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Статті в журналах з теми "Cancer identity"

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Автор: Grafiati

Опубліковано: 10 грудня 2022

Оновлено: 28 січня 2023

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1

Mathieson, Cynthia M., and Henderikus J. Stam. "Renegotiating identity: cancer narratives." Sociology of Health and Illness 17, no. 3 (June 1995): 283–306. http://dx.doi.org/10.1111/1467-9566.ep10933316.

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2

Male, Dana A., Karen D. Fergus, and Kimberley Cullen. "Sexual identity after breast cancer." Current Opinion in Supportive and Palliative Care 10, no. 1 (March 2016): 66–74. http://dx.doi.org/10.1097/spc.0000000000000184.

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3

Kiberstis, Paula A. "Evading cancer drugs by identity fraud." Science 355, no. 6320 (January 5, 2017): 35.16–37. http://dx.doi.org/10.1126/science.355.6320.35-p.

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4

Wou, C., N. Chaston, and S. Doughan. "Mistaken identity: endometrial or rectal cancer?" Case Reports 2014, may20 1 (May 20, 2014): bcr2013202874. http://dx.doi.org/10.1136/bcr-2013-202874.

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5

Roy, Nilotpal, and Matthias Hebrok. "Regulation of Cellular Identity in Cancer." Developmental Cell 35, no. 6 (December 2015): 674–84. http://dx.doi.org/10.1016/j.devcel.2015.12.001.

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6

Ruffenach, G., S. Bonnet, S. Rousseaux, S. Khochbin, S. Provencher, and F. Perros. "Identity crisis in pulmonary arterial hypertension." Pulmonary Circulation 8, no. 1 (December 5, 2017): 204589321774605. http://dx.doi.org/10.1177/2045893217746054.

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Pulmonary arterial hypertension (PAH) shares many hallmarks with cancer. Cancer cells acquire their hallmarks by a pathological Darwinian evolution process built on the so-called cancer cell “identity crisis.” Here we demonstrate that PAH shares the most striking features of the cancer identity crisis: the ectopic expression of normally silent tissue-specific genes.

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7

Sehjae Chun. "Identity Excised: Mastectomy and Women’s Identity in Audre Lorde’s The Cancer Journals." English & American Cultural Studies 9, no. 2 (August 2009): 185–206. http://dx.doi.org/10.15839/eacs.9.2.200908.185.

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8

Cheung, Sze Yan, and Paul Delfabbro. "Are you a cancer survivor? A review on cancer identity." Journal of Cancer Survivorship 10, no. 4 (February 11, 2016): 759–71. http://dx.doi.org/10.1007/s11764-016-0521-z.

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9

Huang, Qin, Matthew Read, Jason S. Gold, and Xiao Ping Zou. "Unraveling the identity of gastric cardiac cancer." Journal of Digestive Diseases 21, no. 12 (October 28, 2020): 674–86. http://dx.doi.org/10.1111/1751-2980.12945.

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10

Kiberstis, P. A. "Clues to cancer from an identity change." Science 352, no. 6293 (June 23, 2016): 1530–32. http://dx.doi.org/10.1126/science.352.6293.1530-q.

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11

Gavaghan, Mary P., and Jane E. Roach. "Ego Identity Development of Adolescents with Cancer." Journal of Pediatric Psychology 12, no. 2 (1987): 203–13. http://dx.doi.org/10.1093/jpepsy/12.2.203.

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12

Madan-Swain, A. "Identity in Adolescent Survivors of Childhood Cancer." Journal of Pediatric Psychology 25, no. 2 (March 1, 2000): 105–15. http://dx.doi.org/10.1093/jpepsy/25.2.105.

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13

Maliski, Sally L., Steve Rivera, Sarah Connor, Griselda Lopez, and Mark S. Litwin. "Renegotiating Masculine Identity After Prostate Cancer Treatment." Qualitative Health Research 18, no. 12 (December 2008): 1609–20. http://dx.doi.org/10.1177/1049732308326813.

