoms for survivors of childhood brain cancer. \u003C\u002Fjats:p>\u003C\u002Fjats:sec>\u003Cjats:sec>\u003Cjats:title>Conclusion\u003C\u002Fjats:title>\u003Cjats:p> Cancer treatment does not appear to contribute directly to increased psychological distress. Instead, distress appears to be associated with diminished social functioning that may be related to cancer type or treatment. 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