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Because little is known about how low-income Latino and African American men attribute meaning and adapt to prostate cancer treatment —related symptoms relative to masculine identity, in this study we sought to develop a descriptive model of this process. Using qualitative methods, 60 Latino and 35 African American/Black men were interviewed by language- and ethnicity-matched male interviewers using a semistructured guide. Interviews were audiotaped and transcribed verbatim. Spanish transcripts were rigorously translated to produce English transcripts. Analysis using grounded theory techniques found that men constructed masculine identities that were influenced by early experience, challenged by several factors including prostate cancer treatment, and underwent a renegotiation process that resulted in the maintenance of their identity as men. Development and testing of interventions that support this process will facilitate the adaptation process for men in a culturally relevant manner.

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14

Knapp, Sarah, Allison Marziliano, and Anne Moyer. "Identity threat and stigma in cancer patients." Health Psychology Open 1, no. 1 (September 30, 2014): 205510291455228. http://dx.doi.org/10.1177/2055102914552281.

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15

Clark, Amander T. "The Stem Cell Identity of Testicular Cancer." Stem Cell Reviews 3, no. 1 (July 3, 2007): 49–59. http://dx.doi.org/10.1007/s12015-007-0002-x.

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16

Zebrack, Brad J. "Cancer Survivor Identity and Quality of Life." Cancer Practice 8, no. 5 (September 2000): 238–42. http://dx.doi.org/10.1046/j.1523-5394.2000.85004.x.

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17

Tabaac, Ariella R., Megan E. Sutter, Catherine S. J. Wall, and Kellan E. Baker. "Gender Identity Disparities in Cancer Screening Behaviors." American Journal of Preventive Medicine 54, no. 3 (March 2018): 385–93. http://dx.doi.org/10.1016/j.amepre.2017.11.009.

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18

Carstens, Julienne L., Sujuan Yang, Pedro Correa de Sampaio, Xiaofeng Zheng, Souptik Barua, Kathleen M. McAndrews, Arvind Rao, Jared K. Burks, Andrew D. Rhim, and Raghu Kalluri. "Abstract PO-059: Epithelial/mesenchymal identity dictates pancreatic cancer cell metastasis." Cancer Research 81, no. 22_Supplement (November 15, 2021): PO—059—PO—059. http://dx.doi.org/10.1158/1538-7445.panca21-po-059.

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Abstract Metastatic pancreatic adenocarcinoma (PDAC) is the dominant clinical presentation and highly treatment-resistant. However, not all metastasis is equal with metastatic disease in the lung having improved outcomes over the liver. These clinical differences suggest a therapeutic opportunity and urge analysis of the molecular underpinnings of PDAC metastasis. The acquisition of mesenchymal features by epithelial cancer cells is commonly associated with solid tumor metastasis and has been linked to the pancreatic cancer basal subtype and its association with treatment resistance and poorer outcomes, but its impact on pancreatic cancer metastasis needs further understanding. We explored the impact on metastasis of stabilized epithelial, partial-mesenchymal and mesenchymal cancer cells by generating several genetic mouse models based on the lineage-traced KPC mouse model (KrasLSL-G12D;p53R172H; or p53LSL; PDX1-Cre;EYFPLSL). Using single-cell RNA-sequencing we confirmed the KPC mouse model recapitulates the spectrum of epithelial-mesenchymal phenotypes observed in patients and can be genetically engineered to stabilize specific phenotypes. The stabilization of epithelial phenotypes through the homozygous loss of the mesenchymal-driving transcription factors Snail and Twist (Snai1F/F;Twist1F/F) had no impact on primary tumor progression but increased liver colonization. This increase in liver colonization was supported by a second epithelial-stabilized mouse model based on the loss of Zeb1 (Zeb1F/F). The stabilization of mesenchymal features through the heterozygous or homozygous loss of the epithelial adherin junction E-cadherin (Cdh1F/+ or Cdh1F/F) promoted lung metastasis. Interestingly, epithelial plasticity was still required for efficient lung colonization, but not rare liver metastasis. Additionally, mesenchymal gene expression correlated with an improved patient survival as well as metastatic localization, supporting the clinical observations of improved survival in lung metastasis. Using gene expression analysis of sorted bulk cancer cells and single-cells, migration assays, and multiplexed-immunohistochemistry, we observed that the epithelial/mesenchymal status of the cancer cells dictated different mechanisms for motility and interaction with the immune system. Mesenchymal cancer cells migrate as single-cells and attract fewer T-cells where epithelial cancer cells migrate collectively and have increased immune regulation gene expression. These data suggest the epithelial/mesenchymal status of cancers cells dictate the where and how of metastatic disease and could inform therapeutic interventions. Citation Format: Julienne L. Carstens, Sujuan Yang, Pedro Correa de Sampaio, Xiaofeng Zheng, Souptik Barua, Kathleen M. McAndrews, Arvind Rao, Jared K. Burks, Andrew D. Rhim, Raghu Kalluri. Epithelial/mesenchymal identity dictates pancreatic cancer cell metastasis [abstract]. In: Proceedings of the AACR Virtual Special Conference on Pancreatic Cancer; 2021 Sep 29-30. Philadelphia (PA): AACR; Cancer Res 2021;81(22 Suppl):Abstract nr PO-059.

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19

Smith, Zyoud, and Allegrucci. "A Case of Identity: HOX Genes in Normal and Cancer Stem Cells." Cancers 11, no. 4 (April 10, 2019): 512. http://dx.doi.org/10.3390/cancers11040512.

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Stem cells are undifferentiated cells that have the unique ability to self-renew and differentiate into many different cell types. Their function is controlled by core gene networks whose misregulation can result in aberrant stem cell function and defects of regeneration or neoplasia. HOX genes are master regulators of cell identity and cell fate during embryonic development. They play a crucial role in embryonic stem cell differentiation into specific lineages and their expression is maintained in adult stem cells along differentiation hierarchies. Aberrant HOX gene expression is found in several cancers where they can function as either oncogenes by sustaining cell proliferation or tumor-suppressor genes by controlling cell differentiation. Emerging evidence shows that abnormal expression of HOX genes is involved in the transformation of adult stem cells into cancer stem cells. Cancer stem cells have been identified in most malignancies and proved to be responsible for cancer initiation, recurrence, and metastasis. In this review, we consider the role of HOX genes in normal and cancer stem cells and discuss how the modulation of HOX gene function could lead to the development of novel therapeutic strategies that target cancer stem cells to halt tumor initiation, progression, and resistance to treatment.

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20

Park, Crystal L., Ianita Zlateva, and Thomas O. Blank. "Self-identity After Cancer: “Survivor”, “Victim”, “Patient”, and “Person with Cancer”." Journal of General Internal Medicine 24, S2 (October 18, 2009): 430–35. http://dx.doi.org/10.1007/s11606-009-0993-x.

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21

Bellizzi, Keith M., and Thomas O. Blank. "Cancer-related identity and positive affect in survivors of prostate cancer." Journal of Cancer Survivorship: Research and Practice 1, no. 1 (January 30, 2007): 44–48. http://dx.doi.org/10.1007/s11764-007-0005-2.

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22

Alpert, Ash B., George A. Komatsoulis, Stephen C. Meersman, Elizabeth Garrett-Mayer, Suanna S. Bruinooge, Robert S. Miller, Danielle Potter, Becky Koronkowski, Edward Stepanski, and Don S. Dizon. "Identification of Transgender People With Cancer in Electronic Health Records: Recommendations Based on CancerLinQ Observations." JCO Oncology Practice 17, no. 3 (March 2021): e336-e342. http://dx.doi.org/10.1200/op.20.00634.

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PURPOSE: Cancer prevalence and outcomes data, necessary to understand disparities in transgender populations, are significantly hampered because gender identity data are not routinely collected. A database of clinical data on people with cancer, CancerLinQ, is operated by the ASCO and collected from practices across the United States and multiple electronic health records. METHODS: To attempt to identify transgender people with cancer within CancerLinQ, we used three criteria: (1) International Classification of Diseases 9/10 diagnosis (Dx) code suggestive of transgender identity; (2) male gender and Dx of cervical, endometrial, ovarian, fallopian tube, or other related cancer; and (3) female gender and Dx of prostate, testicular, penile, or other related cancer. Charts were abstracted to confirm transgender identity. RESULTS: Five hundred fifty-seven cases matched inclusion criteria and two hundred and forty-two were abstracted. Seventy-six percent of patients with Dx codes suggestive of transgender identity were transgender. Only 2% and 3% of the people identified by criteria 2 and 3 had evidence of transgender identity, respectively. Extrapolating to nonabstracted data, we would expect to identify an additional four individuals in category 2 and an additional three individuals in category 3, or a total of 44. The total population in CancerLinQ is approximately 1,300,000. Thus, our methods could identify 0.003% of the total population as transgender. CONCLUSION: Given the need for data regarding transgender people with cancer and the deficiencies of current data resources, a national concerted effort is needed to prospectively collect gender identity data. These efforts will require systemic efforts to create safe healthcare environments for transgender people.

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23

Stringer-Reasor, Erica M., Ahmed Elkhanany, Katia Khoury, Melissa A. Simon, and Lisa A. Newman. "Disparities in Breast Cancer Associated With African American Identity." American Society of Clinical Oncology Educational Book, no. 41 (June 2021): e29-e46. http://dx.doi.org/10.1200/edbk_319929.

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Persistent disparities in the burden of breast cancer between African Americans and White Americans have been documented over many decades. Features characterizing breast cancer in the African American community include a 40% higher mortality rate, younger age distribution, greater advanced-stage distribution, increased risk of biologically aggressive disease such as the triple-negative phenotype, and increased incidence of male breast cancer. Public health experts, genetics researchers, clinical trialists, multidisciplinary oncology teams, and advocates must collaborate to comprehensively address the multifactorial etiology of and remedies for breast cancer disparities. Efforts to achieve breast health equity through improved access to affordable, high-quality care are especially imperative in the context of the COVID-19 pandemic and its disproportionately high economic toll on African Americans.

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24

Shapiro, Sharon, Lynne Angus, and Christine Davis. "Identity and Meaning in the Experience of Cancer." Journal of Health Psychology 2, no. 4 (October 1997): 539–54. http://dx.doi.org/10.1177/135910539700200410.

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25

Dolgin, Elie. "Venerable brain-cancer cell line faces identity crisis." Nature 537, no. 7619 (August 31, 2016): 149–50. http://dx.doi.org/10.1038/nature.2016.20515.

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26

Deimling, Gary T., Karen F. Bowman, and Louis J. Wagner. "Cancer Survivorship and Identity among Long-Term Survivors." Cancer Investigation 25, no. 8 (January 2007): 758–65. http://dx.doi.org/10.1080/07357900600896323.

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27

Sullivan, James P., and John D. Minna. "Tumor Oncogenotypes and Lung Cancer Stem Cell Identity." Cell Stem Cell 7, no. 1 (July 2010): 2–4. http://dx.doi.org/10.1016/j.stem.2010.06.005.

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28

Dalerba, Piero. "The Dynamic Identity of Intestinal Cancer Stem Cells." Cell Stem Cell 20, no. 6 (June 2017): 743–45. http://dx.doi.org/10.1016/j.stem.2017.05.018.

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29

Incrocci, L. "Male identity, couple sexual satisfaction and genital cancer." Sexologies 17 (April 2008): S24. http://dx.doi.org/10.1016/s1158-1360(08)72570-2.

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30

Lee, Gregory, Emily Laflamme, Chin-Hsiang Chien, and Hong Hoi Ting. "Molecular identity of a pan cancer marker, CA215." Cancer Biology & Therapy 7, no. 12 (December 2008): 2007–14. http://dx.doi.org/10.4161/cbt.7.12.6984.

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31

Trusson, Diane, and Alison Pilnick. "The Role of Hair Loss in Cancer Identity." Cancer Nursing 40, no. 2 (2017): E9—E16. http://dx.doi.org/10.1097/ncc.0000000000000373.

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32

Jahangiri, Leila, Loukia Tsaprouni, Ricky M. Trigg, John A. Williams, Georgios V. Gkoutos, Suzanne D. Turner, and Joao Pereira. "Core regulatory circuitries in defining cancer cell identity across the malignant spectrum." Open Biology 10, no. 7 (July 2020): 200121. http://dx.doi.org/10.1098/rsob.200121.

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Gene expression programmes driving cell identity are established by tightly regulated transcription factors that auto- and cross-regulate in a feed-forward manner, forming core regulatory circuitries (CRCs). CRC transcription factors create and engage super-enhancers by recruiting acetylation writers depositing permissive H3K27ac chromatin marks. These super-enhancers are largely associated with BET proteins, including BRD4, that influence higher-order chromatin structure. The orchestration of these events triggers accessibility of RNA polymerase machinery and the imposition of lineage-specific gene expression. In cancers, CRCs drive cell identity by superimposing developmental programmes on a background of genetic alterations. Further, the establishment and maintenance of oncogenic states are reliant on CRCs that drive factors involved in tumour development. Hence, the molecular dissection of CRC components driving cell identity and cancer state can contribute to elucidating mechanisms of diversion from pre-determined developmental programmes and highlight cancer dependencies. These insights can provide valuable opportunities for identifying and re-purposing drug targets. In this article, we review the current understanding of CRCs across solid and liquid malignancies and avenues of investigation for drug development efforts. We also review techniques used to understand CRCs and elaborate the indication of discussed CRC transcription factors in the wider context of cancer CRC models.

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33

Dalton, Kathryn L., Sheila N. Garland, Peggy Miller, Bret Miller, Cheri Ambrose, and Richard J. Wassersug. "Factors Associated with “Survivor Identity” in Men with Breast Cancer." Current Oncology 28, no. 3 (April 30, 2021): 1696–705. http://dx.doi.org/10.3390/curroncol28030158.

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Cancer patients vary in their comfort with the label “survivor”. Here, we explore how comfortable males with breast cancer (BC) are about accepting the label cancer “survivor”. Separate univariate logistic regressions were performed to assess whether time since diagnosis, age, treatment status, and cancer stage were associated with comfort with the “survivor” label. Of the 70 males treated for BC who participated in the study, 58% moderately-to-strongly liked the term “survivor”, 26% were neutral, and 16% moderately-to-strongly disliked the term. Of the factors we explored, only a longer time since diagnosis was significantly associated with the men endorsing a survivor identity (OR = 1.02, p = 0.05). We discuss how our findings compare with literature reports on the comfort with the label “survivor” for women with BC and men with prostate cancer. Unlike males with prostate cancer, males with BC identify as “survivors” in line with women with BC. This suggests that survivor identity is more influenced by disease type and treatments received than with sex/gender identities.

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34

Alpert, Ash, Suanna S. Bruinooge, Don S. Dizon, Becky Koronkowski, Elizabeth Garrett-Mayer, Stephen C. Meersman, Robert S. Miller, Danielle Potter, and George Anthony Komatsoulis. "Identification of transgender people with cancer in electronic health records (EHR): Recommendations based on CancerLinQ observations." Journal of Clinical Oncology 38, no. 15_suppl (May 20, 2020): e19046-e19046. http://dx.doi.org/10.1200/jco.2020.38.15_suppl.e19046.

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e19046 Background: Data regarding people who are gender minorities are not well-captured in oncology practices or large cohorts. Given this, collection of cancer prevalence and outcomes data, which are necessary to understand disparities in this population, are significantly hampered. Real-world data may be the most readily available source to explore outcomes in transgender populations. A database of EHR data on people with cancer, CancerLinQ is housed by the American Society of Clinical Oncology and collected from nation-wide practices and multiple EHRs. Methods: In order to identify people with cancer who may be transgender within CancerLinQ, we used three criteria: 1. ICD 9/10 diagnosis (Dx) code indicating likely transgender or non-binary gender conforming status 2. Male gender and Dx of cervical, endometrial, ovarian, or Fallopian tube cancers 3. Female gender and Dx of prostate, testicular, or penile cancers . We reviewed medical records for gender, cancer diagnosis, Dx indicating transgender identity and surgical history of transition-related surgeries, in other words surgeries that align bodies with identities and constructed a de-identified dataset of people who met one of the three criteria listed above. People without evidence of transgender identity were assigned as: (1) likely Dx error, because the person had either (a) no cancer, (b) an alternate cancer Dx consistent with sex assigned at birth, or (c) a cancer not listed in the above criteria (e.g. lung); or (2) likely error in gender data, if the cancer Dx was confirmed, but gender data was not; or (3) unknown. Results: Of ~1.3 million records in CancerLinQ at time of case selection, 557 matched inclusion criteria and 242 were abstracted. 76% of patients with ICD9/10 gender related Dx codes had evidence confirming transgender identity. By contrast, only 2% and 3% of the people identified by criteria 2 and 3 had evidence of transgender identity, respectively. Conclusions: Given the need for data regarding transgender people with cancer and the deficiencies of current data resources, a national concerted effort is needed to broaden terminology in EHRs to include whether people are transgender or not as routine and required data elements, provided by patients at their discretion. [Table: see text]

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35

He, Ruicen, Arthur Dantas, and Karl Riabowol. "Histone Acetyltransferases and Stem Cell Identity." Cancers 13, no. 10 (May 17, 2021): 2407. http://dx.doi.org/10.3390/cancers13102407.

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Acetylation of histones is a key epigenetic modification involved in transcriptional regulation. The addition of acetyl groups to histone tails generally reduces histone-DNA interactions in the nucleosome leading to increased accessibility for transcription factors and core transcriptional machinery to bind their target sequences. There are approximately 30 histone acetyltransferases and their corresponding complexes, each of which affect the expression of a subset of genes. Because cell identity is determined by gene expression profile, it is unsurprising that the HATs responsible for inducing expression of these genes play a crucial role in determining cell fate. Here, we explore the role of HATs in the maintenance and differentiation of various stem cell types. Several HAT complexes have been characterized to play an important role in activating genes that allow stem cells to self-renew. Knockdown or loss of their activity leads to reduced expression and or differentiation while particular HATs drive differentiation towards specific cell fates. In this study we review functions of the HAT complexes active in pluripotent stem cells, hematopoietic stem cells, muscle satellite cells, mesenchymal stem cells, neural stem cells, and cancer stem cells.

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36

Alderton, Gemma K. "Luminal cells with an identity crisis." Nature Reviews Cancer 11, no. 3 (February 24, 2011): 159. http://dx.doi.org/10.1038/nrc3030.

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37

Pearson, Amy W. Farnbach, Shoshana Adler Jaffe, Lila A. Baca, Nina Dimauro, Kendal A. Jacobson, and Miria Kano. "Abstract B066: Rejection of cancer identity among sexual and gender minority patients." Cancer Epidemiology, Biomarkers & Prevention 32, no. 1_Supplement (January 1, 2023): B066. http://dx.doi.org/10.1158/1538-7755.disp22-b066.

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Abstract For sexual and gender minority (SGM) populations, minority stress exacerbates the physical and emotional challenges of cancer diagnosis, treatment and survivorship; mitigating these effects will require improved understanding of SGM individuals’ cancer experiences both within and beyond the clinic. Among SGM cancer health disparities are increased stress surrounding diagnosis and treatment and poorer post-treatment mental and overall health. Emotional distress accompanying significant or chronic diseases such as cancer results in part from the threat illness poses to personal identity, often leading to disruption and subsequent realignment of one’s self-conception to a “new normal” as a cancer patient or cancer survivor. However, the process of aligning multiple stigmatized identities, as when SGM individuals experience cancer, is relatively unexplored. To this end, transcripts of semi-structured interviews with 11 SGM cancer patients and 8 cisgender, heterosexual (CH) patients matched for sex assigned at birth and cancer type were coded for indicators of health and illness in personal identity. Codes included (1) assertion of prior healthy behavior, (2) rejection of cancer identity, and (3) assertion of cancer identity; these were not mutually exclusive. SGM patients were less likely than CH peers to report engaging in healthy behaviors (exercise, dietary choices): 4 of 11 (36%) SGM patients did so, compared with 7 of 8 CH patients (88%). In contrast, SGM patients were more likely to explicitly reject self-identification as a cancer patient or cancer survivor: this occurred in interviews with 7 of 11 (64%) SGM patients but only 2 of 8 (25%) CH patients. Assertion of cancer identity – either through self-identification with a survivor label or intentional disclosure to reduce cancer stigma or obtain formal health accommodations – did not differ among SGM and CH patients. Five of 11 (46%) SGM patients and 4 of 8 (50%) CH patients identified as a cancer patient or cancer survivor in these ways. Notably for this sample, compared with CH peers SGM cancer patients were both less likely to volunteer a history of engaging in healthy behaviors and more likely to explicitly reject personal identity as a cancer patient or cancer survivor. This may indicate reluctance on the part of already-minoritized individuals to take on additional stigmatized identities, or may represent particular difficulty faced by SGM cancer patients in realigning their personal identities to accommodate their illness experiences. The ways individuals with cancer navigate personal identity following diagnosis and treatment has implications for cancer survivorship care: some aspects of cancer survivor identity are associated with positive outcomes, including improved mental health, more positive engagement with peers, and better quality of life. Understanding the ways cancer shapes personal identity among SGM patients and other minoritized individuals may offer pathways to constructive emotional processing of cancer experiences to reduce post-treatment cancer health disparities. Citation Format: Amy W. Farnbach Pearson, Shoshana Adler Jaffe, Lila A. Baca, Nina Dimauro, Kendal A. Jacobson, Miria Kano. Rejection of cancer identity among sexual and gender minority patients [abstract]. In: Proceedings of the 15th AACR Conference on the Science of Cancer Health Disparities in Racial/Ethnic Minorities and the Medically Underserved; 2022 Sep 16-19; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2022;31(1 Suppl):Abstract nr B066.

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Campesino, Maureen, Delia S. Saenz, Myunghan Choi, and Robert S. Krouse. "Perceived Discrimination and Ethnic Identity Among Breast Cancer Survivors." Oncology Nursing Forum 39, no. 2 (February 28, 2012): E91—E100. http://dx.doi.org/10.1188/12.onf.e91-e100.

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Strach, Patricia. "Gender practice as political practice: cancer, culture, and identity." Politics, Groups and Identities 1, no. 2 (June 2013): 247–50. http://dx.doi.org/10.1080/21565503.2013.785970.

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Miller, Mark. "Identity and prostate cancer: Comments on a messy life." Journal of Gay & Lesbian Mental Health 9, no. 1 (2005): 119–29. http://dx.doi.org/10.1080/19359705.2005.9962400.

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Song, Hayeon, Yujung Nam, Jessica Gould, W. Scott Sanders, Margaret McLaughlin, Janet Fulk, Kathleen A. Meeske, and Kathleen S. Ruccione. "Cancer Survivor Identity Shared in a Social Media Intervention." Journal of Pediatric Oncology Nursing 29, no. 2 (March 2012): 80–91. http://dx.doi.org/10.1177/1043454212438964.

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